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Disease on EC 3.4.24.B12 - ADAMTS5 endopeptidase and Organism(s) Homo sapiens

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DISEASE
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adamts5 endopeptidase deficiency
ADAMTS-5 deficiency does not block aggrecanolysis at preferred cleavage sites in the chondroitin sulfate-rich region of aggrecan.
ADAMTS5 Deficiency in Calcified Aortic Valves Is Associated With Elevated Pro-Osteogenic Activity in Valvular Interstitial Cells.
ADAMTS5 deficiency in mice does not affect cardiac function.
ADAMTS5 deficiency protects against non-alcoholic steatohepatitis in obesity.
Adamts5 Deficiency Protects Mice from Chronic Tobacco Smoking-induced Intervertebral Disc Degeneration.
Adamts5 Deletion Blocks Murine Dermal Repair through CD44-mediated Aggrecan Accumulation and Modulation of Transforming Growth Factor {beta}1 (TGF{beta}1) Signaling.
Insufficient versican cleavage and Smad2 phosphorylation results in bicuspid aortic and pulmonary valves.
Adenoviridae Infections
Sox4 is involved in osteoarthritic cartilage deterioration through induction of ADAMTS4 and ADAMTS5.
Aneurysm
Internal modulation of proteolysis in vascular extracellular matrix remodeling: role of ADAM metallopeptidase with thrombospondin type 1 motif 5 in the development of intracranial aneurysm rupture.
The Investigation of a Disintegrin and Metalloproteinase with ThromboSpondin Motifs (ADAMTS) 1, 5 and 16 in Thoracic Aortic Aneurysms and Dissections.
Aneurysm, Dissecting
ADAMTS-5 Decreases in Aortas and Plasma From Aortic Dissection Patients and Alleviates Angiotensin II-Induced Smooth Muscle-Cell Apoptosis.
Aortic Valve Disease
ADAMTS5 Deficiency in Calcified Aortic Valves Is Associated With Elevated Pro-Osteogenic Activity in Valvular Interstitial Cells.
Arthritis
ADAMTS-5 deficiency does not block aggrecanolysis at preferred cleavage sites in the chondroitin sulfate-rich region of aggrecan.
ADAMTS-5: the story so far.
Adamts5 (aggrecanase-2) is widely expressed in the mouse musculoskeletal system and is induced in specific regions of knee joint explants by inflammatory cytokines.
ADAMTS5 is the major aggrecanase in mouse cartilage in vivo and in vitro.
Adamts5, the gene encoding a proteoglycan-degrading metalloprotease, is expressed by specific cell lineages during mouse embryonic development and in adult tissues.
ADAMTS5-mediated aggrecanolysis in murine epiphyseal chondrocyte cultures.
Aggrecanase-mediated cartilage degradation.
Anti-ADAMTS5 monoclonal antibodies: implications for aggrecanase inhibition in osteoarthritis.
Characterization of proADAMTS5 processing by proprotein convertases.
Kinetics of aggrecanase- and metalloproteinase-induced neoepitopes in various stages of cartilage destruction in murine arthritis.
Matrix-degrading protease ADAMTS-5 cleaves inter-?-inhibitor and release active heavy chain 2 in synovial fluids from arthritic patients.
The nutraceutical flavonoid luteolin inhibits ADAMTS-4 and ADAMTS-5 aggrecanase activities.
Upper zone of growth plate and cartilage matrix associated protein protects cartilage during inflammatory arthritis.
Arthritis, Rheumatoid
ADAMTS5 is a biomarker for prediction of response to infliximab in patients with rheumatoid arthritis.
Current and emerging therapeutic strategies for preventing inflammation and aggrecanase-mediated cartilage destruction in arthritis.
Interleukin-6 upregulates expression of ADAMTS-4 in fibroblast-like synoviocytes from patients with rheumatoid arthritis.
Asthenozoospermia
An in silico analysis of human sperm genes associated with asthenozoospermia and its implication in male infertility.
Atherosclerosis
Novel role of ADAMTS-5 protein in proteoglycan turnover and lipoprotein retention in atherosclerosis.
Azoospermia
ADAMTS1 and ADAMTS5 metalloproteases produced by Sertoli cells: a potential diagnostic marker in azoospermia.
Bicuspid Aortic Valve Disease
Targeted next-generation sequencing identified ADAMTS5 as novel genetic substrate in patients with bicuspid aortic valve.
Breast Neoplasms
Cleavage of Fibulin-2 by the aggrecanases ADAMTS-4 and ADAMTS-5 contributes to the tumorigenic potential of breast cancer cells.
Towards the early detection of ductal carcinoma (a common type of breast cancer) using biomarkers linked to the PPAR(?) signaling pathway.
Carcinogenesis
ADAMTS5 Functions as an Anti-Angiogenic and Anti-Tumorigenic Protein Independent of Its Proteoglycanase Activity.
Epigenetic silencing of ADAMTS5 is associated with increased invasiveness and poor survival in patients with colorectal cancer.
Lost expression of ADAMTS5 protein associates with progression and poor prognosis of hepatocellular carcinoma.
Carcinoma
Expression and distribution of aggrecanases in human larynx: ADAMTS-5/aggrecanase-2 is the main aggrecanase in laryngeal carcinoma.
Host-produced ADAMTS4 Inhibits Early-Stage Tumor Growth.
Carcinoma, Hepatocellular
Association Between a Variant in ADAMTS5 and the Susceptibility to Hepatocellular Carcinoma in a Chinese Han Population.
Expression of ADAMTS-1, ADAMTS-4, ADAMTS-5 and TIMP3 by hepatocellular carcinoma cell lines.
In Silico Identification of Contradictory Role of ADAMTS5 in Hepatocellular Carcinoma.
Lost expression of ADAMTS5 protein associates with progression and poor prognosis of hepatocellular carcinoma.
Polymorphisms of a Disintegrin and Metalloproteinase with Thrombospondin Motifs 5 and Aflatoxin B1-Related Hepatocellular Carcinoma.
Carcinoma, Lewis Lung
Host-produced ADAMTS4 Inhibits Early-Stage Tumor Growth.
Carcinoma, Non-Small-Cell Lung
Overexpression of ADAMTS5 can regulate the migration and invasion of non-small cell lung cancer.
Cardiovascular Diseases
ADAMTS5 deficiency in mice does not affect cardiac function.
Cerebrovascular Disorders
Internal modulation of proteolysis in vascular extracellular matrix remodeling: role of ADAM metallopeptidase with thrombospondin type 1 motif 5 in the development of intracranial aneurysm rupture.
Chondrosarcoma
Characterization of the human ADAMTS-5 (aggrecanase-2) gene promoter.
NF-?? upregulates ADAMTS5 expression by direct binding after TNF-? treatment in OUMS-27 chondrosarcoma cell line.
Colorectal Neoplasms
ADAMTS expression in colorectal cancer.
Epigenetic silencing of ADAMTS5 is associated with increased invasiveness and poor survival in patients with colorectal cancer.
High expression of ADAMTS5 is a potent marker for lymphatic invasion and lymph node metastasis in colorectal cancer.
microRNA -140-5p inhibits colorectal cancer invasion and metastasis by targeting ADAMTS5 and IGFBP5.
Retraction Note: microRNA-140-5p inhibits colorectal cancer invasion and metastasis by targeting ADAMTS5 and IGFBP5.
Coronary Artery Disease
ADAMTS-5 Decreases in Coronary Arteries and Plasma from Patients with Coronary Artery Disease.
Coronary Stenosis
ADAMTS-5 Decreases in Coronary Arteries and Plasma from Patients with Coronary Artery Disease.
Diabetes, Gestational
Evaluation of second trimester amniotic fluid ADAMTS4, ADAMTS5, interleukin-6 and tumor necrosis factor-? levels in patients with gestational diabetes mellitus.
Down Syndrome
Metalloproteinase ADAMTS-1 but not ADAMTS-5 is manifold overexpressed in neurodegenerative disorders as Down syndrome, Alzheimer's and Pick's disease.
Fatty Liver
ADAMTS5 deficiency protects against non-alcoholic steatohepatitis in obesity.
Fetal Growth Retardation
Role of ADAMTS5 in Unexplained Fetal Growth Restriction (FGR).
Glioblastoma
High expression of ADAMTS5 is a potent marker for lymphatic invasion and lymph node metastasis in colorectal cancer.
Human glioblastomas overexpress ADAMTS-5 that degrades brevican.
Matrix-degrading proteases ADAMTS4 and ADAMTS5 (disintegrins and metalloproteinases with thrombospondin motifs 4 and 5) are expressed in human glioblastomas.
Glioma
Human glioblastomas overexpress ADAMTS-5 that degrades brevican.
Glomerulonephritis, IGA
The Metalloproteinase ADAMTS5 Is Expressed by Interstitial Inflammatory Cells in IgA Nephropathy and Is Proteolytically Active on the Kidney Matrix.
Head and Neck Neoplasms
High expression of ADAMTS5 is a potent marker for lymphatic invasion and lymph node metastasis in colorectal cancer.
Hemangioma, Cavernous, Central Nervous System
Cerebral cavernous malformations are driven by ADAMTS5 proteolysis of versican.
Hemophilia A
Serological biomarkers detect active joint destruction and inflammation in patients with haemophilic arthropathy.
Serological biomarkers in hemophilic arthropathy: Can they be used to monitor bleeding and ongoing progression of blood-induced joint disease in patients with hemophilia?
Hyperalgesia
ADAMTS-5 deficient mice do not develop mechanical allodynia associated with osteoarthritis following medial meniscal destabilization.
Spinal Microglial Activation in a Murine Surgical Model of Knee Osteoarthritis.
Therapeutic effects of an anti-ADAMTS-5 antibody on joint damage and mechanical allodynia in a murine model of osteoarthritis.
Infertility
Role of ADAMTS1 and ADAMTS5 in male infertility.
Infertility, Male
ADAMTS1 and ADAMTS5 metalloproteases produced by Sertoli cells: a potential diagnostic marker in azoospermia.
Role of ADAMTS1 and ADAMTS5 in male infertility.
Influenza, Human
ADAMTS5 Is a Critical Regulator of Virus-Specific T Cell Immunity.
Insulin Resistance
ADAMTS5 deficiency protects against non-alcoholic steatohepatitis in obesity.
Are serum levels of ADAMTS5, TAS and TOS at 24-28 gestational weeks associated with adverse perinatal outcomes in gestational diabetic women?
Intervertebral Disc Degeneration
ADAMTS-5 and Intervertebral Disc Degeneration: The Results of Tissue Immunohistochemistry and In Vitro Cell Culture.
Adamts5 Deficiency Protects Mice from Chronic Tobacco Smoking-induced Intervertebral Disc Degeneration.
APOE-knockout in rabbits causes loss of cells in nucleus pulposus and enhances the levels of inflammatory catabolic cytokines damaging the intervertebral disc matrix.
Effect of small interference RNA (siRNA) for ADAMTS5 on intervertebral disc degeneration in the rabbit anular needle-puncture model.
Efficiency of dual siRNA-mediated gene therapy for intervertebral disc degeneration (IVDD).
Interleukin-1? exacerbates the catabolic effects of human nucleus pulposus cells through activation of the Nuclear Factor kappa B signaling pathway under hypoxic conditions.
Resistin Promotes Intervertebral Disc Degeneration by Up-Regulation of ADAMTS-5 Through p38 MAPK Signaling Pathway.
The involvement of ADAMTS-5 genetic polymorphisms in predisposition and diffusion tensor imaging alterations of lumbar disc degeneration.
The noncoding RNA linc-ADAMTS5 cooperates with RREB1 to protect from intervertebral disc degeneration through inhibiting ADAMTS5 expression.
TNF-? and IL-1? promote a disintegrin-like and metalloprotease with thrombospondin type I motif-5-mediated aggrecan degradation through syndecan-4 in intervertebral disc.
Intracranial Hemorrhages
Internal modulation of proteolysis in vascular extracellular matrix remodeling: role of ADAM metallopeptidase with thrombospondin type 1 motif 5 in the development of intracranial aneurysm rupture.
Joint Diseases
ADAMTS4 and ADAMTS5 may be considered as new molecular therapeutic targets for cartilage damages with Kashin-Beck Disease.
Joint Instability
ADAMTS5-/- mice have less subchondral bone changes after induction of osteoarthritis through surgical instability: implications for a link between cartilage and subchondral bone changes.
Deletion of active ADAMTS5 prevents cartilage degradation in a murine model of osteoarthritis.
Kashin-Beck Disease
ADAMTS4 and ADAMTS5 may be considered as new molecular therapeutic targets for cartilage damages with Kashin-Beck Disease.
Leukemia
High molecular weight hyaluronic acid down-regulates the gene expression of osteoarthritis-associated cytokines and enzymes in fibroblast-like synoviocytes from patients with early osteoarthritis.
Liver Diseases
Polymorphisms of a Disintegrin and Metalloproteinase with Thrombospondin Motifs 5 and Aflatoxin B1-Related Hepatocellular Carcinoma.
Lung Neoplasms
Overexpression of ADAMTS5 can regulate the migration and invasion of non-small cell lung cancer.
Lymphatic Metastasis
High expression of ADAMTS5 is a potent marker for lymphatic invasion and lymph node metastasis in colorectal cancer.
Lymphoma
Evaluation of Anti-inflammatory and Regenerative Efficiency of Naringin and Naringenin in Degenerated Human Nucleus Pulposus Cells: Biological and Molecular Modeling Studies.
Melanoma
Recombinant TSR1 of ADAMTS5 Suppresses Melanoma Growth in Mice via an Anti-angiogenic Mechanism.
Melanoma, Experimental
ADAMTS5 Functions as an Anti-Angiogenic and Anti-Tumorigenic Protein Independent of Its Proteoglycanase Activity.
Metabolic Diseases
Loss of ADAMTS5 enhances brown adipose tissue mass and promotes browning of white adipose tissue via CREB signaling.
Neoplasm Metastasis
ADAMTS5 acts as a tumor suppressor by inhibiting migration, invasion and angiogenesis in human gastric cancer.
High expression of ADAMTS5 is a potent marker for lymphatic invasion and lymph node metastasis in colorectal cancer.
microRNA -140-5p inhibits colorectal cancer invasion and metastasis by targeting ADAMTS5 and IGFBP5.
Retraction Note: microRNA-140-5p inhibits colorectal cancer invasion and metastasis by targeting ADAMTS5 and IGFBP5.
Transcriptional control of PAX4-regulated miR-144/451 modulates metastasis by suppressing ADAMs expression.
Neoplasms
ADAMs in cancer cell proliferation and progression.
ADAMTS expression in colorectal cancer.
ADAMTS-5 Decreases in Aortas and Plasma From Aortic Dissection Patients and Alleviates Angiotensin II-Induced Smooth Muscle-Cell Apoptosis.
ADAMTS-9 is synergistically induced by interleukin-1beta and tumor necrosis factor alpha in OUMS-27 chondrosarcoma cells and in human chondrocytes.
ADAMTS5 acts as a tumor suppressor by inhibiting migration, invasion and angiogenesis in human gastric cancer.
ADAMTS5 Functions as an Anti-Angiogenic and Anti-Tumorigenic Protein Independent of Its Proteoglycanase Activity.
ADAMTS5: A New Player in the Vascular Field.
Associations between second-trimester amniotic fluid levels of ADAMTS4, ADAMTS5, IL-6, and TNF-? and spontaneous preterm delivery in singleton pregnancies.
Astragaloside inhibits IL-1?-induced inflammatory response in human osteoarthritis chondrocytes and ameliorates the progression of osteoarthritis in mice.
Azilsartan prevented AGE-induced inflammatory response and degradation of aggrecan in human chondrocytes through inhibition of Sox4.
Central and peripheral region tibial plateau chondrocytes respond differently to in vitro dynamic compression.
Chondroprotective effects of platelet lysate towards monoiodoacetate-induced arthritis by suppression of TNF-?-induced activation of NF-?B pathway in chondrocytes.
Cytokine and catabolic enzyme expression in synovium, synovial fluid and articular cartilage of naturally osteoarthritic equine carpi.
Does it go to right address to measure amniotic fluid DAMTS4, ADAMTS5, interleukin-6 and tumor necrosis factor-? without an ELISA assay validation?
Drug insight: aggrecanases as therapeutic targets for osteoarthritis.
Epigenetic silencing of ADAMTS5 is associated with increased invasiveness and poor survival in patients with colorectal cancer.
Evaluation of second trimester amniotic fluid ADAMTS4, ADAMTS5, interleukin-6 and tumor necrosis factor-? levels in patients with gestational diabetes mellitus.
Fibulin-3 is uniquely upregulated in malignant gliomas and promotes tumor cell motility and invasion.
High molecular weight hyaluronic acid down-regulates the gene expression of osteoarthritis-associated cytokines and enzymes in fibroblast-like synoviocytes from patients with early osteoarthritis.
Host-produced ADAMTS4 Inhibits Early-Stage Tumor Growth.
Identification of Downstream Genes of the mTOR Pathway that Predict Recurrence and Progression in Non-Muscle Invasive High-Grade Urothelial Carcinoma of the Bladder.
In Silico Identification of Contradictory Role of ADAMTS5 in Hepatocellular Carcinoma.
In vitro effects of meloxicam on metabolism in articular chondrocytes from dogs with naturally occurring osteoarthritis.
Increased type II collagen degradation and very early focal cartilage degeneration is associated with upregulation of chondrocyte differentiation related genes in early human articular cartilage lesions.
Influence of an n-3 long-chain polyunsaturated fatty acid-enriched diet on experimentally induced synovitis in horses.
Interleukin-6 upregulates expression of ADAMTS-4 in fibroblast-like synoviocytes from patients with rheumatoid arthritis.
Long non-coding RNA HOTAIR promotes expression of ADAMTS-5 in human osteoarthritic articular chondrocytes.
Lost expression of ADAMTS5 protein associates with progression and poor prognosis of hepatocellular carcinoma.
Matrix-degrading proteases ADAMTS4 and ADAMTS5 (disintegrins and metalloproteinases with thrombospondin motifs 4 and 5) are expressed in human glioblastomas.
Mechanical impact induces cartilage degradation via mitogen activated protein kinases.
Muscone Protects Vertebral End-plate Degeneration by Antiinflammatory Property.
NF-?? upregulates ADAMTS5 expression by direct binding after TNF-? treatment in OUMS-27 chondrosarcoma cell line.
Polymorphisms of a Disintegrin and Metalloproteinase with Thrombospondin Motifs 5 and Aflatoxin B1-Related Hepatocellular Carcinoma.
Prognostic Value of ADAMTS Proteases and Their Substrates in Epithelial Ovarian Cancer.
Prostaglandin EP2 receptor signalling inhibits the expression of matrix metalloproteinase 13 in human osteoarthritic chondrocytes.
Regulation of the inflammatory cycle by a controllable release hydrogel for eliminating postoperative inflammation after discectomy.
Relative efficacies of omega-3 polyunsaturated fatty acids in reducing expression of key proteins in a model system for studying osteoarthritis.
Salvianolic Acid A Has Anti-Osteoarthritis Effect In Vitro and In Vivo.
Sinomenine contributes to the inhibition of the inflammatory response and the improvement of osteoarthritis in mouse-cartilage cells by acting on the Nrf2/HO-1 and NF-?B signaling pathways.
The role of ADAM-TS4 (aggrecanase-1) and ADAM-TS5 (aggrecanase-2) in a model of cartilage degradation.
Transcriptional control of PAX4-regulated miR-144/451 modulates metastasis by suppressing ADAMs expression.
Upregulation of tumor necrosis factor ? and ADAMTS-5, but not ADAMTS-4, in human intervertebral cartilage endplate with modic changes.
Neurodegenerative Diseases
Metalloproteinase ADAMTS-1 but not ADAMTS-5 is manifold overexpressed in neurodegenerative disorders as Down syndrome, Alzheimer's and Pick's disease.
Obesity
ADAMTS5 deficiency in mice does not affect cardiac function.
ADAMTS5 deficiency protects against non-alcoholic steatohepatitis in obesity.
Expression of aggrecan(ases) during murine preadipocyte differentiation and adipose tissue development.
Loss of ADAMTS5 enhances brown adipose tissue mass and promotes browning of white adipose tissue via CREB signaling.
Oligodendroglioma
Microvesicles shed by oligodendroglioma cells and rheumatoid synovial fibroblasts contain aggrecanase activity.
Osteoarthritis
10mM glucosamine prevents activation of proADAMTS5 (aggrecanase-2) in transfected cells by interference with post-translational modification of furin.
5'-Phenyl-3'H-spiro[indoline-3,2'-[1,3,4]thiadiazol]-2-one inhibitors of ADAMTS-5 (Aggrecanase-2).
ADAMTS proteins in human disorders.
ADAMTS-4 and ADAMTS-5: Key enzymes in osteoarthritis.
ADAMTS-5 deficient mice do not develop mechanical allodynia associated with osteoarthritis following medial meniscal destabilization.
ADAMTS-5: A difficult teenager turning 20.
ADAMTS4 and ADAMTS5 may be considered as new molecular therapeutic targets for cartilage damages with Kashin-Beck Disease.
Adamts5 Deletion Blocks Murine Dermal Repair through CD44-mediated Aggrecan Accumulation and Modulation of Transforming Growth Factor {beta}1 (TGF{beta}1) Signaling.
ADAMTS5 in Osteoarthritis: Biological Functions, Regulatory Network, and Potential Targeting Therapies.
ADAMTS5 Is a Critical Regulator of Virus-Specific T Cell Immunity.
Advances in understanding cartilage remodeling.
An aggrecan fragment drives osteoarthritis pain through Toll-like receptor 2.
Animal models of osteoarthritis: lessons learned while seeking the 'Holy Grail'.
Arylsulfonamide inhibitors of aggrecanases as potential therapeutic agents for osteoarthritis: Synthesis and biological evaluation.
Association of ADAMTS5 gene polymorphisms with osteoarthritis in Chinese Han population: a community-based case-control study.
Catabolism of Fibromodulin in Developmental Rudiment and Pathologic Articular Cartilage Demonstrates Novel Roles for MMP-13 and ADAMTS-4 in C-terminal Processing of SLRPs.
Changes in Synovial Fluid Biomarkers after Experimental Equine Osteoarthritis.
Characterization of proADAMTS5 processing by proprotein convertases.
Characterization of the human ADAMTS-5 (aggrecanase-2) gene promoter.
Chondroprotection of PPAR? activation by WY14643 via autophagy involving Akt and ERK in LPS-treated mouse chondrocytes and osteoarthritis model.
Cirsium japonicum var. maackii and apigenin block Hif-2?-induced osteoarthritic cartilage destruction.
Computational Insights into ADAMTS4, ADAMTS5 and MMP13 Inhibitor Selectivity.
Conserved sequence in the aggrecan interglobular domain modulates cleavage by ADAMTS-4 and ADAMTS-5.
Curcumin downregulates expression of opioid-related nociceptin receptor gene (OPRL1) in isolated neuroglia cells.
Curcumin slows osteoarthritis progression and relieves osteoarthritis-associated pain symptoms in a post-traumatic osteoarthritis mouse model.
Current and emerging therapeutic strategies for preventing inflammation and aggrecanase-mediated cartilage destruction in arthritis.
Deletion of active ADAMTS5 prevents cartilage degradation in a murine model of osteoarthritis.
Development of human neutralizing antibody to ADAMTS4 (aggrecanase-1) and ADAMTS5 (aggrecanase-2).
Discovery of (1S,2R,3R)-2,3-Dimethyl-2-phenyl-1-sulfamidocyclopropanecarboxylates: Novel and Highly Selective Aggrecanase Inhibitors.
Discovery of GLPG1972/S201086, a Potent, Selective, and Orally Bioavailable ADAMTS-5 Inhibitor for the Treatment of Osteoarthritis.
Discovery of Highly Potent and Selective Small Molecule ADAMTS-5 Inhibitors That Inhibit Human Cartilage Degradation via Encoded Library Technology (ELT).
Double-knockout of ADAMTS-4 and ADAMTS-5 in mice results in physiologically normal animals and prevents the progression of osteoarthritis.
Effect of inhibiting MMP13 and ADAMTS5 by intra-articular injection of small interfering RNA in a surgically induced osteoarthritis model of mice.
Elucidation of the Mechanism by Which a ADAMTS5 Gene MicroRNA-Binding Site Single Nucleotide Polymorphism Affects the Risk of Osteoarthritis.
Epigallocatechin-3-O-gallate modulates global microRNA expression in interleukin-1?-stimulated human osteoarthritis chondrocytes: potential role of EGCG on negative co-regulation of microRNA-140-3p and ADAMTS5.
Exosite inhibition of ADAMTS-5 by a glycoconjugated arylsulfonamide.
Expression of ADAMTS-4 by chondrocytes in the surface zone of human osteoarthritic cartilage is regulated by epigenetic DNA de-methylation.
Expression of ADAMTs-5 and TIMP-3 in the condylar cartilage of rats induced by experimentally created osteoarthritis.
Fibrin-hyaluronic acid hydrogel-based delivery of antisense oligonucleotides for ADAMTS5 inhibition in co-delivered and resident joint cells in osteoarthritis.
Fibroblast growth factor 2 is an intrinsic chondroprotective agent that suppresses ADAMTS-5 and delays cartilage degradation in murine osteoarthritis.
Gene expression profiling suggests a pathological role of human bone marrow-derived mesenchymal stem cells in aging-related skeletal diseases.
Genetic variation including nonsynonymous polymorphisms of a major aggrecanase, ADAMTS-5, in susceptibility to osteoarthritis.
Genetic variation of aggrecanase-2 (ADAMTS5) in susceptibility to osteoarthritis.
Genetically Engineered Mouse Models Reveal the Importance of Proteases as Osteoarthritis Drug Targets.
Hedgehog signalling does not stimulate cartilage catabolism and is inhibited by Interleukin-1?.
hsa-miR-15a exerts protective effects against osteoarthritis by targeting aggrecanase-2 (ADAMTS5) in human chondrocytes.
Human osteoarthritis synovial fluid and joint cartilage contain both aggrecanase- and matrix metalloproteinase-generated aggrecan fragments.
Identification of an ADAMTS-4 cleavage motif using phage display leads to the development of fluorogenic peptide substrates and reveals matrilin-3 as a novel substrate.
Identification of potent and selective hydantoin inhibitors of aggrecanase-1 and aggrecanase-2 that are efficacious in both chemical and surgical models of osteoarthritis.
IL-17A induction of ADAMTS-5 in differentiated THP-1 cells is modulated by the ERK signaling pathway.
Inhibition of ADAM-TS4 and ADAM-TS5 prevents aggrecan degradation in osteoarthritic cartilage.
Knockout of ADAMTS5 does not eliminate cartilage aggrecanase activity but abrogates joint fibrosis and promotes cartilage aggrecan deposition in murine osteoarthritis models.
LncRNA MALAT1/MiR-145 Adjusts IL-1?-Induced Chondrocytes Viability and Cartilage Matrix Degradation by Regulating ADAMTS5 in Human Osteoarthritis.
Long non-coding RNA HOTAIR promotes expression of ADAMTS-5 in human osteoarthritic articular chondrocytes.
Low-density lipoprotein receptor-related protein 1 (LRP1)-mediated endocytic clearance of a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS)-4: Functional differences of non-catalytic domains of ADAMTS-4 and ADAMTS-5 in LRP1 binding.
Matrilin-4 is processed by ADAMTS-5 in late Golgi vesicles present in growth plate chondrocytes of defined differentiation state.
Mechanical impact induces cartilage degradation via mitogen activated protein kinases.
MicroRNA-140 and the silencing of osteoarthritis.
MicroRNA-92a-3p Regulates Aggrecanase-1 and Aggrecanase-2 Expression in Chondrogenesis and IL-1?-Induced Catabolism in Human Articular Chondrocytes.
MiR-132-3p regulates ADAMTS-5 expression and promotes chondrogenic differentiation of rat mesenchymal stem cells.
N-((8-hydroxy-5-substituted-quinolin-7-yl)(phenyl)methyl)-2-phenyloxy/amino-acetamide inhibitors of ADAMTS-5 (Aggrecanase-2).
Orally active achiral N-hydroxyformamide inhibitors of ADAM-TS4 (aggrecanase-1) and ADAM-TS5 (aggrecanase-2) for the treatment of osteoarthritis.
Osthole ameliorates cartilage degradation by downregulation of NF-?B and HIF-2? pathways in an osteoarthritis murine model.
Polymorphic variation within the ADAMTS2, ADAMTS14, ADAMTS5, ADAM12 and TIMP2 genes and the risk of Achilles tendon pathology: A genetic association study.
Polymorphisms in ADAMTS4 and ADAMTS5 are not linked to susceptibility to knee osteoarthritis in the Turkish population.
Proline-Serine-Threonine Phosphatase-Interacting Protein 2 Alleviates Diabetes Mellitus-Osteoarthritis in Rats through Attenuating Synovial Inflammation and Cartilage Injury.
Protective effect of lentivirus-mediated siRNA targeting ADAMTS-5 on cartilage degradation in a rat model of osteoarthritis.
Purification and Activity Determination of ADAMTS-4 and ADAMTS-5 and Their Domain Deleted Mutants.
Syndecan-4 regulates ADAMTS-5 activation and cartilage breakdown in osteoarthritis.
Targeting of ADAMTS5's ancillary domain with the recombinant mAb CRB0017 ameliorates disease progression in a spontaneous murine model of osteoarthritis.
The "elusive DMOAD": Aggrecanase inhibition from laboratory to clinic.
The Anti-ADAMTS-5 Nanobody® M6495 Protects Cartilage Degradation Ex Vivo.
The protective effect of licofelone on experimental osteoarthritis is correlated with the downregulation of gene expression and protein synthesis of several major cartilage catabolic factors: MMP-13, cathepsin K and aggrecanases.
The regulation of the ADAMTS4 and ADAMTS5 aggrecanases in osteoarthritis: a review.
The role of ADAMTS genes in the end stage of hip osteoarthritis.
Transcriptional Induction of ADAMTS5 Protein by Nuclear Factor-?B (NF-?B) Family Member RelA/p65 in Chondrocytes during Osteoarthritis Development.
Transcriptomics of wild type and mice lacking ADAMTS-5 activity identifies genes involved in osteoarthritis initiation and cartilage destruction.
Translational development of an ADAMTS-5 antibody for osteoarthritis disease modification.
Validation of the Diagnostic and Prognostic Values of ADAMTS5 and FSTL1 in Osteoarthritis Rat Model.
Zinc: the Other Suspected Environmental Factor in Kashin-Beck Disease in Addition to Selenium.
[Protective effect of LR-90 on articular cartilage in rabbit model of osteoarthritis].
[Research progress of a disintegrin and metalloproteinase with thrombospondin motif 4 and 5 in osteoarthritis].
Osteoarthritis, Knee
ADAMTS-5 deficient mice do not develop mechanical allodynia associated with osteoarthritis following medial meniscal destabilization.
Effect of osteopontin on the mRNA expression of ADAMTS4 and ADAMTS5 in chondrocytes from patients with knee osteoarthritis.
Elucidation of the Mechanism by Which a ADAMTS5 Gene MicroRNA-Binding Site Single Nucleotide Polymorphism Affects the Risk of Osteoarthritis.
Increased serum ADAMTS-4 in knee osteoarthritis: a potential indicator for the diagnosis of osteoarthritis in early stages.
Polymorphisms in ADAMTS4 and ADAMTS5 are not linked to susceptibility to knee osteoarthritis in the Turkish population.
Osteophyte
Inhibition of Notch1 promotes hedgehog signalling in a HES1-dependent manner in chondrocytes and exacerbates experimental osteoarthritis.
Therapeutic effects of an anti-ADAMTS-5 antibody on joint damage and mechanical allodynia in a murine model of osteoarthritis.
Osteoporosis
5-((1H-pyrazol-4-yl)methylene)-2-thioxothiazolidin-4-one inhibitors of ADAMTS-5.
Gene expression profiling suggests a pathological role of human bone marrow-derived mesenchymal stem cells in aging-related skeletal diseases.
Periodontitis
Expression Levels of A disintegrin-like metalloproteinase with thrombospondin motifs-4 and -5 (ADAMTS-4 and ADAMTS-5) in inflamed and healthy gingival tissues.
Pick Disease of the Brain
Metalloproteinase ADAMTS-1 but not ADAMTS-5 is manifold overexpressed in neurodegenerative disorders as Down syndrome, Alzheimer's and Pick's disease.
Placental Insufficiency
Role of ADAMTS5 in Unexplained Fetal Growth Restriction (FGR).
Polycystic Ovary Syndrome
Clinical significance of ADAMTS1, ADAMTS5, ADAMTS9 aggrecanases and IL-17A, IL-23, IL-33 cytokines in polycystic ovary syndrome.
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
Lack of CpG island methylator phenotype defines a clinical subtype of T-cell acute lymphoblastic leukemia associated with good prognosis.
Premature Birth
Associations between second-trimester amniotic fluid levels of ADAMTS4, ADAMTS5, IL-6, and TNF-? and spontaneous preterm delivery in singleton pregnancies.
Pruritus
The role of kinin B1 and B2 receptors in the mouse model of oxazolone-induced atopic dermatitis.
receptor protein-tyrosine kinase deficiency
Loss of Fgfr1 in chondrocytes inhibits osteoarthritis by promoting autophagic activity in temporomandibular joint.
Spinal Cord Injuries
ADAMTS1, ADAMTS5, ADAMTS9 and aggrecanase-generated proteoglycan fragments are induced following spinal cord injury in mouse.
ADAMTS4 and ADAMTS5 knockout mice are protected from versican but not aggrecan or brevican proteolysis during spinal cord injury.
Stomach Neoplasms
ADAMTS5 acts as a tumor suppressor by inhibiting migration, invasion and angiogenesis in human gastric cancer.
Stroke
ADAMTS5 deficiency in mice does not affect cardiac function.
Syndactyly
A new Adamts9 conditional mouse allele identifies its non-redundant role in interdigital web regression.
ADAMTS metalloproteases generate active versican fragments that regulate interdigital web regression.
Synovitis
Curcumin slows osteoarthritis progression and relieves osteoarthritis-associated pain symptoms in a post-traumatic osteoarthritis mouse model.
Temporomandibular Joint Disorders
Activation of ?-catenin signalling leads to temporomandibular joint defects.
Tendinopathy
ADAMTS5 is required for biomechanically-stimulated healing of murine tendinopathy.
Trigger finger, tendinosis, and intratendinous gene expression.
Virus Diseases
ADAMTS5 Is a Critical Regulator of Virus-Specific T Cell Immunity.