3.4.23.24 Acquired Immunodeficiency Syndrome https://pubmed.ncbi.nlm.nih.gov/7952656/ Structure-assisted design of nonpeptide human immunodeficiency virus-1 protease inhibitors. causal interaction 1 3.4.23.24 Acquired Immunodeficiency Syndrome https://pubmed.ncbi.nlm.nih.gov/10395861/ In vitro and in vivo anticandidal activity of human immunodeficiency virus protease inhibitors. causal interaction 4 3.4.23.24 Acquired Immunodeficiency Syndrome https://pubmed.ncbi.nlm.nih.gov/15305695/ [Highly Active AntiRetroviral Therapy and cryptosporidiosis] causal interaction 2 3.4.23.24 Acquired Immunodeficiency Syndrome https://pubmed.ncbi.nlm.nih.gov/30393404/ Syntheses of FDA Approved HIV Protease Inhibitors. causal interaction 3 3.4.23.24 Acquired Immunodeficiency Syndrome https://pubmed.ncbi.nlm.nih.gov/32601166/ The FDA-Approved Drug Nelfinavir Inhibits Lytic Cell-Free but Not Cell-Associated Nonlytic Transmission of Human Adenovirus. causal interaction 2 3.4.23.24 Acquired Immunodeficiency Syndrome https://pubmed.ncbi.nlm.nih.gov/10395861/ In vitro and in vivo anticandidal activity of human immunodeficiency virus protease inhibitors. therapeutic application 4 3.4.23.24 Acquired Immunodeficiency Syndrome https://pubmed.ncbi.nlm.nih.gov/10770752/ Enhanced extracellular production of aspartyl proteinase, a virulence factor, by Candida albicans isolates following growth in subinhibitory concentrations of fluconazole. therapeutic application 1 3.4.23.24 Acquired Immunodeficiency Syndrome https://pubmed.ncbi.nlm.nih.gov/15305695/ [Highly Active AntiRetroviral Therapy and cryptosporidiosis] therapeutic application 4 3.4.23.24 Acquired Immunodeficiency Syndrome https://pubmed.ncbi.nlm.nih.gov/30393404/ Syntheses of FDA Approved HIV Protease Inhibitors. therapeutic application 4 3.4.23.24 Acquired Immunodeficiency Syndrome https://pubmed.ncbi.nlm.nih.gov/32601166/ The FDA-Approved Drug Nelfinavir Inhibits Lytic Cell-Free but Not Cell-Associated Nonlytic Transmission of Human Adenovirus. therapeutic application 4 3.4.23.24 Acquired Immunodeficiency Syndrome https://pubmed.ncbi.nlm.nih.gov/10770752/ Enhanced extracellular production of aspartyl proteinase, a virulence factor, by Candida albicans isolates following growth in subinhibitory concentrations of fluconazole. ongoing research 2 3.4.23.24 Acquired Immunodeficiency Syndrome https://pubmed.ncbi.nlm.nih.gov/8317922/ Characterization of two structurally novel HIV-1 protease inhibitors identified by rational selection. unassigned - 3.4.23.24 Acquired Immunodeficiency Syndrome https://pubmed.ncbi.nlm.nih.gov/10770752/ Enhanced extracellular production of aspartyl proteinase, a virulence factor, by Candida albicans isolates following growth in subinhibitory concentrations of fluconazole. unassigned - 3.4.23.24 Acquired Immunodeficiency Syndrome https://pubmed.ncbi.nlm.nih.gov/7952656/ Structure-assisted design of nonpeptide human immunodeficiency virus-1 protease inhibitors. unassigned - 3.4.23.24 Acquired Immunodeficiency Syndrome https://pubmed.ncbi.nlm.nih.gov/10395861/ In vitro and in vivo anticandidal activity of human immunodeficiency virus protease inhibitors. unassigned - 3.4.23.24 Acquired Immunodeficiency Syndrome https://pubmed.ncbi.nlm.nih.gov/15305695/ [Highly Active AntiRetroviral Therapy and cryptosporidiosis] unassigned - 3.4.23.24 Acquired Immunodeficiency Syndrome https://pubmed.ncbi.nlm.nih.gov/30393404/ Syntheses of FDA Approved HIV Protease Inhibitors. unassigned - 3.4.23.24 Acquired Immunodeficiency Syndrome https://pubmed.ncbi.nlm.nih.gov/32601166/ The FDA-Approved Drug Nelfinavir Inhibits Lytic Cell-Free but Not Cell-Associated Nonlytic Transmission of Human Adenovirus. unassigned - 3.4.23.24 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/27149201/ Procathepsin E is highly abundant but minimally active in pancreatic ductal adenocarcinoma tumors. causal interaction 4 3.4.23.24 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/27149201/ Procathepsin E is highly abundant but minimally active in pancreatic ductal adenocarcinoma tumors. diagnostic usage 3 3.4.23.24 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/27149201/ Procathepsin E is highly abundant but minimally active in pancreatic ductal adenocarcinoma tumors. therapeutic application 4 3.4.23.24 Adenocarcinoma https://pubmed.ncbi.nlm.nih.gov/27149201/ Procathepsin E is highly abundant but minimally active in pancreatic ductal adenocarcinoma tumors. ongoing research 2 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/11444983/ Aspartyl protease inhibitor pepstatin binds to the presenilins of Alzheimer's disease. causal interaction 2 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/19323561/ Harnessing nature's insight: design of aspartyl protease inhibitors from treatment of drug-resistant HIV to Alzheimer's disease. causal interaction 3 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/22363289/ The Membrane-Bound Aspartyl Protease BACE1: Molecular and Functional Properties in Alzheimer's Disease and Beyond. causal interaction 3 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/10498202/ Synthesis and structure activity relationships of novel small molecule cathepsin D inhibitors. causal interaction 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/10899409/ The genetic association between Cathepsin D and Alzheimer's disease. causal interaction 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/11278841/ Phosphorylation regulates intracellular trafficking of beta-secretase. causal interaction 1 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/11922623/ Prediction of the tertiary structure of the beta-secretase zymogen. causal interaction 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/12151789/ Cerebrospinal fluid levels of beta-amyloid(42) in patients with Alzheimer's disease are related to the exon 2 polymorphism of the cathepsin D gene. causal interaction 2 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/12811635/ Modulation of disease risk according to a cathepsin D / apolipoprotein E genotype in Parkinson's disease. causal interaction 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/14507929/ The cell adhesion protein P-selectin glycoprotein ligand-1 is a substrate for the aspartyl protease BACE1. causal interaction 3 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/14692784/ Determination of the active site protonation state of beta-secretase from molecular dynamics simulation and docking experiment: implications for structure-based inhibitor design. causal interaction 2 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/15080893/ BACE (beta-secretase) modulates the processing of APLP2 in vivo. causal interaction 3 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/15167888/ Expression of the Alzheimer protease BACE1 is suppressed via its 5'-untranslated region. causal interaction 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/15485862/ Dimerization of beta-site beta-amyloid precursor protein-cleaving enzyme. causal interaction 3 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/15953349/ Length and overall sequence of the PEN-2 C-terminal domain determines its function in the stabilization of presenilin fragments. causal interaction 1 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/16354928/ BACE1, a major determinant of selective vulnerability of the brain to amyloid-beta amyloidogenesis, is essential for cognitive, emotional, and synaptic functions. causal interaction 3 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/16696577/ Inhibition of gamma-secretase as a therapeutic intervention for Alzheimer's disease: prospects, limitations and strategies. causal interaction 3 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/16965550/ Reticulons RTN3 and RTN4-B/C interact with BACE1 and inhibit its ability to produce amyloid beta-protein. causal interaction 3 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/17034121/ Acylguanidines as small-molecule beta-secretase inhibitors. causal interaction 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/17105873/ Unnatural amino acid-substituted (hydroxyethyl)urea peptidomimetics inhibit gamma-secretase and promote the neuronal differentiation of neuroblastoma cells. causal interaction 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/17349981/ Familial Alzheimer's disease presenilin 1 mutation M146V increases gamma secretase cutting of p75NTR in vitro. causal interaction 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/17466415/ Interaction between the APOE epsilon4 allele and the APH-1b c + 651T > G SNP in Alzheimer's disease. causal interaction 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/17616527/ Partial reduction of BACE1 has dramatic effects on Alzheimer plaque and synaptic pathology in APP Transgenic Mice. causal interaction 1 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/17827153/ Epidermal Growth Factor Receptor and Notch Pathways Participate in the Tumor Suppressor Function of {gamma}-Secretase. causal interaction 3 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/17913918/ Moderate reduction of gamma-secretase attenuates amyloid burden and limits mechanism-based liabilities. causal interaction 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/18171614/ BACE-1 inhibitors part 1: identification of novel hydroxy ethylamines (HEAs). causal interaction 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/18221231/ BACE inhibitors as potential therapeutics for Alzheimer's disease. causal interaction 1 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/18801744/ Chemical cross-linking provides a model of the gamma-secretase complex subunit architecture and evidence for close proximity of the C-terminal fragment of presenilin with APH-1. causal interaction 3 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/19079786/ Assigning the protonation states of the key aspartates in beta-Secretase using QM/MM X-ray structure refinement. causal interaction 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/19109900/ Translational control of BACE1 may go awry in Alzheimer's disease. causal interaction 2 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/19200034/ Large scale refolding and purification of the catalytic domain of human BACE-2 produced in E. coli. causal interaction 3 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/19284778/ Fragment-Based Discovery of Nonpeptidic BACE-1 Inhibitors Using Tethering. causal interaction 3 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/19302194/ Identification of a cis-acting element involved in the regulation of BACE1 mRNA alternative splicing. causal interaction 1 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/19428244/ Second generation of BACE-1 inhibitors. Part 1: The need for improved pharmacokinetics. causal interaction 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/19486882/ Calcium enhances the proteolytic activity of BACE1: An in vitro biophysical and biochemical characterization of the BACE1-calcium interaction. causal interaction 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/20097169/ Evidence for dimeric BACE-mediated APP processing. causal interaction 3 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/20421416/ In vivo Reconstitution of {gamma}-Secretase in Drosophila Results in Substrate Specificity. causal interaction 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/20482315/ Structure, mechanism and inhibition of gamma-secretase and presenilin-like proteases. causal interaction 3 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/20485791/ A paramagnetic chemical exchange-based MRI probe metabolized by cathepsin D: design, synthesis and cellular uptake studies. causal interaction 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/20579874/ BACE-1 hydroxyethylamine inhibitors using novel edge-to-face interaction with Arg-296. causal interaction 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/20731541/ Is BACE1 a suitable therapeutic target for the treatment of Alzheimer's disease? Current strategies and future directions. causal interaction 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/20817005/ BACE: Therapeutic target and potential biomarker for Alzheimer's disease. causal interaction 1 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/21490216/ Reduced BACE1 activity enhances clearance of myelin debris and regeneration of axons in the injured peripheral nervous system. causal interaction 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/21889954/ Development of a specific ELISA to measure BACE1 levels in human tissues. causal interaction 3 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/22303960/ A G-Rich element forms a G-quadruplex and regulates BACE1 mRNA alternative splicing. causal interaction 3 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/22309842/ Therapeutic approaches to modulating Notch signaling: Current challenges and future prospects. causal interaction 3 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/22468999/ Discovery and Optimization of a Novel Spiropyrrolidine Inhibitor of ?-Secretase (BACE1) through Fragment-Based Drug Design. causal interaction 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/22926063/ BACE1 in Alzheimer's disease. causal interaction 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/23457027/ Label-free quantitative analysis of the membrane proteome of Bace1 protease knock-out zebrafish brains. causal interaction 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/23484877/ Structure-guided design of ?-secretase (BACE-1) inhibitors. causal interaction 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/24099007/ Toward the structure of presenilin/?-secretase and presenilin homologs. causal interaction 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/25288897/ Application of a Bioinformatics-Based Approach to Identify Novel Putative in vivo BACE1 Substrates. causal interaction 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/26126792/ Significance of transcytosis in Alzheimer's disease: BACE1 takes the scenic route to axons. causal interaction 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/26840340/ Identification of Human Islet Amyloid Polypeptide as a BACE2 Substrate. causal interaction 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/27111489/ Determination of the protonation state for the catalytic dyad in ?-secretase when bound to hydroxyethylamine transition state analogue inhibitors: A molecular dynamics simulation study. causal interaction 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/27474865/ Modeling the protonation states of ?-secretase binding pocket by molecular dynamics simulations and docking studies. causal interaction 1 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/27750187/ A molecular dynamics study of the BACE1 conformational change from Apo to closed form induced by hydroxyethylamine derived compounds. causal interaction 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/27853315/ A?42 oligomers modulate ?-secretase through an XBP-1s-dependent pathway involving HRD1. causal interaction 3 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/29078331/ Lack of BACE1 S-palmitoylation reduces amyloid burden and mitigates memory deficits in transgenic mouse models of Alzheimer's disease. causal interaction 2 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/29649434/ Evaluation of an Allosteric BACE Inhibitor Peptide to Identify Mimetics that Can Interact with the Loop F Region of the Enzyme and Prevent APP Cleavage. causal interaction 3 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/30264484/ pH-dependent conformational dynamics of beta-secretase 1: A molecular dynamics study. causal interaction 3 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/30979338/ APH-1A Component of ?-Secretase Forms an Internal Water and Ion-Containing Cavity. causal interaction 1 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/31424395/ Safety, Tolerability, Pharmacokinetics, and Pharmacodynamic Effects of PF-06751979, a Potent and Selective Oral BACE1 Inhibitor: Results from Phase I Studies in Healthy Adults and Healthy Older Subjects. causal interaction 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/31589043/ Discovery of AM-6494: A Potent and Orally Efficacious ?-Site Amyloid Precursor Protein Cleaving Enzyme 1 (BACE1) Inhibitor with in Vivo Selectivity over BACE2. causal interaction 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/31625391/ Designed Helical Peptides as Functional Probes for ?-Secretase. causal interaction 1 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/33349218/ Design, Synthesis and Evaluation of 2,4,6-substituted Pyrimidine Derivatives as BACE-1 inhibitor: Plausible lead for Alzheimer's Disease. causal interaction 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/33722254/ The influence of BACE1 on macrophage recruitment and activity in the injured peripheral nerve. causal interaction 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/11444983/ Aspartyl protease inhibitor pepstatin binds to the presenilins of Alzheimer's disease. diagnostic usage 1 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/10498202/ Synthesis and structure activity relationships of novel small molecule cathepsin D inhibitors. diagnostic usage 2 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/12151789/ Cerebrospinal fluid levels of beta-amyloid(42) in patients with Alzheimer's disease are related to the exon 2 polymorphism of the cathepsin D gene. diagnostic usage 1 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/12811635/ Modulation of disease risk according to a cathepsin D / apolipoprotein E genotype in Parkinson's disease. diagnostic usage 3 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/15059975/ Gene structure and organization of the human beta-secretase (BACE) promoter. diagnostic usage 1 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/15167888/ Expression of the Alzheimer protease BACE1 is suppressed via its 5'-untranslated region. diagnostic usage 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/17616527/ Partial reduction of BACE1 has dramatic effects on Alzheimer plaque and synaptic pathology in APP Transgenic Mice. diagnostic usage 3 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/20485791/ A paramagnetic chemical exchange-based MRI probe metabolized by cathepsin D: design, synthesis and cellular uptake studies. diagnostic usage 2 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/24874077/ Leptin attenuates BACE1 expression and amyloid-? genesis via the activation of SIRT1 signaling pathway. diagnostic usage 3 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/11922623/ Prediction of the tertiary structure of the beta-secretase zymogen. therapeutic application 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/12811635/ Modulation of disease risk according to a cathepsin D / apolipoprotein E genotype in Parkinson's disease. therapeutic application 1 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/16354928/ BACE1, a major determinant of selective vulnerability of the brain to amyloid-beta amyloidogenesis, is essential for cognitive, emotional, and synaptic functions. therapeutic application 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/16696577/ Inhibition of gamma-secretase as a therapeutic intervention for Alzheimer's disease: prospects, limitations and strategies. therapeutic application 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/17105873/ Unnatural amino acid-substituted (hydroxyethyl)urea peptidomimetics inhibit gamma-secretase and promote the neuronal differentiation of neuroblastoma cells. therapeutic application 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/17349981/ Familial Alzheimer's disease presenilin 1 mutation M146V increases gamma secretase cutting of p75NTR in vitro. therapeutic application 3 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/17827153/ Epidermal Growth Factor Receptor and Notch Pathways Participate in the Tumor Suppressor Function of {gamma}-Secretase. therapeutic application 3 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/17913918/ Moderate reduction of gamma-secretase attenuates amyloid burden and limits mechanism-based liabilities. therapeutic application 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/18171614/ BACE-1 inhibitors part 1: identification of novel hydroxy ethylamines (HEAs). therapeutic application 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/19200034/ Large scale refolding and purification of the catalytic domain of human BACE-2 produced in E. coli. therapeutic application 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/19284778/ Fragment-Based Discovery of Nonpeptidic BACE-1 Inhibitors Using Tethering. therapeutic application 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/19428244/ Second generation of BACE-1 inhibitors. Part 1: The need for improved pharmacokinetics. therapeutic application 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/20579874/ BACE-1 hydroxyethylamine inhibitors using novel edge-to-face interaction with Arg-296. therapeutic application 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/20731541/ Is BACE1 a suitable therapeutic target for the treatment of Alzheimer's disease? Current strategies and future directions. therapeutic application 3 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/22303960/ A G-Rich element forms a G-quadruplex and regulates BACE1 mRNA alternative splicing. therapeutic application 3 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/22309842/ Therapeutic approaches to modulating Notch signaling: Current challenges and future prospects. therapeutic application 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/29052456/ Population density analysis for determining the protonation state of the catalytic dyad in BACE1-tertiary carbinamine-based inhibitor complex. therapeutic application 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/29649434/ Evaluation of an Allosteric BACE Inhibitor Peptide to Identify Mimetics that Can Interact with the Loop F Region of the Enzyme and Prevent APP Cleavage. therapeutic application 3 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/31589043/ Discovery of AM-6494: A Potent and Orally Efficacious ?-Site Amyloid Precursor Protein Cleaving Enzyme 1 (BACE1) Inhibitor with in Vivo Selectivity over BACE2. therapeutic application 3 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/33349218/ Design, Synthesis and Evaluation of 2,4,6-substituted Pyrimidine Derivatives as BACE-1 inhibitor: Plausible lead for Alzheimer's Disease. therapeutic application 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/11444983/ Aspartyl protease inhibitor pepstatin binds to the presenilins of Alzheimer's disease. ongoing research 2 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/22363289/ The Membrane-Bound Aspartyl Protease BACE1: Molecular and Functional Properties in Alzheimer's Disease and Beyond. ongoing research 1 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/10498202/ Synthesis and structure activity relationships of novel small molecule cathepsin D inhibitors. ongoing research 1 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/15167888/ Expression of the Alzheimer protease BACE1 is suppressed via its 5'-untranslated region. ongoing research 1 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/16965550/ Reticulons RTN3 and RTN4-B/C interact with BACE1 and inhibit its ability to produce amyloid beta-protein. ongoing research 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/17827153/ Epidermal Growth Factor Receptor and Notch Pathways Participate in the Tumor Suppressor Function of {gamma}-Secretase. ongoing research 1 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/21865451/ Synaptic Autoregulation by Metalloproteases and {gamma}-Secretase. ongoing research 1 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/23951005/ Gadd153 and NF-?B Crosstalk Regulates 27-Hydroxycholesterol-Induced Increase in BACE1 and ?-Amyloid Production in Human Neuroblastoma SH-SY5Y Cells. ongoing research 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/24874077/ Leptin attenuates BACE1 expression and amyloid-? genesis via the activation of SIRT1 signaling pathway. ongoing research 4 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/29078331/ Lack of BACE1 S-palmitoylation reduces amyloid burden and mitigates memory deficits in transgenic mouse models of Alzheimer's disease. ongoing research 2 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/10591213/ Membrane-anchored aspartyl protease with Alzheimer's disease beta-secretase activity. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/11493036/ Endoproteolysis of the ER stress transducer ATF6 in the presence of functionally inactive presenilins. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/12679784/ Reconstitution of gamma-secretase activity. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/15059975/ Gene structure and organization of the human beta-secretase (BACE) promoter. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/15087467/ Presenilin 1 stabilizes the C-terminal fragment of the amyloid precursor protein independently of gamma-secretase activity. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/15210705/ Co-expression of nicastrin and presenilin rescues a loss of function mutant of APH-1. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/16597736/ The GxGD motif of presenilin contributes to catalytic function and substrate identification of gamma-secretase. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/17360493/ Regulation of Alzheimer's disease amyloid-beta formation by casein kinase I. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/21865451/ Synaptic Autoregulation by Metalloproteases and {gamma}-Secretase. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/23133641/ A peptide binding to the ?-site of APP improves spatial memory and attenuates A? burden in Alzheimer's disease transgenic mice. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/23951005/ Gadd153 and NF-?B Crosstalk Regulates 27-Hydroxycholesterol-Induced Increase in BACE1 and ?-Amyloid Production in Human Neuroblastoma SH-SY5Y Cells. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/24874077/ Leptin attenuates BACE1 expression and amyloid-? genesis via the activation of SIRT1 signaling pathway. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/29052456/ Population density analysis for determining the protonation state of the catalytic dyad in BACE1-tertiary carbinamine-based inhibitor complex. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/32354467/ Successive cleavage of ?-amyloid precursor protein by ?-secretase. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/19323561/ Harnessing nature's insight: design of aspartyl protease inhibitors from treatment of drug-resistant HIV to Alzheimer's disease. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/22363289/ The Membrane-Bound Aspartyl Protease BACE1: Molecular and Functional Properties in Alzheimer's Disease and Beyond. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/10899409/ The genetic association between Cathepsin D and Alzheimer's disease. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/11278841/ Phosphorylation regulates intracellular trafficking of beta-secretase. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/11922623/ Prediction of the tertiary structure of the beta-secretase zymogen. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/14507929/ The cell adhesion protein P-selectin glycoprotein ligand-1 is a substrate for the aspartyl protease BACE1. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/14692784/ Determination of the active site protonation state of beta-secretase from molecular dynamics simulation and docking experiment: implications for structure-based inhibitor design. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/15080893/ BACE (beta-secretase) modulates the processing of APLP2 in vivo. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/15485862/ Dimerization of beta-site beta-amyloid precursor protein-cleaving enzyme. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/15953349/ Length and overall sequence of the PEN-2 C-terminal domain determines its function in the stabilization of presenilin fragments. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/16354928/ BACE1, a major determinant of selective vulnerability of the brain to amyloid-beta amyloidogenesis, is essential for cognitive, emotional, and synaptic functions. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/16696577/ Inhibition of gamma-secretase as a therapeutic intervention for Alzheimer's disease: prospects, limitations and strategies. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/16965550/ Reticulons RTN3 and RTN4-B/C interact with BACE1 and inhibit its ability to produce amyloid beta-protein. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/17034121/ Acylguanidines as small-molecule beta-secretase inhibitors. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/17105873/ Unnatural amino acid-substituted (hydroxyethyl)urea peptidomimetics inhibit gamma-secretase and promote the neuronal differentiation of neuroblastoma cells. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/17349981/ Familial Alzheimer's disease presenilin 1 mutation M146V increases gamma secretase cutting of p75NTR in vitro. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/17466415/ Interaction between the APOE epsilon4 allele and the APH-1b c + 651T > G SNP in Alzheimer's disease. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/17827153/ Epidermal Growth Factor Receptor and Notch Pathways Participate in the Tumor Suppressor Function of {gamma}-Secretase. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/17913918/ Moderate reduction of gamma-secretase attenuates amyloid burden and limits mechanism-based liabilities. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/18171614/ BACE-1 inhibitors part 1: identification of novel hydroxy ethylamines (HEAs). unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/18221231/ BACE inhibitors as potential therapeutics for Alzheimer's disease. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/18801744/ Chemical cross-linking provides a model of the gamma-secretase complex subunit architecture and evidence for close proximity of the C-terminal fragment of presenilin with APH-1. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/19079786/ Assigning the protonation states of the key aspartates in beta-Secretase using QM/MM X-ray structure refinement. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/19109900/ Translational control of BACE1 may go awry in Alzheimer's disease. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/19200034/ Large scale refolding and purification of the catalytic domain of human BACE-2 produced in E. coli. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/19284778/ Fragment-Based Discovery of Nonpeptidic BACE-1 Inhibitors Using Tethering. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/19302194/ Identification of a cis-acting element involved in the regulation of BACE1 mRNA alternative splicing. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/19428244/ Second generation of BACE-1 inhibitors. Part 1: The need for improved pharmacokinetics. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/19486882/ Calcium enhances the proteolytic activity of BACE1: An in vitro biophysical and biochemical characterization of the BACE1-calcium interaction. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/20097169/ Evidence for dimeric BACE-mediated APP processing. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/20421416/ In vivo Reconstitution of {gamma}-Secretase in Drosophila Results in Substrate Specificity. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/20482315/ Structure, mechanism and inhibition of gamma-secretase and presenilin-like proteases. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/20579874/ BACE-1 hydroxyethylamine inhibitors using novel edge-to-face interaction with Arg-296. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/20731541/ Is BACE1 a suitable therapeutic target for the treatment of Alzheimer's disease? Current strategies and future directions. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/20817005/ BACE: Therapeutic target and potential biomarker for Alzheimer's disease. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/21490216/ Reduced BACE1 activity enhances clearance of myelin debris and regeneration of axons in the injured peripheral nervous system. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/21889954/ Development of a specific ELISA to measure BACE1 levels in human tissues. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/22303960/ A G-Rich element forms a G-quadruplex and regulates BACE1 mRNA alternative splicing. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/22309842/ Therapeutic approaches to modulating Notch signaling: Current challenges and future prospects. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/22468999/ Discovery and Optimization of a Novel Spiropyrrolidine Inhibitor of ?-Secretase (BACE1) through Fragment-Based Drug Design. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/22926063/ BACE1 in Alzheimer's disease. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/23457027/ Label-free quantitative analysis of the membrane proteome of Bace1 protease knock-out zebrafish brains. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/23484877/ Structure-guided design of ?-secretase (BACE-1) inhibitors. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/24099007/ Toward the structure of presenilin/?-secretase and presenilin homologs. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/25288897/ Application of a Bioinformatics-Based Approach to Identify Novel Putative in vivo BACE1 Substrates. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/26126792/ Significance of transcytosis in Alzheimer's disease: BACE1 takes the scenic route to axons. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/26840340/ Identification of Human Islet Amyloid Polypeptide as a BACE2 Substrate. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/27111489/ Determination of the protonation state for the catalytic dyad in ?-secretase when bound to hydroxyethylamine transition state analogue inhibitors: A molecular dynamics simulation study. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/27474865/ Modeling the protonation states of ?-secretase binding pocket by molecular dynamics simulations and docking studies. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/27750187/ A molecular dynamics study of the BACE1 conformational change from Apo to closed form induced by hydroxyethylamine derived compounds. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/27853315/ A?42 oligomers modulate ?-secretase through an XBP-1s-dependent pathway involving HRD1. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/29078331/ Lack of BACE1 S-palmitoylation reduces amyloid burden and mitigates memory deficits in transgenic mouse models of Alzheimer's disease. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/29649434/ Evaluation of an Allosteric BACE Inhibitor Peptide to Identify Mimetics that Can Interact with the Loop F Region of the Enzyme and Prevent APP Cleavage. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/30264484/ pH-dependent conformational dynamics of beta-secretase 1: A molecular dynamics study. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/30979338/ APH-1A Component of ?-Secretase Forms an Internal Water and Ion-Containing Cavity. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/31424395/ Safety, Tolerability, Pharmacokinetics, and Pharmacodynamic Effects of PF-06751979, a Potent and Selective Oral BACE1 Inhibitor: Results from Phase I Studies in Healthy Adults and Healthy Older Subjects. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/31589043/ Discovery of AM-6494: A Potent and Orally Efficacious ?-Site Amyloid Precursor Protein Cleaving Enzyme 1 (BACE1) Inhibitor with in Vivo Selectivity over BACE2. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/31625391/ Designed Helical Peptides as Functional Probes for ?-Secretase. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/33349218/ Design, Synthesis and Evaluation of 2,4,6-substituted Pyrimidine Derivatives as BACE-1 inhibitor: Plausible lead for Alzheimer's Disease. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/33722254/ The influence of BACE1 on macrophage recruitment and activity in the injured peripheral nerve. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/11444983/ Aspartyl protease inhibitor pepstatin binds to the presenilins of Alzheimer's disease. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/10498202/ Synthesis and structure activity relationships of novel small molecule cathepsin D inhibitors. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/12151789/ Cerebrospinal fluid levels of beta-amyloid(42) in patients with Alzheimer's disease are related to the exon 2 polymorphism of the cathepsin D gene. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/15167888/ Expression of the Alzheimer protease BACE1 is suppressed via its 5'-untranslated region. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/17616527/ Partial reduction of BACE1 has dramatic effects on Alzheimer plaque and synaptic pathology in APP Transgenic Mice. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/20485791/ A paramagnetic chemical exchange-based MRI probe metabolized by cathepsin D: design, synthesis and cellular uptake studies. unassigned - 3.4.23.24 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/12811635/ Modulation of disease risk according to a cathepsin D / apolipoprotein E genotype in Parkinson's disease. unassigned - 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/9271363/ Release of the aspartyl protease cathepsin D is associated with and facilitates human breast cancer cell invasion. causal interaction 1 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/1622626/ Biological and clinical significance of cathepsin D in breast cancer. causal interaction 4 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/7749141/ Cathepsin D in primary breast carcinoma: adverse prognosis is associated with expression of cathepsin D in stromal cells. causal interaction 4 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/8419924/ Cathepsin D gene is controlled by a mixed promoter, and estrogens stimulate only TATA-dependent transcription in breast cancer cells. causal interaction 4 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/8428368/ The role of cathepsin D in the invasiveness of human breast cancer cells. causal interaction 4 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/9065599/ Mitogenic activity toward human breast cancer cell line MCF-7 of two bFGFs purified from sera of breast cancer patients: co-operative role of cathepsin D. causal interaction 2 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/9493971/ Low cathepsin D and low plasminogen activator type 1 inhibitor in tumor cytosols defines a group of node negative breast cancer patients with low risk of recurrence. causal interaction 4 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/9917508/ Characterization of purified cathepsin D from malignant human breast tissue. causal interaction 4 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/12113579/ Clinical significance of pepsinogen C tumor expression in patients with stage D2 prostate carcinoma. causal interaction 4 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/21559613/ Prognostic indicators for early-stage breast-carcinoma .2. Value of cathepsin-d expression, detected by immunocytochemistry - a multiparametric study. causal interaction 4 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/21607525/ Immunohistochemical detection of cathepsin-d expression in prostate-cancer. causal interaction 4 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/24026424/ Cathepsin D stimulates the activities of secreted plasminogen activators in the breast cancer acidic environment. causal interaction 4 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/9271363/ Release of the aspartyl protease cathepsin D is associated with and facilitates human breast cancer cell invasion. diagnostic usage 3 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/1622626/ Biological and clinical significance of cathepsin D in breast cancer. diagnostic usage 4 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/7749141/ Cathepsin D in primary breast carcinoma: adverse prognosis is associated with expression of cathepsin D in stromal cells. diagnostic usage 4 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/8419924/ Cathepsin D gene is controlled by a mixed promoter, and estrogens stimulate only TATA-dependent transcription in breast cancer cells. diagnostic usage 3 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/8428368/ The role of cathepsin D in the invasiveness of human breast cancer cells. diagnostic usage 4 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/9065599/ Mitogenic activity toward human breast cancer cell line MCF-7 of two bFGFs purified from sera of breast cancer patients: co-operative role of cathepsin D. diagnostic usage 1 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/9493971/ Low cathepsin D and low plasminogen activator type 1 inhibitor in tumor cytosols defines a group of node negative breast cancer patients with low risk of recurrence. diagnostic usage 3 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/12113579/ Clinical significance of pepsinogen C tumor expression in patients with stage D2 prostate carcinoma. diagnostic usage 4 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/21559613/ Prognostic indicators for early-stage breast-carcinoma .2. Value of cathepsin-d expression, detected by immunocytochemistry - a multiparametric study. diagnostic usage 4 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/21607525/ Immunohistochemical detection of cathepsin-d expression in prostate-cancer. diagnostic usage 4 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/24026424/ Cathepsin D stimulates the activities of secreted plasminogen activators in the breast cancer acidic environment. diagnostic usage 3 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/7749141/ Cathepsin D in primary breast carcinoma: adverse prognosis is associated with expression of cathepsin D in stromal cells. therapeutic application 2 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/9493971/ Low cathepsin D and low plasminogen activator type 1 inhibitor in tumor cytosols defines a group of node negative breast cancer patients with low risk of recurrence. therapeutic application 4 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/12113579/ Clinical significance of pepsinogen C tumor expression in patients with stage D2 prostate carcinoma. therapeutic application 2 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/21559613/ Prognostic indicators for early-stage breast-carcinoma .2. Value of cathepsin-d expression, detected by immunocytochemistry - a multiparametric study. therapeutic application 1 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/24026424/ Cathepsin D stimulates the activities of secreted plasminogen activators in the breast cancer acidic environment. therapeutic application 1 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/9271363/ Release of the aspartyl protease cathepsin D is associated with and facilitates human breast cancer cell invasion. ongoing research 4 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/1622626/ Biological and clinical significance of cathepsin D in breast cancer. ongoing research 4 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/7749141/ Cathepsin D in primary breast carcinoma: adverse prognosis is associated with expression of cathepsin D in stromal cells. ongoing research 4 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/8419924/ Cathepsin D gene is controlled by a mixed promoter, and estrogens stimulate only TATA-dependent transcription in breast cancer cells. ongoing research 1 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/8428368/ The role of cathepsin D in the invasiveness of human breast cancer cells. ongoing research 4 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/9065599/ Mitogenic activity toward human breast cancer cell line MCF-7 of two bFGFs purified from sera of breast cancer patients: co-operative role of cathepsin D. ongoing research 4 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/9493971/ Low cathepsin D and low plasminogen activator type 1 inhibitor in tumor cytosols defines a group of node negative breast cancer patients with low risk of recurrence. ongoing research 4 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/12113579/ Clinical significance of pepsinogen C tumor expression in patients with stage D2 prostate carcinoma. ongoing research 4 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/21559613/ Prognostic indicators for early-stage breast-carcinoma .2. Value of cathepsin-d expression, detected by immunocytochemistry - a multiparametric study. ongoing research 4 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/21607525/ Immunohistochemical detection of cathepsin-d expression in prostate-cancer. ongoing research 3 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/24026424/ Cathepsin D stimulates the activities of secreted plasminogen activators in the breast cancer acidic environment. ongoing research 4 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/23755096/ Prolactin-induced protein (PIP) regulates proliferation of luminal A type breast cancer cells in an estrogen-independent manner. unassigned - 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/9917508/ Characterization of purified cathepsin D from malignant human breast tissue. unassigned - 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/9271363/ Release of the aspartyl protease cathepsin D is associated with and facilitates human breast cancer cell invasion. unassigned - 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/1622626/ Biological and clinical significance of cathepsin D in breast cancer. unassigned - 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/8419924/ Cathepsin D gene is controlled by a mixed promoter, and estrogens stimulate only TATA-dependent transcription in breast cancer cells. unassigned - 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/8428368/ The role of cathepsin D in the invasiveness of human breast cancer cells. unassigned - 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/9065599/ Mitogenic activity toward human breast cancer cell line MCF-7 of two bFGFs purified from sera of breast cancer patients: co-operative role of cathepsin D. unassigned - 3.4.23.24 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/21607525/ Immunohistochemical detection of cathepsin-d expression in prostate-cancer. unassigned - 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/12761103/ The secreted aspartyl proteinases Sap1 and Sap2 cause tissue damage in an in vitro model of vaginal candidiasis based on reconstituted human vaginal epithelium. causal interaction 1 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/20679440/ Limited role of secreted aspartyl proteinases Sap1 to Sap6 in Candida albicans virulence and host immune response in murine hematogenously disseminated candidiasis. causal interaction 1 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/11807692/ Antiretroviral therapy with protease inhibitors has an early, immune reconstitution-independent beneficial effect on Candida virulence and oral candidiasis in human immunodeficiency virus-infected subjects. causal interaction 2 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/24378182/ Sap6, a secreted aspartyl proteinase, participates in maintenance the cell surface integrity of Candida albicans. causal interaction 1 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/12965914/ Competitive binding inhibition enzyme-linked immunosorbent assay that uses the secreted aspartyl proteinase of Candida albicans as an antigenic marker for diagnosis of disseminated candidiasis. diagnostic usage 4 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/17472610/ Production of hybrid phage displaying secreted aspartyl proteinase epitope of Candida albicans and its application for the diagnosis of disseminated candidiasis. diagnostic usage 3 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/17641856/ Expression of Candida albicans secreted aspartyl proteinase in acute vaginal candidiasis. diagnostic usage 3 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/12870130/ Differential expression of Candida albicans secreted aspartyl proteinase and phospholipase B genes in humans correlates with active oral and vaginal infections. diagnostic usage 1 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/12898449/ Hydrolytic gene expression during oroesophageal and gastric candidiasis in immunocompetent and immunodeficient gnotobiotic mice. diagnostic usage 3 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/19737582/ A modified in situ RT-PCR method for localizing fungal-specific gene expression in Candida-infected mice renal cells. diagnostic usage 1 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/12761103/ The secreted aspartyl proteinases Sap1 and Sap2 cause tissue damage in an in vitro model of vaginal candidiasis based on reconstituted human vaginal epithelium. therapeutic application 1 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/12965914/ Competitive binding inhibition enzyme-linked immunosorbent assay that uses the secreted aspartyl proteinase of Candida albicans as an antigenic marker for diagnosis of disseminated candidiasis. therapeutic application 2 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/15009435/ Protection against systemic candidiasis in mice immunized with secreted aspartic proteinase 2. therapeutic application 3 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/17472610/ Production of hybrid phage displaying secreted aspartyl proteinase epitope of Candida albicans and its application for the diagnosis of disseminated candidiasis. therapeutic application 1 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/20679440/ Limited role of secreted aspartyl proteinases Sap1 to Sap6 in Candida albicans virulence and host immune response in murine hematogenously disseminated candidiasis. therapeutic application 1 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/32661125/ Vaccination with Secreted Aspartyl Proteinase 2 Protein from Candida parapsilosis Can Enhance Survival of Mice during C. tropicalis-Mediated Systemic Candidiasis. therapeutic application 2 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/11807692/ Antiretroviral therapy with protease inhibitors has an early, immune reconstitution-independent beneficial effect on Candida virulence and oral candidiasis in human immunodeficiency virus-infected subjects. therapeutic application 4 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/12870130/ Differential expression of Candida albicans secreted aspartyl proteinase and phospholipase B genes in humans correlates with active oral and vaginal infections. therapeutic application 1 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/29763829/ Silver-loaded graphene as an effective SERS substrate for clotrimazole detection: DFT and spectroscopic studies. therapeutic application 2 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/12761103/ The secreted aspartyl proteinases Sap1 and Sap2 cause tissue damage in an in vitro model of vaginal candidiasis based on reconstituted human vaginal epithelium. ongoing research 3 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/15009435/ Protection against systemic candidiasis in mice immunized with secreted aspartic proteinase 2. ongoing research 4 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/17641856/ Expression of Candida albicans secreted aspartyl proteinase in acute vaginal candidiasis. ongoing research 4 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/18957581/ Quantitative expression of the Candida albicans secreted aspartyl proteinase gene family in human oral and vaginal candidiasis. ongoing research 2 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/9720053/ Overexpression of Candida albicans secretory aspartyl proteinase 2 and its expression in Saccharomyces cerevisiae do not augment virulence in mice. ongoing research 2 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/10225911/ In vivo analysis of secreted aspartyl proteinase expression in human oral candidiasis. ongoing research 4 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/12870130/ Differential expression of Candida albicans secreted aspartyl proteinase and phospholipase B genes in humans correlates with active oral and vaginal infections. ongoing research 2 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/12898449/ Hydrolytic gene expression during oroesophageal and gastric candidiasis in immunocompetent and immunodeficient gnotobiotic mice. ongoing research 4 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/17577331/ IL-1alpha, IL-1ra and IL-8 are differentially induced by Candida in experimental oral candidiasis. ongoing research 2 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/19737582/ A modified in situ RT-PCR method for localizing fungal-specific gene expression in Candida-infected mice renal cells. ongoing research 1 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/12965914/ Competitive binding inhibition enzyme-linked immunosorbent assay that uses the secreted aspartyl proteinase of Candida albicans as an antigenic marker for diagnosis of disseminated candidiasis. unassigned - 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/15009435/ Protection against systemic candidiasis in mice immunized with secreted aspartic proteinase 2. unassigned - 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/17472610/ Production of hybrid phage displaying secreted aspartyl proteinase epitope of Candida albicans and its application for the diagnosis of disseminated candidiasis. unassigned - 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/17641856/ Expression of Candida albicans secreted aspartyl proteinase in acute vaginal candidiasis. unassigned - 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/18957581/ Quantitative expression of the Candida albicans secreted aspartyl proteinase gene family in human oral and vaginal candidiasis. unassigned - 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/23139737/ Secreted aspartic protease cleavage of Candida albicans Msb2 activates Cek1 MAPK signaling affecting biofilm formation and oropharyngeal candidiasis. unassigned - 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/23990858/ Correction: Secreted Aspartic Protease Cleavage of Candida albicans Msb2 Activates Cek1 MAPK Signaling Affecting Biofilm Formation and Oropharyngeal Candidiasis. unassigned - 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/32661125/ Vaccination with Secreted Aspartyl Proteinase 2 Protein from Candida parapsilosis Can Enhance Survival of Mice during C. tropicalis-Mediated Systemic Candidiasis. unassigned - 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/9043112/ Analysis of secreted aspartic proteinases from Candida albicans: purification and characterization of individual Sap1, Sap2 and Sap3 isoenzymes. unassigned - 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/9720053/ Overexpression of Candida albicans secretory aspartyl proteinase 2 and its expression in Saccharomyces cerevisiae do not augment virulence in mice. unassigned - 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/10225911/ In vivo analysis of secreted aspartyl proteinase expression in human oral candidiasis. unassigned - 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/12427964/ Differential secretion of Sap4-6 proteins in Candida albicans during hyphae formation. unassigned - 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/12870130/ Differential expression of Candida albicans secreted aspartyl proteinase and phospholipase B genes in humans correlates with active oral and vaginal infections. unassigned - 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/12898449/ Hydrolytic gene expression during oroesophageal and gastric candidiasis in immunocompetent and immunodeficient gnotobiotic mice. unassigned - 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/17577331/ IL-1alpha, IL-1ra and IL-8 are differentially induced by Candida in experimental oral candidiasis. unassigned - 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/19737582/ A modified in situ RT-PCR method for localizing fungal-specific gene expression in Candida-infected mice renal cells. unassigned - 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/23829781/ Engineering Candida albicans to secrete a host immunomodulatory factor. unassigned - 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/29763829/ Silver-loaded graphene as an effective SERS substrate for clotrimazole detection: DFT and spectroscopic studies. unassigned - 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/12761103/ The secreted aspartyl proteinases Sap1 and Sap2 cause tissue damage in an in vitro model of vaginal candidiasis based on reconstituted human vaginal epithelium. unassigned - 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/20679440/ Limited role of secreted aspartyl proteinases Sap1 to Sap6 in Candida albicans virulence and host immune response in murine hematogenously disseminated candidiasis. unassigned - 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/11807692/ Antiretroviral therapy with protease inhibitors has an early, immune reconstitution-independent beneficial effect on Candida virulence and oral candidiasis in human immunodeficiency virus-infected subjects. unassigned - 3.4.23.24 Candidiasis https://pubmed.ncbi.nlm.nih.gov/24378182/ Sap6, a secreted aspartyl proteinase, participates in maintenance the cell surface integrity of Candida albicans. unassigned - 3.4.23.24 Candidiasis, Invasive https://pubmed.ncbi.nlm.nih.gov/10548587/ Use of monoclonal antibody in diagnosis of candidiasis caused by Candida albicans: detection of circulating aspartyl proteinase antigen. diagnostic usage 4 3.4.23.24 Candidiasis, Invasive https://pubmed.ncbi.nlm.nih.gov/10548587/ Use of monoclonal antibody in diagnosis of candidiasis caused by Candida albicans: detection of circulating aspartyl proteinase antigen. therapeutic application 1 3.4.23.24 Candidiasis, Invasive https://pubmed.ncbi.nlm.nih.gov/10548587/ Use of monoclonal antibody in diagnosis of candidiasis caused by Candida albicans: detection of circulating aspartyl proteinase antigen. ongoing research 2 3.4.23.24 Candidiasis, Invasive https://pubmed.ncbi.nlm.nih.gov/10548587/ Use of monoclonal antibody in diagnosis of candidiasis caused by Candida albicans: detection of circulating aspartyl proteinase antigen. unassigned - 3.4.23.24 Candidiasis, Oral https://pubmed.ncbi.nlm.nih.gov/24329754/ Enzymatic activity profile of a Brazilian culture collection of Candida albicans isolated from diabetics and non-diabetics with oral candidiasis. diagnostic usage 2 3.4.23.24 Candidiasis, Oral https://pubmed.ncbi.nlm.nih.gov/24908598/ In vitro evaluation of the enzymatic activity profile of non-albicans Candida species isolated from patients with oral candidiasis with or without diabetes. diagnostic usage 2 3.4.23.24 Candidiasis, Oral https://pubmed.ncbi.nlm.nih.gov/10084319/ In vivo expression and localization of Candida albicans secreted aspartyl proteinases during oral candidiasis in HIV-infected patients. ongoing research 2 3.4.23.24 Candidiasis, Oral https://pubmed.ncbi.nlm.nih.gov/10225911/ In vivo analysis of secreted aspartyl proteinase expression in human oral candidiasis. ongoing research 4 3.4.23.24 Candidiasis, Oral https://pubmed.ncbi.nlm.nih.gov/24329754/ Enzymatic activity profile of a Brazilian culture collection of Candida albicans isolated from diabetics and non-diabetics with oral candidiasis. ongoing research 3 3.4.23.24 Candidiasis, Oral https://pubmed.ncbi.nlm.nih.gov/24908598/ In vitro evaluation of the enzymatic activity profile of non-albicans Candida species isolated from patients with oral candidiasis with or without diabetes. ongoing research 2 3.4.23.24 Candidiasis, Oral https://pubmed.ncbi.nlm.nih.gov/10084319/ In vivo expression and localization of Candida albicans secreted aspartyl proteinases during oral candidiasis in HIV-infected patients. unassigned - 3.4.23.24 Candidiasis, Oral https://pubmed.ncbi.nlm.nih.gov/10225911/ In vivo analysis of secreted aspartyl proteinase expression in human oral candidiasis. unassigned - 3.4.23.24 Candidiasis, Oral https://pubmed.ncbi.nlm.nih.gov/25870228/ Novel Aggregation Properties of Candida albicans Secreted Aspartyl Proteinase Sap6 Mediate Virulence in Oral Candidiasis. unassigned - 3.4.23.24 Candidiasis, Oral https://pubmed.ncbi.nlm.nih.gov/24329754/ Enzymatic activity profile of a Brazilian culture collection of Candida albicans isolated from diabetics and non-diabetics with oral candidiasis. unassigned - 3.4.23.24 Candidiasis, Oral https://pubmed.ncbi.nlm.nih.gov/24908598/ In vitro evaluation of the enzymatic activity profile of non-albicans Candida species isolated from patients with oral candidiasis with or without diabetes. unassigned - 3.4.23.24 Candidiasis, Oral https://pubmed.ncbi.nlm.nih.gov/28588252/ Candida albicans Sap6 amyloid regions function in cellular aggregation and zinc binding, and contribute to zinc acquisition. unassigned - 3.4.23.24 Candidiasis, Vulvovaginal https://pubmed.ncbi.nlm.nih.gov/26473934/ Studies of Immune Responses in Candida vaginitis. causal interaction 3 3.4.23.24 Candidiasis, Vulvovaginal https://pubmed.ncbi.nlm.nih.gov/17714358/ Differential expression of Candida albicans secreted aspartyl proteinase in human vulvovaginal candidiasis. diagnostic usage 1 3.4.23.24 Candidiasis, Vulvovaginal https://pubmed.ncbi.nlm.nih.gov/33689812/ Virulence of "white-gray-opaque" tri-stable transformation in clinical Candida albicans in vitro and in vivo. diagnostic usage 1 3.4.23.24 Candidiasis, Vulvovaginal https://pubmed.ncbi.nlm.nih.gov/26473934/ Studies of Immune Responses in Candida vaginitis. therapeutic application 4 3.4.23.24 Candidiasis, Vulvovaginal https://pubmed.ncbi.nlm.nih.gov/33689812/ Virulence of "white-gray-opaque" tri-stable transformation in clinical Candida albicans in vitro and in vivo. ongoing research 1 3.4.23.24 Candidiasis, Vulvovaginal https://pubmed.ncbi.nlm.nih.gov/17714358/ Differential expression of Candida albicans secreted aspartyl proteinase in human vulvovaginal candidiasis. unassigned - 3.4.23.24 Candidiasis, Vulvovaginal https://pubmed.ncbi.nlm.nih.gov/33689812/ Virulence of "white-gray-opaque" tri-stable transformation in clinical Candida albicans in vitro and in vivo. unassigned - 3.4.23.24 Candidiasis, Vulvovaginal https://pubmed.ncbi.nlm.nih.gov/26473934/ Studies of Immune Responses in Candida vaginitis. unassigned - 3.4.23.24 Carcinoma https://pubmed.ncbi.nlm.nih.gov/22167025/ Spectrophotometric analysis of the expression of secreted aspartyl proteinases from Candida in leukoplakia and oral squamous cell carcinoma. causal interaction 4 3.4.23.24 Carcinoma https://pubmed.ncbi.nlm.nih.gov/22167025/ Spectrophotometric analysis of the expression of secreted aspartyl proteinases from Candida in leukoplakia and oral squamous cell carcinoma. diagnostic usage 2 3.4.23.24 Carcinoma https://pubmed.ncbi.nlm.nih.gov/22167025/ Spectrophotometric analysis of the expression of secreted aspartyl proteinases from Candida in leukoplakia and oral squamous cell carcinoma. ongoing research 3 3.4.23.24 Carcinoma https://pubmed.ncbi.nlm.nih.gov/22167025/ Spectrophotometric analysis of the expression of secreted aspartyl proteinases from Candida in leukoplakia and oral squamous cell carcinoma. unassigned - 3.4.23.24 Cholera https://pubmed.ncbi.nlm.nih.gov/11953420/ Intravaginal and intranasal immunizations are equally effective in inducing vaginal antibodies and conferring protection against vaginal candidiasis. ongoing research 1 3.4.23.24 Cholera https://pubmed.ncbi.nlm.nih.gov/11953420/ Intravaginal and intranasal immunizations are equally effective in inducing vaginal antibodies and conferring protection against vaginal candidiasis. unassigned - 3.4.23.24 Coccidioidomycosis https://pubmed.ncbi.nlm.nih.gov/16369008/ A recombinant aspartyl protease of Coccidioides posadasii induces protection against pulmonary coccidioidomycosis in mice. therapeutic application 3 3.4.23.24 Coccidioidomycosis https://pubmed.ncbi.nlm.nih.gov/16369008/ A recombinant aspartyl protease of Coccidioides posadasii induces protection against pulmonary coccidioidomycosis in mice. ongoing research 3 3.4.23.24 Coccidioidomycosis https://pubmed.ncbi.nlm.nih.gov/16369008/ A recombinant aspartyl protease of Coccidioides posadasii induces protection against pulmonary coccidioidomycosis in mice. unassigned - 3.4.23.24 Coinfection https://pubmed.ncbi.nlm.nih.gov/22593238/ Analysis of heavy-chain antibody responses and resistance to Parelaphostrongylus tenuis in experimentally infected alpacas. therapeutic application 2 3.4.23.24 Coinfection https://pubmed.ncbi.nlm.nih.gov/22593238/ Analysis of heavy-chain antibody responses and resistance to Parelaphostrongylus tenuis in experimentally infected alpacas. unassigned - 3.4.23.24 Coinfection https://pubmed.ncbi.nlm.nih.gov/27190184/ Streptococcus oralis and Candida albicans Synergistically Activate ?-Calpain to Degrade E-cadherin From Oral Epithelial Junctions. unassigned - 3.4.23.24 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/16246305/ Blockade of gamma-secretase activity within the hippocampus enhances long-term memory. therapeutic application 1 3.4.23.24 Colorectal Neoplasms https://pubmed.ncbi.nlm.nih.gov/16246305/ Blockade of gamma-secretase activity within the hippocampus enhances long-term memory. unassigned - 3.4.23.24 Decompression Sickness https://pubmed.ncbi.nlm.nih.gov/16195226/ Sap1p binds to Ter1 at the ribosomal DNA of Schizosaccharomyces pombe and causes polar replication fork arrest. diagnostic usage 1 3.4.23.24 Decompression Sickness https://pubmed.ncbi.nlm.nih.gov/16195226/ Sap1p binds to Ter1 at the ribosomal DNA of Schizosaccharomyces pombe and causes polar replication fork arrest. therapeutic application 1 3.4.23.24 Decompression Sickness https://pubmed.ncbi.nlm.nih.gov/16195226/ Sap1p binds to Ter1 at the ribosomal DNA of Schizosaccharomyces pombe and causes polar replication fork arrest. unassigned - 3.4.23.24 Enteritis https://pubmed.ncbi.nlm.nih.gov/15305695/ [Highly Active AntiRetroviral Therapy and cryptosporidiosis] causal interaction 2 3.4.23.24 Enteritis https://pubmed.ncbi.nlm.nih.gov/15305695/ [Highly Active AntiRetroviral Therapy and cryptosporidiosis] therapeutic application 4 3.4.23.24 Enteritis https://pubmed.ncbi.nlm.nih.gov/15305695/ [Highly Active AntiRetroviral Therapy and cryptosporidiosis] unassigned - 3.4.23.24 Hepatitis B https://pubmed.ncbi.nlm.nih.gov/2685358/ Biosynthesis of hepatitis B virus e antigen: directed mutagenesis of the putative aspartyl protease site. therapeutic application 1 3.4.23.24 Hepatitis B https://pubmed.ncbi.nlm.nih.gov/2685358/ Biosynthesis of hepatitis B virus e antigen: directed mutagenesis of the putative aspartyl protease site. ongoing research 3 3.4.23.24 Hepatitis B https://pubmed.ncbi.nlm.nih.gov/2685358/ Biosynthesis of hepatitis B virus e antigen: directed mutagenesis of the putative aspartyl protease site. unassigned - 3.4.23.24 Herpes Simplex https://pubmed.ncbi.nlm.nih.gov/25709648/ Nelfinavir impairs glycosylation of herpes simplex virus 1 envelope proteins and blocks virus maturation. ongoing research 4 3.4.23.24 Herpes Simplex https://pubmed.ncbi.nlm.nih.gov/25709648/ Nelfinavir impairs glycosylation of herpes simplex virus 1 envelope proteins and blocks virus maturation. unassigned - 3.4.23.24 HIV Infections https://pubmed.ncbi.nlm.nih.gov/22472853/ Candida and candidiasis in HIV-infected patients: where commensalism, opportunistic behavior and frank pathogenicity lose their borders. causal interaction 2 3.4.23.24 HIV Infections https://pubmed.ncbi.nlm.nih.gov/15938881/ [In vitro study of oral Candida albicans in virulence from HIV-positive individuals] diagnostic usage 3 3.4.23.24 HIV Infections https://pubmed.ncbi.nlm.nih.gov/22472853/ Candida and candidiasis in HIV-infected patients: where commensalism, opportunistic behavior and frank pathogenicity lose their borders. therapeutic application 1 3.4.23.24 HIV Infections https://pubmed.ncbi.nlm.nih.gov/15938881/ [In vitro study of oral Candida albicans in virulence from HIV-positive individuals] ongoing research 4 3.4.23.24 HIV Infections https://pubmed.ncbi.nlm.nih.gov/15938881/ [In vitro study of oral Candida albicans in virulence from HIV-positive individuals] unassigned - 3.4.23.24 HIV Infections https://pubmed.ncbi.nlm.nih.gov/22472853/ Candida and candidiasis in HIV-infected patients: where commensalism, opportunistic behavior and frank pathogenicity lose their borders. unassigned - 3.4.23.24 Hypersensitivity https://pubmed.ncbi.nlm.nih.gov/16087741/ Yapsins are a family of aspartyl proteases required for cell wall integrity in Saccharomyces cerevisiae. ongoing research 1 3.4.23.24 Hypersensitivity https://pubmed.ncbi.nlm.nih.gov/16087741/ Yapsins are a family of aspartyl proteases required for cell wall integrity in Saccharomyces cerevisiae. unassigned - 3.4.23.24 Hypertension https://pubmed.ncbi.nlm.nih.gov/16787263/ Development of inhibitors of the aspartyl protease renin for the treatment of hypertension. causal interaction 4 3.4.23.24 Hypertension https://pubmed.ncbi.nlm.nih.gov/21840215/ Structure-based design and optimization of potent renin inhibitors on 5- or 7-azaindole-scaffolds. causal interaction 3 3.4.23.24 Hypertension https://pubmed.ncbi.nlm.nih.gov/33356221/ Exploring the pH-Dependent Structure-Dynamics-Function Relationship of Human Renin. causal interaction 3 3.4.23.24 Hypertension https://pubmed.ncbi.nlm.nih.gov/21840218/ Structure-based optimization of potent 4- and 6-azaindole-3-carboxamides as renin inhibitors. diagnostic usage 3 3.4.23.24 Hypertension https://pubmed.ncbi.nlm.nih.gov/16787263/ Development of inhibitors of the aspartyl protease renin for the treatment of hypertension. therapeutic application 4 3.4.23.24 Hypertension https://pubmed.ncbi.nlm.nih.gov/20850300/ Discovery and optimization of a new class of potent and non-chiral indole-3-carboxamide-based renin inhibitors. therapeutic application 3 3.4.23.24 Hypertension https://pubmed.ncbi.nlm.nih.gov/25754490/ trans-3,4-Disubstituted pyrrolidines as inhibitors of the human aspartyl protease renin. Part II: Prime site exploration using an oxygen linker. therapeutic application 4 3.4.23.24 Hypertension https://pubmed.ncbi.nlm.nih.gov/33356221/ Exploring the pH-Dependent Structure-Dynamics-Function Relationship of Human Renin. therapeutic application 4 3.4.23.24 Hypertension https://pubmed.ncbi.nlm.nih.gov/20850300/ Discovery and optimization of a new class of potent and non-chiral indole-3-carboxamide-based renin inhibitors. unassigned - 3.4.23.24 Hypertension https://pubmed.ncbi.nlm.nih.gov/21840218/ Structure-based optimization of potent 4- and 6-azaindole-3-carboxamides as renin inhibitors. unassigned - 3.4.23.24 Hypertension https://pubmed.ncbi.nlm.nih.gov/25754490/ trans-3,4-Disubstituted pyrrolidines as inhibitors of the human aspartyl protease renin. Part II: Prime site exploration using an oxygen linker. unassigned - 3.4.23.24 Hypertension https://pubmed.ncbi.nlm.nih.gov/16787263/ Development of inhibitors of the aspartyl protease renin for the treatment of hypertension. unassigned - 3.4.23.24 Hypertension https://pubmed.ncbi.nlm.nih.gov/21840215/ Structure-based design and optimization of potent renin inhibitors on 5- or 7-azaindole-scaffolds. unassigned - 3.4.23.24 Hypertension https://pubmed.ncbi.nlm.nih.gov/33356221/ Exploring the pH-Dependent Structure-Dynamics-Function Relationship of Human Renin. unassigned - 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/15731084/ Profile of Candida albicans-secreted aspartic proteinase elicited during vaginal infection. causal interaction 1 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/30260953/ Secreted aspartyl proteinase (PbSap) contributes to the virulence of Paracoccidioides brasiliensis infection. causal interaction 4 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/8591036/ The crystal structure of a major secreted aspartic proteinase from Candida albicans in complexes with two inhibitors. causal interaction 3 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/11836127/ Insights into the selective inhibition of Candida albicans secreted aspartyl protease: a docking analysis study. causal interaction 4 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/12761103/ The secreted aspartyl proteinases Sap1 and Sap2 cause tissue damage in an in vitro model of vaginal candidiasis based on reconstituted human vaginal epithelium. causal interaction 1 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/15845479/ Candida albicans-secreted aspartic proteinases modify the epithelial cytokine response in an in vitro model of vaginal candidiasis. causal interaction 3 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/22167025/ Spectrophotometric analysis of the expression of secreted aspartyl proteinases from Candida in leukoplakia and oral squamous cell carcinoma. causal interaction 4 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/27037957/ An effector of apple proliferation phytoplasma targets TCP transcription factors - a generalized virulence strategy of phytoplasma? causal interaction 2 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/28541793/ Inhibition of secreted aspartyl proteinase activity in biofilms of Candida species by mycogenic silver nanoparticles. causal interaction 1 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/29139623/ Extracellular proteinases of Candida species pathogenic yeasts. causal interaction 2 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/33787770/ Gene expression of Paracoccidioides virulence factors after interaction with macrophages and fibroblasts. causal interaction 1 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/34420500/ Effect of HIV aspartyl protease inhibitors on experimental infection with a cystogenic Me49 strain of Toxoplasma gondii. causal interaction 1 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/9920319/ Antibody to the Dirofilaria immitis aspartyl protease inhibitor homologue is a diagnostic marker for feline heartworm infections. diagnostic usage 1 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/12870130/ Differential expression of Candida albicans secreted aspartyl proteinase and phospholipase B genes in humans correlates with active oral and vaginal infections. diagnostic usage 1 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/17641856/ Expression of Candida albicans secreted aspartyl proteinase in acute vaginal candidiasis. diagnostic usage 3 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/22167025/ Spectrophotometric analysis of the expression of secreted aspartyl proteinases from Candida in leukoplakia and oral squamous cell carcinoma. diagnostic usage 2 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/30766582/ Relationship between Sap prevalence and biofilm formation among resistant clinical isolates of Candida albicans. diagnostic usage 3 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/33787770/ Gene expression of Paracoccidioides virulence factors after interaction with macrophages and fibroblasts. diagnostic usage 3 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/9920319/ Antibody to the Dirofilaria immitis aspartyl protease inhibitor homologue is a diagnostic marker for feline heartworm infections. therapeutic application 1 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/12870130/ Differential expression of Candida albicans secreted aspartyl proteinase and phospholipase B genes in humans correlates with active oral and vaginal infections. therapeutic application 1 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/8591036/ The crystal structure of a major secreted aspartic proteinase from Candida albicans in complexes with two inhibitors. therapeutic application 4 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/12761103/ The secreted aspartyl proteinases Sap1 and Sap2 cause tissue damage in an in vitro model of vaginal candidiasis based on reconstituted human vaginal epithelium. therapeutic application 1 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/16741514/ Hyphal invasion of Candida albicans inhibits the expression of human beta-defensins in experimental oral candidiasis. therapeutic application 1 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/18032516/ Inhibition of endosome-lysosome system acidification enhances porcine circovirus 2 infection of porcine epithelial cells. therapeutic application 1 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/22110651/ Wild-type Drosophila melanogaster as a model host to analyze nitrogen source dependent virulence of Candida albicans. therapeutic application 1 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/26890982/ Genetically Engineered Virus Nanofibers as an Efficient Vaccine for Preventing Fungal Infection. therapeutic application 1 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/28541793/ Inhibition of secreted aspartyl proteinase activity in biofilms of Candida species by mycogenic silver nanoparticles. therapeutic application 4 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/34420500/ Effect of HIV aspartyl protease inhibitors on experimental infection with a cystogenic Me49 strain of Toxoplasma gondii. therapeutic application 4 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/12870130/ Differential expression of Candida albicans secreted aspartyl proteinase and phospholipase B genes in humans correlates with active oral and vaginal infections. ongoing research 2 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/15731084/ Profile of Candida albicans-secreted aspartic proteinase elicited during vaginal infection. ongoing research 2 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/9720053/ Overexpression of Candida albicans secretory aspartyl proteinase 2 and its expression in Saccharomyces cerevisiae do not augment virulence in mice. ongoing research 2 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/12761103/ The secreted aspartyl proteinases Sap1 and Sap2 cause tissue damage in an in vitro model of vaginal candidiasis based on reconstituted human vaginal epithelium. ongoing research 3 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/16269404/ Glycosylphosphatidylinositol-anchored proteases of Candida albicans target proteins necessary for both cellular processes and host-pathogen interactions. ongoing research 3 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/17641856/ Expression of Candida albicans secreted aspartyl proteinase in acute vaginal candidiasis. ongoing research 4 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/18957581/ Quantitative expression of the Candida albicans secreted aspartyl proteinase gene family in human oral and vaginal candidiasis. ongoing research 2 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/22167025/ Spectrophotometric analysis of the expression of secreted aspartyl proteinases from Candida in leukoplakia and oral squamous cell carcinoma. ongoing research 3 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/30766582/ Relationship between Sap prevalence and biofilm formation among resistant clinical isolates of Candida albicans. ongoing research 2 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/33787770/ Gene expression of Paracoccidioides virulence factors after interaction with macrophages and fibroblasts. ongoing research 4 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/34420500/ Effect of HIV aspartyl protease inhibitors on experimental infection with a cystogenic Me49 strain of Toxoplasma gondii. ongoing research 2 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/9920319/ Antibody to the Dirofilaria immitis aspartyl protease inhibitor homologue is a diagnostic marker for feline heartworm infections. unassigned - 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/12870130/ Differential expression of Candida albicans secreted aspartyl proteinase and phospholipase B genes in humans correlates with active oral and vaginal infections. unassigned - 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/7599606/ Cleavage of human big endothelin-1 by Candida albicans aspartic proteinase. unassigned - 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/9720053/ Overexpression of Candida albicans secretory aspartyl proteinase 2 and its expression in Saccharomyces cerevisiae do not augment virulence in mice. unassigned - 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/16269404/ Glycosylphosphatidylinositol-anchored proteases of Candida albicans target proteins necessary for both cellular processes and host-pathogen interactions. unassigned - 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/16741514/ Hyphal invasion of Candida albicans inhibits the expression of human beta-defensins in experimental oral candidiasis. unassigned - 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/17641856/ Expression of Candida albicans secreted aspartyl proteinase in acute vaginal candidiasis. unassigned - 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/18032516/ Inhibition of endosome-lysosome system acidification enhances porcine circovirus 2 infection of porcine epithelial cells. unassigned - 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/18957581/ Quantitative expression of the Candida albicans secreted aspartyl proteinase gene family in human oral and vaginal candidiasis. unassigned - 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/22110651/ Wild-type Drosophila melanogaster as a model host to analyze nitrogen source dependent virulence of Candida albicans. unassigned - 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/25033657/ Quantitative expression of Candida albicans aspartyl proteinase genes SAP7, SAP8, SAP9, SAP10 in human serum in vitro. unassigned - 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/26890982/ Genetically Engineered Virus Nanofibers as an Efficient Vaccine for Preventing Fungal Infection. unassigned - 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/30377279/ Aspartyl Protease 5 Matures Dense Granule Proteins That Reside at the Host-Parasite Interface in Toxoplasma gondii. unassigned - 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/30766582/ Relationship between Sap prevalence and biofilm formation among resistant clinical isolates of Candida albicans. unassigned - 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/31602591/ Upregulation of secreted aspartyl proteinase genes of fluconazole-sensitive Candida albicans isolates. unassigned - 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/15731084/ Profile of Candida albicans-secreted aspartic proteinase elicited during vaginal infection. unassigned - 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/30260953/ Secreted aspartyl proteinase (PbSap) contributes to the virulence of Paracoccidioides brasiliensis infection. unassigned - 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/8591036/ The crystal structure of a major secreted aspartic proteinase from Candida albicans in complexes with two inhibitors. unassigned - 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/11836127/ Insights into the selective inhibition of Candida albicans secreted aspartyl protease: a docking analysis study. unassigned - 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/12761103/ The secreted aspartyl proteinases Sap1 and Sap2 cause tissue damage in an in vitro model of vaginal candidiasis based on reconstituted human vaginal epithelium. unassigned - 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/15845479/ Candida albicans-secreted aspartic proteinases modify the epithelial cytokine response in an in vitro model of vaginal candidiasis. unassigned - 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/27037957/ An effector of apple proliferation phytoplasma targets TCP transcription factors - a generalized virulence strategy of phytoplasma? unassigned - 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/28541793/ Inhibition of secreted aspartyl proteinase activity in biofilms of Candida species by mycogenic silver nanoparticles. unassigned - 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/29139623/ Extracellular proteinases of Candida species pathogenic yeasts. unassigned - 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/34420500/ Effect of HIV aspartyl protease inhibitors on experimental infection with a cystogenic Me49 strain of Toxoplasma gondii. unassigned - 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/22167025/ Spectrophotometric analysis of the expression of secreted aspartyl proteinases from Candida in leukoplakia and oral squamous cell carcinoma. unassigned - 3.4.23.24 Infections https://pubmed.ncbi.nlm.nih.gov/33787770/ Gene expression of Paracoccidioides virulence factors after interaction with macrophages and fibroblasts. unassigned - 3.4.23.24 Insulin Resistance https://pubmed.ncbi.nlm.nih.gov/15075198/ Diarrhea-associated HIV-1 APIs potentiate muscarinic activation of Cl- secretion by T84 cells via prolongation of cytosolic Ca2+ signaling. causal interaction 2 3.4.23.24 Insulin Resistance https://pubmed.ncbi.nlm.nih.gov/15075198/ Diarrhea-associated HIV-1 APIs potentiate muscarinic activation of Cl- secretion by T84 cells via prolongation of cytosolic Ca2+ signaling. ongoing research 1 3.4.23.24 Insulin Resistance https://pubmed.ncbi.nlm.nih.gov/15075198/ Diarrhea-associated HIV-1 APIs potentiate muscarinic activation of Cl- secretion by T84 cells via prolongation of cytosolic Ca2+ signaling. unassigned - 3.4.23.24 Intestinal Volvulus https://pubmed.ncbi.nlm.nih.gov/9920319/ Antibody to the Dirofilaria immitis aspartyl protease inhibitor homologue is a diagnostic marker for feline heartworm infections. diagnostic usage 1 3.4.23.24 Intestinal Volvulus https://pubmed.ncbi.nlm.nih.gov/9920319/ Antibody to the Dirofilaria immitis aspartyl protease inhibitor homologue is a diagnostic marker for feline heartworm infections. therapeutic application 1 3.4.23.24 Intestinal Volvulus https://pubmed.ncbi.nlm.nih.gov/9920319/ Antibody to the Dirofilaria immitis aspartyl protease inhibitor homologue is a diagnostic marker for feline heartworm infections. unassigned - 3.4.23.24 Keratitis https://pubmed.ncbi.nlm.nih.gov/17652724/ The role of secreted aspartyl proteinases in Candida albicans keratitis. ongoing research 1 3.4.23.24 Keratitis https://pubmed.ncbi.nlm.nih.gov/17652724/ The role of secreted aspartyl proteinases in Candida albicans keratitis. unassigned - 3.4.23.24 Leukoplakia https://pubmed.ncbi.nlm.nih.gov/22167025/ Spectrophotometric analysis of the expression of secreted aspartyl proteinases from Candida in leukoplakia and oral squamous cell carcinoma. causal interaction 4 3.4.23.24 Leukoplakia https://pubmed.ncbi.nlm.nih.gov/22167025/ Spectrophotometric analysis of the expression of secreted aspartyl proteinases from Candida in leukoplakia and oral squamous cell carcinoma. diagnostic usage 2 3.4.23.24 Leukoplakia https://pubmed.ncbi.nlm.nih.gov/22167025/ Spectrophotometric analysis of the expression of secreted aspartyl proteinases from Candida in leukoplakia and oral squamous cell carcinoma. ongoing research 3 3.4.23.24 Leukoplakia https://pubmed.ncbi.nlm.nih.gov/22167025/ Spectrophotometric analysis of the expression of secreted aspartyl proteinases from Candida in leukoplakia and oral squamous cell carcinoma. unassigned - 3.4.23.24 Lipodystrophy https://pubmed.ncbi.nlm.nih.gov/15075198/ Diarrhea-associated HIV-1 APIs potentiate muscarinic activation of Cl- secretion by T84 cells via prolongation of cytosolic Ca2+ signaling. causal interaction 2 3.4.23.24 Lipodystrophy https://pubmed.ncbi.nlm.nih.gov/15075198/ Diarrhea-associated HIV-1 APIs potentiate muscarinic activation of Cl- secretion by T84 cells via prolongation of cytosolic Ca2+ signaling. ongoing research 1 3.4.23.24 Lipodystrophy https://pubmed.ncbi.nlm.nih.gov/15075198/ Diarrhea-associated HIV-1 APIs potentiate muscarinic activation of Cl- secretion by T84 cells via prolongation of cytosolic Ca2+ signaling. unassigned - 3.4.23.24 Lung Injury https://pubmed.ncbi.nlm.nih.gov/30260953/ Secreted aspartyl proteinase (PbSap) contributes to the virulence of Paracoccidioides brasiliensis infection. causal interaction 4 3.4.23.24 Lung Injury https://pubmed.ncbi.nlm.nih.gov/30260953/ Secreted aspartyl proteinase (PbSap) contributes to the virulence of Paracoccidioides brasiliensis infection. unassigned - 3.4.23.24 Malaria https://pubmed.ncbi.nlm.nih.gov/9873534/ Identification of potent inhibitors of Plasmodium falciparum plasmepsin II from an encoded statine combinatorial library. causal interaction 2 3.4.23.24 Malaria https://pubmed.ncbi.nlm.nih.gov/26214367/ Structural basis for plasmepsin V inhibition that blocks export of malaria proteins to human erythrocytes. causal interaction 1 3.4.23.24 Malaria https://pubmed.ncbi.nlm.nih.gov/31883707/ Targeting Plasmodium Plasmepsin V: Hitting Two Birds with One Stone. causal interaction 4 3.4.23.24 Malaria https://pubmed.ncbi.nlm.nih.gov/9873534/ Identification of potent inhibitors of Plasmodium falciparum plasmepsin II from an encoded statine combinatorial library. therapeutic application 4 3.4.23.24 Malaria https://pubmed.ncbi.nlm.nih.gov/26214367/ Structural basis for plasmepsin V inhibition that blocks export of malaria proteins to human erythrocytes. therapeutic application 2 3.4.23.24 Malaria https://pubmed.ncbi.nlm.nih.gov/31883707/ Targeting Plasmodium Plasmepsin V: Hitting Two Birds with One Stone. therapeutic application 1 3.4.23.24 Malaria https://pubmed.ncbi.nlm.nih.gov/20130643/ An aspartyl protease directs malaria effector proteins to the host cell. ongoing research 2 3.4.23.24 Malaria https://pubmed.ncbi.nlm.nih.gov/20130643/ An aspartyl protease directs malaria effector proteins to the host cell. unassigned - 3.4.23.24 Malaria https://pubmed.ncbi.nlm.nih.gov/29800827/ Enhanced antimalarial activity of plasmepsin V inhibitors by modification of the P2 position of PEXEL peptidomimetics. unassigned - 3.4.23.24 Malaria https://pubmed.ncbi.nlm.nih.gov/9873534/ Identification of potent inhibitors of Plasmodium falciparum plasmepsin II from an encoded statine combinatorial library. unassigned - 3.4.23.24 Malaria https://pubmed.ncbi.nlm.nih.gov/26214367/ Structural basis for plasmepsin V inhibition that blocks export of malaria proteins to human erythrocytes. unassigned - 3.4.23.24 Malaria https://pubmed.ncbi.nlm.nih.gov/31883707/ Targeting Plasmodium Plasmepsin V: Hitting Two Birds with One Stone. unassigned - 3.4.23.24 Melanoma https://pubmed.ncbi.nlm.nih.gov/18343923/ Gamma-IFN-inducible-lysosomal thiol reductase modulates acidic proteases and HLA class II antigen processing in melanoma. therapeutic application 1 3.4.23.24 Melanoma https://pubmed.ncbi.nlm.nih.gov/18343923/ Gamma-IFN-inducible-lysosomal thiol reductase modulates acidic proteases and HLA class II antigen processing in melanoma. ongoing research 1 3.4.23.24 Melanoma https://pubmed.ncbi.nlm.nih.gov/18343923/ Gamma-IFN-inducible-lysosomal thiol reductase modulates acidic proteases and HLA class II antigen processing in melanoma. unassigned - 3.4.23.24 Mycoses https://pubmed.ncbi.nlm.nih.gov/30431632/ Novel non-peptidic small molecule inhibitors of secreted aspartic protease 2 (SAP2) for the treatment of resistant fungal infections. causal interaction 3 3.4.23.24 Mycoses https://pubmed.ncbi.nlm.nih.gov/11836127/ Insights into the selective inhibition of Candida albicans secreted aspartyl protease: a docking analysis study. causal interaction 4 3.4.23.24 Mycoses https://pubmed.ncbi.nlm.nih.gov/30431632/ Novel non-peptidic small molecule inhibitors of secreted aspartic protease 2 (SAP2) for the treatment of resistant fungal infections. therapeutic application 4 3.4.23.24 Mycoses https://pubmed.ncbi.nlm.nih.gov/22146051/ The crystal structure of protease Sapp1p from Candida parapsilosis in complex with the HIV protease inhibitor ritonavir. therapeutic application 4 3.4.23.24 Mycoses https://pubmed.ncbi.nlm.nih.gov/22146051/ The crystal structure of protease Sapp1p from Candida parapsilosis in complex with the HIV protease inhibitor ritonavir. unassigned - 3.4.23.24 Mycoses https://pubmed.ncbi.nlm.nih.gov/30431632/ Novel non-peptidic small molecule inhibitors of secreted aspartic protease 2 (SAP2) for the treatment of resistant fungal infections. unassigned - 3.4.23.24 Mycoses https://pubmed.ncbi.nlm.nih.gov/11836127/ Insights into the selective inhibition of Candida albicans secreted aspartyl protease: a docking analysis study. unassigned - 3.4.23.24 Nematode Infections https://pubmed.ncbi.nlm.nih.gov/13678638/ Identification and characterisation of an aspartyl protease inhibitor homologue as a major allergen of Trichostrongylus colubriformis. causal interaction 2 3.4.23.24 Nematode Infections https://pubmed.ncbi.nlm.nih.gov/13678638/ Identification and characterisation of an aspartyl protease inhibitor homologue as a major allergen of Trichostrongylus colubriformis. diagnostic usage 1 3.4.23.24 Nematode Infections https://pubmed.ncbi.nlm.nih.gov/13678638/ Identification and characterisation of an aspartyl protease inhibitor homologue as a major allergen of Trichostrongylus colubriformis. therapeutic application 1 3.4.23.24 Nematode Infections https://pubmed.ncbi.nlm.nih.gov/13678638/ Identification and characterisation of an aspartyl protease inhibitor homologue as a major allergen of Trichostrongylus colubriformis. unassigned - 3.4.23.24 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/1395002/ Cathepsin D concentration in breast cancer cytosols: correlation with disease-free interval and overall survival. causal interaction 2 3.4.23.24 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/7541934/ Quantitative immunohistochemical determination of cathepsin D levels in prostatic carcinoma biopsies. Correlation with tumor grade, stage, PSA level, and DNA ploidy status. causal interaction 3 3.4.23.24 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/21559613/ Prognostic indicators for early-stage breast-carcinoma .2. Value of cathepsin-d expression, detected by immunocytochemistry - a multiparametric study. causal interaction 4 3.4.23.24 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/1395002/ Cathepsin D concentration in breast cancer cytosols: correlation with disease-free interval and overall survival. diagnostic usage 3 3.4.23.24 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/7541934/ Quantitative immunohistochemical determination of cathepsin D levels in prostatic carcinoma biopsies. Correlation with tumor grade, stage, PSA level, and DNA ploidy status. diagnostic usage 4 3.4.23.24 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/9033633/ Differential targeting and processing of procathepsin D in normal and transformed murine 3T3 fibroblasts. diagnostic usage 3 3.4.23.24 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/21559613/ Prognostic indicators for early-stage breast-carcinoma .2. Value of cathepsin-d expression, detected by immunocytochemistry - a multiparametric study. diagnostic usage 4 3.4.23.24 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/7541934/ Quantitative immunohistochemical determination of cathepsin D levels in prostatic carcinoma biopsies. Correlation with tumor grade, stage, PSA level, and DNA ploidy status. therapeutic application 1 3.4.23.24 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/21559613/ Prognostic indicators for early-stage breast-carcinoma .2. Value of cathepsin-d expression, detected by immunocytochemistry - a multiparametric study. therapeutic application 1 3.4.23.24 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/1395002/ Cathepsin D concentration in breast cancer cytosols: correlation with disease-free interval and overall survival. ongoing research 2 3.4.23.24 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/7541934/ Quantitative immunohistochemical determination of cathepsin D levels in prostatic carcinoma biopsies. Correlation with tumor grade, stage, PSA level, and DNA ploidy status. ongoing research 4 3.4.23.24 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/21559613/ Prognostic indicators for early-stage breast-carcinoma .2. Value of cathepsin-d expression, detected by immunocytochemistry - a multiparametric study. ongoing research 4 3.4.23.24 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/9033633/ Differential targeting and processing of procathepsin D in normal and transformed murine 3T3 fibroblasts. unassigned - 3.4.23.24 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/1395002/ Cathepsin D concentration in breast cancer cytosols: correlation with disease-free interval and overall survival. unassigned - 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/9022834/ Muscle aspartyl protease (cathepsin D) activity: detection using a chromophoric substrate and relation to wasting in DBA/2 mice implanted with leukemic L1210 tumor cells. causal interaction 3 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/1395002/ Cathepsin D concentration in breast cancer cytosols: correlation with disease-free interval and overall survival. causal interaction 2 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/7541934/ Quantitative immunohistochemical determination of cathepsin D levels in prostatic carcinoma biopsies. Correlation with tumor grade, stage, PSA level, and DNA ploidy status. causal interaction 3 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/8419924/ Cathepsin D gene is controlled by a mixed promoter, and estrogens stimulate only TATA-dependent transcription in breast cancer cells. causal interaction 4 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/9271363/ Release of the aspartyl protease cathepsin D is associated with and facilitates human breast cancer cell invasion. causal interaction 1 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/9917508/ Characterization of purified cathepsin D from malignant human breast tissue. causal interaction 4 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/11080791/ Nm23 and cathepsin D expression in laryngeal carcinomas. causal interaction 4 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/14766246/ Cathepsin D in ovarian cancer: prognostic value and correlation with p53 expression and microvessel density. causal interaction 4 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/15958563/ Cathepsin D is a potential serum marker for poor prognosis in glioma patients. causal interaction 4 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/16787353/ New cathepsin d inhibitors with hydroxyethylamine isosteres: preparation and characterization. causal interaction 4 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/17827153/ Epidermal Growth Factor Receptor and Notch Pathways Participate in the Tumor Suppressor Function of {gamma}-Secretase. causal interaction 3 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/20485791/ A paramagnetic chemical exchange-based MRI probe metabolized by cathepsin D: design, synthesis and cellular uptake studies. causal interaction 4 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/21607525/ Immunohistochemical detection of cathepsin-d expression in prostate-cancer. causal interaction 4 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22309842/ Therapeutic approaches to modulating Notch signaling: Current challenges and future prospects. causal interaction 3 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22476353/ The potential prognostic value of cathepsin D protein in serous ovarian cancer. causal interaction 3 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24026424/ Cathepsin D stimulates the activities of secreted plasminogen activators in the breast cancer acidic environment. causal interaction 4 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27149201/ Procathepsin E is highly abundant but minimally active in pancreatic ductal adenocarcinoma tumors. causal interaction 4 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/1395002/ Cathepsin D concentration in breast cancer cytosols: correlation with disease-free interval and overall survival. diagnostic usage 3 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/7541934/ Quantitative immunohistochemical determination of cathepsin D levels in prostatic carcinoma biopsies. Correlation with tumor grade, stage, PSA level, and DNA ploidy status. diagnostic usage 4 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/8372434/ Moloney murine leukemia virus protease: bacterial expression and characterization of the purified enzyme. diagnostic usage 2 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/8419924/ Cathepsin D gene is controlled by a mixed promoter, and estrogens stimulate only TATA-dependent transcription in breast cancer cells. diagnostic usage 3 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/9271363/ Release of the aspartyl protease cathepsin D is associated with and facilitates human breast cancer cell invasion. diagnostic usage 3 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/11080791/ Nm23 and cathepsin D expression in laryngeal carcinomas. diagnostic usage 3 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/14766246/ Cathepsin D in ovarian cancer: prognostic value and correlation with p53 expression and microvessel density. diagnostic usage 4 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/15958563/ Cathepsin D is a potential serum marker for poor prognosis in glioma patients. diagnostic usage 4 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/16552483/ Phospholipase and proteinase activities of clinical isolates of Candida from immunocompromised patients. diagnostic usage 2 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/16787353/ New cathepsin d inhibitors with hydroxyethylamine isosteres: preparation and characterization. diagnostic usage 3 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/20485791/ A paramagnetic chemical exchange-based MRI probe metabolized by cathepsin D: design, synthesis and cellular uptake studies. diagnostic usage 2 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/21607525/ Immunohistochemical detection of cathepsin-d expression in prostate-cancer. diagnostic usage 4 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22476353/ The potential prognostic value of cathepsin D protein in serous ovarian cancer. diagnostic usage 4 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24026424/ Cathepsin D stimulates the activities of secreted plasminogen activators in the breast cancer acidic environment. diagnostic usage 3 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27149201/ Procathepsin E is highly abundant but minimally active in pancreatic ductal adenocarcinoma tumors. diagnostic usage 3 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/9022834/ Muscle aspartyl protease (cathepsin D) activity: detection using a chromophoric substrate and relation to wasting in DBA/2 mice implanted with leukemic L1210 tumor cells. therapeutic application 1 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/7541934/ Quantitative immunohistochemical determination of cathepsin D levels in prostatic carcinoma biopsies. Correlation with tumor grade, stage, PSA level, and DNA ploidy status. therapeutic application 1 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/8372434/ Moloney murine leukemia virus protease: bacterial expression and characterization of the purified enzyme. therapeutic application 2 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/11080791/ Nm23 and cathepsin D expression in laryngeal carcinomas. therapeutic application 1 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/14766246/ Cathepsin D in ovarian cancer: prognostic value and correlation with p53 expression and microvessel density. therapeutic application 1 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/15958563/ Cathepsin D is a potential serum marker for poor prognosis in glioma patients. therapeutic application 4 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/16787353/ New cathepsin d inhibitors with hydroxyethylamine isosteres: preparation and characterization. therapeutic application 1 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/17827153/ Epidermal Growth Factor Receptor and Notch Pathways Participate in the Tumor Suppressor Function of {gamma}-Secretase. therapeutic application 3 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22309842/ Therapeutic approaches to modulating Notch signaling: Current challenges and future prospects. therapeutic application 4 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24026424/ Cathepsin D stimulates the activities of secreted plasminogen activators in the breast cancer acidic environment. therapeutic application 1 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27149201/ Procathepsin E is highly abundant but minimally active in pancreatic ductal adenocarcinoma tumors. therapeutic application 4 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33271453/ Identification and structure-activity relationship studies of small molecule inhibitors of the human cathepsin D. therapeutic application 4 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/9022834/ Muscle aspartyl protease (cathepsin D) activity: detection using a chromophoric substrate and relation to wasting in DBA/2 mice implanted with leukemic L1210 tumor cells. ongoing research 4 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/1395002/ Cathepsin D concentration in breast cancer cytosols: correlation with disease-free interval and overall survival. ongoing research 2 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/7541934/ Quantitative immunohistochemical determination of cathepsin D levels in prostatic carcinoma biopsies. Correlation with tumor grade, stage, PSA level, and DNA ploidy status. ongoing research 4 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/8372434/ Moloney murine leukemia virus protease: bacterial expression and characterization of the purified enzyme. ongoing research 2 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/8419924/ Cathepsin D gene is controlled by a mixed promoter, and estrogens stimulate only TATA-dependent transcription in breast cancer cells. ongoing research 1 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/9271363/ Release of the aspartyl protease cathepsin D is associated with and facilitates human breast cancer cell invasion. ongoing research 4 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/11080791/ Nm23 and cathepsin D expression in laryngeal carcinomas. ongoing research 4 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/14766246/ Cathepsin D in ovarian cancer: prognostic value and correlation with p53 expression and microvessel density. ongoing research 3 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/15958563/ Cathepsin D is a potential serum marker for poor prognosis in glioma patients. ongoing research 4 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/16552483/ Phospholipase and proteinase activities of clinical isolates of Candida from immunocompromised patients. ongoing research 2 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/17827153/ Epidermal Growth Factor Receptor and Notch Pathways Participate in the Tumor Suppressor Function of {gamma}-Secretase. ongoing research 1 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/21607525/ Immunohistochemical detection of cathepsin-d expression in prostate-cancer. ongoing research 3 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22476353/ The potential prognostic value of cathepsin D protein in serous ovarian cancer. ongoing research 4 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/24026424/ Cathepsin D stimulates the activities of secreted plasminogen activators in the breast cancer acidic environment. ongoing research 4 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/27149201/ Procathepsin E is highly abundant but minimally active in pancreatic ductal adenocarcinoma tumors. ongoing research 2 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33294784/ Non-canonical Shedding of TNF? by SPPL2a Is Determined by the Conformational Flexibility of Its Transmembrane Helix. ongoing research 3 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/8372434/ Moloney murine leukemia virus protease: bacterial expression and characterization of the purified enzyme. unassigned - 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/16552483/ Phospholipase and proteinase activities of clinical isolates of Candida from immunocompromised patients. unassigned - 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33271453/ Identification and structure-activity relationship studies of small molecule inhibitors of the human cathepsin D. unassigned - 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33294784/ Non-canonical Shedding of TNF? by SPPL2a Is Determined by the Conformational Flexibility of Its Transmembrane Helix. unassigned - 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33343338/ ?-Secretase Modulatory Proteins: The Guiding Hand Behind the Running Scissors. unassigned - 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/9022834/ Muscle aspartyl protease (cathepsin D) activity: detection using a chromophoric substrate and relation to wasting in DBA/2 mice implanted with leukemic L1210 tumor cells. unassigned - 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/9917508/ Characterization of purified cathepsin D from malignant human breast tissue. unassigned - 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/17827153/ Epidermal Growth Factor Receptor and Notch Pathways Participate in the Tumor Suppressor Function of {gamma}-Secretase. unassigned - 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22309842/ Therapeutic approaches to modulating Notch signaling: Current challenges and future prospects. unassigned - 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/1395002/ Cathepsin D concentration in breast cancer cytosols: correlation with disease-free interval and overall survival. unassigned - 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/8419924/ Cathepsin D gene is controlled by a mixed promoter, and estrogens stimulate only TATA-dependent transcription in breast cancer cells. unassigned - 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/9271363/ Release of the aspartyl protease cathepsin D is associated with and facilitates human breast cancer cell invasion. unassigned - 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/20485791/ A paramagnetic chemical exchange-based MRI probe metabolized by cathepsin D: design, synthesis and cellular uptake studies. unassigned - 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/21607525/ Immunohistochemical detection of cathepsin-d expression in prostate-cancer. unassigned - 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/22476353/ The potential prognostic value of cathepsin D protein in serous ovarian cancer. unassigned - 3.4.23.24 Neoplasms https://pubmed.ncbi.nlm.nih.gov/16787353/ New cathepsin d inhibitors with hydroxyethylamine isosteres: preparation and characterization. unassigned - 3.4.23.24 Neurodegenerative Diseases https://pubmed.ncbi.nlm.nih.gov/23250759/ Role of cathepsin D in U18666A-induced neuronal cell death: potential implication in Niemann-Pick type C disease pathogenesis. causal interaction 4 3.4.23.24 Neurodegenerative Diseases https://pubmed.ncbi.nlm.nih.gov/23484877/ Structure-guided design of ?-secretase (BACE-1) inhibitors. causal interaction 4 3.4.23.24 Neurodegenerative Diseases https://pubmed.ncbi.nlm.nih.gov/29078331/ Lack of BACE1 S-palmitoylation reduces amyloid burden and mitigates memory deficits in transgenic mouse models of Alzheimer's disease. causal interaction 2 3.4.23.24 Neurodegenerative Diseases https://pubmed.ncbi.nlm.nih.gov/29078331/ Lack of BACE1 S-palmitoylation reduces amyloid burden and mitigates memory deficits in transgenic mouse models of Alzheimer's disease. ongoing research 2 3.4.23.24 Neurodegenerative Diseases https://pubmed.ncbi.nlm.nih.gov/23250759/ Role of cathepsin D in U18666A-induced neuronal cell death: potential implication in Niemann-Pick type C disease pathogenesis. unassigned - 3.4.23.24 Neurodegenerative Diseases https://pubmed.ncbi.nlm.nih.gov/23484877/ Structure-guided design of ?-secretase (BACE-1) inhibitors. unassigned - 3.4.23.24 Neurodegenerative Diseases https://pubmed.ncbi.nlm.nih.gov/29078331/ Lack of BACE1 S-palmitoylation reduces amyloid burden and mitigates memory deficits in transgenic mouse models of Alzheimer's disease. unassigned - 3.4.23.24 Opportunistic Infections https://pubmed.ncbi.nlm.nih.gov/10395861/ In vitro and in vivo anticandidal activity of human immunodeficiency virus protease inhibitors. causal interaction 4 3.4.23.24 Opportunistic Infections https://pubmed.ncbi.nlm.nih.gov/10395861/ In vitro and in vivo anticandidal activity of human immunodeficiency virus protease inhibitors. therapeutic application 4 3.4.23.24 Opportunistic Infections https://pubmed.ncbi.nlm.nih.gov/10395861/ In vitro and in vivo anticandidal activity of human immunodeficiency virus protease inhibitors. unassigned - 3.4.23.24 Osteoarthritis https://pubmed.ncbi.nlm.nih.gov/33271453/ Identification and structure-activity relationship studies of small molecule inhibitors of the human cathepsin D. therapeutic application 4 3.4.23.24 Osteoarthritis https://pubmed.ncbi.nlm.nih.gov/33271453/ Identification and structure-activity relationship studies of small molecule inhibitors of the human cathepsin D. unassigned - 3.4.23.24 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/10498202/ Synthesis and structure activity relationships of novel small molecule cathepsin D inhibitors. causal interaction 4 3.4.23.24 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/10498202/ Synthesis and structure activity relationships of novel small molecule cathepsin D inhibitors. diagnostic usage 2 3.4.23.24 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/10498202/ Synthesis and structure activity relationships of novel small molecule cathepsin D inhibitors. ongoing research 1 3.4.23.24 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/10498202/ Synthesis and structure activity relationships of novel small molecule cathepsin D inhibitors. unassigned - 3.4.23.24 Paracoccidioidomycosis https://pubmed.ncbi.nlm.nih.gov/30260953/ Secreted aspartyl proteinase (PbSap) contributes to the virulence of Paracoccidioides brasiliensis infection. causal interaction 4 3.4.23.24 Paracoccidioidomycosis https://pubmed.ncbi.nlm.nih.gov/30260953/ Secreted aspartyl proteinase (PbSap) contributes to the virulence of Paracoccidioides brasiliensis infection. unassigned - 3.4.23.24 Phytoplasma Disease https://pubmed.ncbi.nlm.nih.gov/30165491/ Alterations of plant architecture and phase transition by the phytoplasma virulence factor SAP11. therapeutic application 1 3.4.23.24 Phytoplasma Disease https://pubmed.ncbi.nlm.nih.gov/24552625/ The small phytoplasma virulence effector SAP11 contains distinct domains required for nuclear targeting and CIN-TCP binding and destabilization. unassigned - 3.4.23.24 Phytoplasma Disease https://pubmed.ncbi.nlm.nih.gov/30165491/ Alterations of plant architecture and phase transition by the phytoplasma virulence factor SAP11. unassigned - 3.4.23.24 Retinal Degeneration https://pubmed.ncbi.nlm.nih.gov/22426392/ Cathepsin proteases mediate photoreceptor cell degeneration in Drosophila. causal interaction 1 3.4.23.24 Retinal Degeneration https://pubmed.ncbi.nlm.nih.gov/33800998/ Rapid and Progressive Loss of Multiple Retinal Cell Types in Cathepsin D-Deficient Mice-An Animal Model of CLN10 Disease. diagnostic usage 3 3.4.23.24 Retinal Degeneration https://pubmed.ncbi.nlm.nih.gov/33800998/ Rapid and Progressive Loss of Multiple Retinal Cell Types in Cathepsin D-Deficient Mice-An Animal Model of CLN10 Disease. therapeutic application 2 3.4.23.24 Retinal Degeneration https://pubmed.ncbi.nlm.nih.gov/33800998/ Rapid and Progressive Loss of Multiple Retinal Cell Types in Cathepsin D-Deficient Mice-An Animal Model of CLN10 Disease. ongoing research 4 3.4.23.24 Retinal Degeneration https://pubmed.ncbi.nlm.nih.gov/33800998/ Rapid and Progressive Loss of Multiple Retinal Cell Types in Cathepsin D-Deficient Mice-An Animal Model of CLN10 Disease. unassigned - 3.4.23.24 Retinal Degeneration https://pubmed.ncbi.nlm.nih.gov/22426392/ Cathepsin proteases mediate photoreceptor cell degeneration in Drosophila. unassigned - 3.4.23.24 Squamous Cell Carcinoma of Head and Neck https://pubmed.ncbi.nlm.nih.gov/22167025/ Spectrophotometric analysis of the expression of secreted aspartyl proteinases from Candida in leukoplakia and oral squamous cell carcinoma. causal interaction 4 3.4.23.24 Squamous Cell Carcinoma of Head and Neck https://pubmed.ncbi.nlm.nih.gov/22167025/ Spectrophotometric analysis of the expression of secreted aspartyl proteinases from Candida in leukoplakia and oral squamous cell carcinoma. diagnostic usage 2 3.4.23.24 Squamous Cell Carcinoma of Head and Neck https://pubmed.ncbi.nlm.nih.gov/22167025/ Spectrophotometric analysis of the expression of secreted aspartyl proteinases from Candida in leukoplakia and oral squamous cell carcinoma. ongoing research 3 3.4.23.24 Squamous Cell Carcinoma of Head and Neck https://pubmed.ncbi.nlm.nih.gov/22167025/ Spectrophotometric analysis of the expression of secreted aspartyl proteinases from Candida in leukoplakia and oral squamous cell carcinoma. unassigned - 3.4.23.24 Starvation https://pubmed.ncbi.nlm.nih.gov/9524217/ Characterization of a gene from the filamentous fungus Podospora anserina encoding an aspartyl protease induced upon carbon starvation. therapeutic application 1 3.4.23.24 Starvation https://pubmed.ncbi.nlm.nih.gov/24464367/ Transgenic plants that express the phytoplasma effector SAP11 show altered phosphate starvation and defense responses. therapeutic application 1 3.4.23.24 Starvation https://pubmed.ncbi.nlm.nih.gov/9524217/ Characterization of a gene from the filamentous fungus Podospora anserina encoding an aspartyl protease induced upon carbon starvation. ongoing research 2 3.4.23.24 Starvation https://pubmed.ncbi.nlm.nih.gov/9524217/ Characterization of a gene from the filamentous fungus Podospora anserina encoding an aspartyl protease induced upon carbon starvation. unassigned - 3.4.23.24 Starvation https://pubmed.ncbi.nlm.nih.gov/24464367/ Transgenic plants that express the phytoplasma effector SAP11 show altered phosphate starvation and defense responses. unassigned - 3.4.23.24 Stomatitis, Denture https://pubmed.ncbi.nlm.nih.gov/25857681/ Expression of Secreted Aspartyl Proteinases in an Experimental Model of Candida albicans-Associated Denture Stomatitis. ongoing research 2 3.4.23.24 Stomatitis, Denture https://pubmed.ncbi.nlm.nih.gov/25857681/ Expression of Secreted Aspartyl Proteinases in an Experimental Model of Candida albicans-Associated Denture Stomatitis. unassigned - 3.4.23.24 Uterine Cervical Neoplasms https://pubmed.ncbi.nlm.nih.gov/33668328/ HIV-1 Protease Inhibitors Slow HPV16-Driven Cell Proliferation through Targeted Depletion of Viral E6 and E7 Oncoproteins. therapeutic application 2 3.4.23.24 Uterine Cervical Neoplasms https://pubmed.ncbi.nlm.nih.gov/33668328/ HIV-1 Protease Inhibitors Slow HPV16-Driven Cell Proliferation through Targeted Depletion of Viral E6 and E7 Oncoproteins. ongoing research 3 3.4.23.24 Uterine Cervical Neoplasms https://pubmed.ncbi.nlm.nih.gov/33668328/ HIV-1 Protease Inhibitors Slow HPV16-Driven Cell Proliferation through Targeted Depletion of Viral E6 and E7 Oncoproteins. unassigned - 3.4.23.24 Vaginitis https://pubmed.ncbi.nlm.nih.gov/10203490/ High aspartyl proteinase production and vaginitis in human immunodeficiency virus-infected women. causal interaction 2 3.4.23.24 Vaginitis https://pubmed.ncbi.nlm.nih.gov/10203490/ High aspartyl proteinase production and vaginitis in human immunodeficiency virus-infected women. diagnostic usage 3 3.4.23.24 Vaginitis https://pubmed.ncbi.nlm.nih.gov/9841840/ Evidence that members of the secretory aspartyl proteinase gene family, in particular SAP2, are virulence factors for Candida vaginitis. ongoing research 1 3.4.23.24 Vaginitis https://pubmed.ncbi.nlm.nih.gov/10203490/ High aspartyl proteinase production and vaginitis in human immunodeficiency virus-infected women. ongoing research 3 3.4.23.24 Vaginitis https://pubmed.ncbi.nlm.nih.gov/9841840/ Evidence that members of the secretory aspartyl proteinase gene family, in particular SAP2, are virulence factors for Candida vaginitis. unassigned - 3.4.23.24 Vaginitis https://pubmed.ncbi.nlm.nih.gov/28760935/ Overexpression of Candida albicans Secreted Aspartyl Proteinases 2 or 5 is not sufficient for exacerbation of immunopathology in a murine model of vaginitis. unassigned - 3.4.23.24 Vaginitis https://pubmed.ncbi.nlm.nih.gov/10203490/ High aspartyl proteinase production and vaginitis in human immunodeficiency virus-infected women. unassigned - 3.4.23.24 Wasting Syndrome https://pubmed.ncbi.nlm.nih.gov/9022834/ Muscle aspartyl protease (cathepsin D) activity: detection using a chromophoric substrate and relation to wasting in DBA/2 mice implanted with leukemic L1210 tumor cells. causal interaction 3 3.4.23.24 Wasting Syndrome https://pubmed.ncbi.nlm.nih.gov/9022834/ Muscle aspartyl protease (cathepsin D) activity: detection using a chromophoric substrate and relation to wasting in DBA/2 mice implanted with leukemic L1210 tumor cells. therapeutic application 1 3.4.23.24 Wasting Syndrome https://pubmed.ncbi.nlm.nih.gov/9022834/ Muscle aspartyl protease (cathepsin D) activity: detection using a chromophoric substrate and relation to wasting in DBA/2 mice implanted with leukemic L1210 tumor cells. ongoing research 4 3.4.23.24 Wasting Syndrome https://pubmed.ncbi.nlm.nih.gov/9022834/ Muscle aspartyl protease (cathepsin D) activity: detection using a chromophoric substrate and relation to wasting in DBA/2 mice implanted with leukemic L1210 tumor cells. unassigned -