2.3.1.255 Atherosclerosis https://pubmed.ncbi.nlm.nih.gov/27755984/ miRNA-27b modulates endothelial cell angiogenesis by directly targeting Naa15 in atherogenesis. unassigned - 2.3.1.255 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/10464641/ Evaluation of genotype data in clinical risk assessment: methods and application to BRCA1, BRCA2, and N-acetyl transferase-2 genotypes in breast cancer. causal interaction 3 2.3.1.255 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/10464641/ Evaluation of genotype data in clinical risk assessment: methods and application to BRCA1, BRCA2, and N-acetyl transferase-2 genotypes in breast cancer. diagnostic usage 3 2.3.1.255 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/10464641/ Evaluation of genotype data in clinical risk assessment: methods and application to BRCA1, BRCA2, and N-acetyl transferase-2 genotypes in breast cancer. therapeutic application 3 2.3.1.255 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/10464641/ Evaluation of genotype data in clinical risk assessment: methods and application to BRCA1, BRCA2, and N-acetyl transferase-2 genotypes in breast cancer. unassigned - 2.3.1.255 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/18794801/ Implication of human N-alpha-acetyltransferase 5 in cellular proliferation and carcinogenesis. causal interaction 2 2.3.1.255 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/20592467/ hNaa10p contributes to tumorigenesis by facilitating DNMT1-mediated tumor suppressor gene silencing. causal interaction 1 2.3.1.255 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/20592467/ hNaa10p contributes to tumorigenesis by facilitating DNMT1-mediated tumor suppressor gene silencing. diagnostic usage 1 2.3.1.255 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/20592467/ hNaa10p contributes to tumorigenesis by facilitating DNMT1-mediated tumor suppressor gene silencing. therapeutic application 1 2.3.1.255 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/18794801/ Implication of human N-alpha-acetyltransferase 5 in cellular proliferation and carcinogenesis. ongoing research 2 2.3.1.255 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/20592467/ hNaa10p contributes to tumorigenesis by facilitating DNMT1-mediated tumor suppressor gene silencing. ongoing research 2 2.3.1.255 Carcinogenesis https://pubmed.ncbi.nlm.nih.gov/18794801/ Implication of human N-alpha-acetyltransferase 5 in cellular proliferation and carcinogenesis. unassigned - 2.3.1.255 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/20419844/ LOH analysis of genes around D4S2964 identifies ARD1B as a prognostic predictor of hepatocellular carcinoma. causal interaction 3 2.3.1.255 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/23258102/ Clinical implications of arrest-defective protein 1 expression in hepatocellular carcinoma: a novel predictor of microvascular invasion. causal interaction 4 2.3.1.255 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/20419844/ LOH analysis of genes around D4S2964 identifies ARD1B as a prognostic predictor of hepatocellular carcinoma. diagnostic usage 4 2.3.1.255 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/23258102/ Clinical implications of arrest-defective protein 1 expression in hepatocellular carcinoma: a novel predictor of microvascular invasion. diagnostic usage 3 2.3.1.255 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/20419844/ LOH analysis of genes around D4S2964 identifies ARD1B as a prognostic predictor of hepatocellular carcinoma. therapeutic application 2 2.3.1.255 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/23258102/ Clinical implications of arrest-defective protein 1 expression in hepatocellular carcinoma: a novel predictor of microvascular invasion. ongoing research 2 2.3.1.255 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/23258102/ Clinical implications of arrest-defective protein 1 expression in hepatocellular carcinoma: a novel predictor of microvascular invasion. unassigned - 2.3.1.255 Carcinoma, Hepatocellular https://pubmed.ncbi.nlm.nih.gov/20419844/ LOH analysis of genes around D4S2964 identifies ARD1B as a prognostic predictor of hepatocellular carcinoma. unassigned - 2.3.1.255 Cardiomyopathy, Hypertrophic https://pubmed.ncbi.nlm.nih.gov/33103328/ Variants in NAA15 cause pediatric hypertrophic cardiomyopathy. causal interaction 3 2.3.1.255 Cardiomyopathy, Hypertrophic https://pubmed.ncbi.nlm.nih.gov/33103328/ Variants in NAA15 cause pediatric hypertrophic cardiomyopathy. diagnostic usage 1 2.3.1.255 Cardiomyopathy, Hypertrophic https://pubmed.ncbi.nlm.nih.gov/33103328/ Variants in NAA15 cause pediatric hypertrophic cardiomyopathy. unassigned - 2.3.1.255 Cleft Lip https://pubmed.ncbi.nlm.nih.gov/33103328/ Variants in NAA15 cause pediatric hypertrophic cardiomyopathy. causal interaction 3 2.3.1.255 Cleft Lip https://pubmed.ncbi.nlm.nih.gov/33103328/ Variants in NAA15 cause pediatric hypertrophic cardiomyopathy. diagnostic usage 1 2.3.1.255 Cleft Lip https://pubmed.ncbi.nlm.nih.gov/33103328/ Variants in NAA15 cause pediatric hypertrophic cardiomyopathy. unassigned - 2.3.1.255 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/22261620/ Combined Phenotype of 4 Markers Improves Prognostic Value of Patients With Colon Cancer. diagnostic usage 1 2.3.1.255 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/22261620/ Combined Phenotype of 4 Markers Improves Prognostic Value of Patients With Colon Cancer. ongoing research 3 2.3.1.255 Colonic Neoplasms https://pubmed.ncbi.nlm.nih.gov/22261620/ Combined Phenotype of 4 Markers Improves Prognostic Value of Patients With Colon Cancer. unassigned - 2.3.1.255 Heart Defects, Congenital https://pubmed.ncbi.nlm.nih.gov/33557580/ Mechanisms of Congenital Heart Disease Caused by NAA15 Haploinsufficiency. causal interaction 4 2.3.1.255 Heart Defects, Congenital https://pubmed.ncbi.nlm.nih.gov/29621621/ Phenotypic consequences of gene disruption by a balanced de novo translocation involving SLC6A1 and NAA15. causal interaction 4 2.3.1.255 Heart Defects, Congenital https://pubmed.ncbi.nlm.nih.gov/33557580/ Mechanisms of Congenital Heart Disease Caused by NAA15 Haploinsufficiency. therapeutic application 1 2.3.1.255 Heart Defects, Congenital https://pubmed.ncbi.nlm.nih.gov/33557580/ Mechanisms of Congenital Heart Disease Caused by NAA15 Haploinsufficiency. unassigned - 2.3.1.255 Heart Defects, Congenital https://pubmed.ncbi.nlm.nih.gov/29621621/ Phenotypic consequences of gene disruption by a balanced de novo translocation involving SLC6A1 and NAA15. unassigned - 2.3.1.255 Infertility https://pubmed.ncbi.nlm.nih.gov/32461302/ NAA50 Is an Enzymatically Active N?-Acetyltransferase That Is Crucial for Development and Regulation of Stress Responses. unassigned - 2.3.1.255 Insulin Resistance https://pubmed.ncbi.nlm.nih.gov/33296651/ Reduction of mNAT1/hNAT2 Contributes to Cerebral Endothelial Necroptosis and A? Accumulation in Alzheimer's Disease. causal interaction 1 2.3.1.255 Insulin Resistance https://pubmed.ncbi.nlm.nih.gov/33296651/ Reduction of mNAT1/hNAT2 Contributes to Cerebral Endothelial Necroptosis and A? Accumulation in Alzheimer's Disease. ongoing research 2 2.3.1.255 Insulin Resistance https://pubmed.ncbi.nlm.nih.gov/33296651/ Reduction of mNAT1/hNAT2 Contributes to Cerebral Endothelial Necroptosis and A? Accumulation in Alzheimer's Disease. unassigned - 2.3.1.255 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/28990276/ Exome sequencing reveals NAA15 and PUF60 as candidate genes associated with intellectual disability. causal interaction 2 2.3.1.255 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/29656860/ Truncating Variants in NAA15 Are Associated with Variable Levels of Intellectual Disability, Autism Spectrum Disorder, and Congenital Anomalies. causal interaction 3 2.3.1.255 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/33103328/ Variants in NAA15 cause pediatric hypertrophic cardiomyopathy. causal interaction 3 2.3.1.255 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/33103328/ Variants in NAA15 cause pediatric hypertrophic cardiomyopathy. diagnostic usage 1 2.3.1.255 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/28990276/ Exome sequencing reveals NAA15 and PUF60 as candidate genes associated with intellectual disability. unassigned - 2.3.1.255 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/29656860/ Truncating Variants in NAA15 Are Associated with Variable Levels of Intellectual Disability, Autism Spectrum Disorder, and Congenital Anomalies. unassigned - 2.3.1.255 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/33103328/ Variants in NAA15 cause pediatric hypertrophic cardiomyopathy. unassigned - 2.3.1.255 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23557624/ Design, Synthesis, and Kinetic Characterization of Protein N-Terminal Acetyltransferase Inhibitors. causal interaction 4 2.3.1.255 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23557624/ Design, Synthesis, and Kinetic Characterization of Protein N-Terminal Acetyltransferase Inhibitors. diagnostic usage 1 2.3.1.255 Neoplasms https://pubmed.ncbi.nlm.nih.gov/19716809/ Phosphorylation of ARD1 by IKKbeta contributes to its destabilization and degradation. ongoing research 4 2.3.1.255 Neoplasms https://pubmed.ncbi.nlm.nih.gov/19716809/ Phosphorylation of ARD1 by IKKbeta contributes to its destabilization and degradation. unassigned - 2.3.1.255 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23557624/ Design, Synthesis, and Kinetic Characterization of Protein N-Terminal Acetyltransferase Inhibitors. unassigned - 2.3.1.255 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/27659526/ Acetylation of androgen receptor by ARD1 promotes dissociation from HSP90 complex and prostate tumorigenesis. causal interaction 3 2.3.1.255 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/27659526/ Acetylation of androgen receptor by ARD1 promotes dissociation from HSP90 complex and prostate tumorigenesis. ongoing research 2 2.3.1.255 Prostatic Neoplasms https://pubmed.ncbi.nlm.nih.gov/27659526/ Acetylation of androgen receptor by ARD1 promotes dissociation from HSP90 complex and prostate tumorigenesis. unassigned - 2.3.1.255 Starvation https://pubmed.ncbi.nlm.nih.gov/25330189/ daf-31 encodes the catalytic subunit of N alpha-acetyltransferase that regulates Caenorhabditis elegans development, metabolism and adult lifespan. therapeutic application 4 2.3.1.255 Starvation https://pubmed.ncbi.nlm.nih.gov/25330189/ daf-31 encodes the catalytic subunit of N alpha-acetyltransferase that regulates Caenorhabditis elegans development, metabolism and adult lifespan. unassigned - 2.3.1.255 Thyroid Neoplasms https://pubmed.ncbi.nlm.nih.gov/20178098/ Depletion of the human N(alpha)-terminal acetyltransferase A (hNatA) induces p53-dependent apoptosis and p53-independent growth inhibition. therapeutic application 1 2.3.1.255 Thyroid Neoplasms https://pubmed.ncbi.nlm.nih.gov/21351257/ Depletion of the human N?-terminal acetyltransferase A induces p53-dependent apoptosis and p53-independent growth inhibition. therapeutic application 1 2.3.1.255 Thyroid Neoplasms https://pubmed.ncbi.nlm.nih.gov/20178098/ Depletion of the human N(alpha)-terminal acetyltransferase A (hNatA) induces p53-dependent apoptosis and p53-independent growth inhibition. ongoing research 2 2.3.1.255 Thyroid Neoplasms https://pubmed.ncbi.nlm.nih.gov/21351257/ Depletion of the human N?-terminal acetyltransferase A induces p53-dependent apoptosis and p53-independent growth inhibition. ongoing research 3 2.3.1.255 Thyroid Neoplasms https://pubmed.ncbi.nlm.nih.gov/20178098/ Depletion of the human N(alpha)-terminal acetyltransferase A (hNatA) induces p53-dependent apoptosis and p53-independent growth inhibition. unassigned - 2.3.1.255 Thyroid Neoplasms https://pubmed.ncbi.nlm.nih.gov/21351257/ Depletion of the human N?-terminal acetyltransferase A induces p53-dependent apoptosis and p53-independent growth inhibition. unassigned - 2.3.1.255 Tuberculosis https://pubmed.ncbi.nlm.nih.gov/31389995/ Biophysical and functional characterizations of recombinant RimI acetyltransferase from Mycobacterium tuberculosis. causal interaction 3 2.3.1.255 Tuberculosis https://pubmed.ncbi.nlm.nih.gov/31389995/ Biophysical and functional characterizations of recombinant RimI acetyltransferase from Mycobacterium tuberculosis. therapeutic application 1 2.3.1.255 Tuberculosis https://pubmed.ncbi.nlm.nih.gov/31389995/ Biophysical and functional characterizations of recombinant RimI acetyltransferase from Mycobacterium tuberculosis. ongoing research 4 2.3.1.255 Tuberculosis https://pubmed.ncbi.nlm.nih.gov/27353550/ Biochemical evidence for relaxed substrate specificity of N?-acetyltransferase (Rv3420c/rimI) of Mycobacterium tuberculosis. unassigned - 2.3.1.255 Tuberculosis https://pubmed.ncbi.nlm.nih.gov/31389995/ Biophysical and functional characterizations of recombinant RimI acetyltransferase from Mycobacterium tuberculosis. unassigned -