2.3.1.255 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18794801&form=6&db=m Implication of human N-alpha-acetyltransferase 5 in cellular proliferation and carcinogenesis. causal interaction,ongoing research,unassigned 2,2,0 2.3.1.255 Colonic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22261620&form=6&db=m Combined Phenotype of 4 Markers Improves Prognostic Value of Patients With Colon Cancer. diagnostic usage,ongoing research,unassigned 1,3,0 2.3.1.255 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20592467&form=6&db=m hNaa10p contributes to tumorigenesis by facilitating DNMT1-mediated tumor suppressor gene silencing. causal interaction,diagnostic usage,ongoing research,therapeutic application 1,1,2,1 2.3.1.255 Starvation http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25330189&form=6&db=m daf-31 encodes the catalytic subunit of N alpha-acetyltransferase that regulates Caenorhabditis elegans development, metabolism and adult lifespan. therapeutic application,unassigned 4,0 2.3.1.255 Atherosclerosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27755984&form=6&db=m miRNA-27b modulates endothelial cell angiogenesis by directly targeting Naa15 in atherogenesis. unassigned - 2.3.1.255 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10464641&form=6&db=m 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,diagnostic usage,therapeutic application,unassigned 3,3,3,0 2.3.1.255 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20419844&form=6&db=m LOH analysis of genes around D4S2964 identifies ARD1B as a prognostic predictor of hepatocellular carcinoma. causal interaction,diagnostic usage,therapeutic application,unassigned 3,4,2,0 2.3.1.255 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23258102&form=6&db=m Clinical implications of arrest-defective protein 1 expression in hepatocellular carcinoma: a novel predictor of microvascular invasion. causal interaction,diagnostic usage,ongoing research,unassigned 4,3,2,0 2.3.1.255 Cardiomyopathy, Hypertrophic http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33103328&form=6&db=m Variants in NAA15 cause pediatric hypertrophic cardiomyopathy. causal interaction,diagnostic usage,unassigned 3,1,0 2.3.1.255 Cleft Lip http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33103328&form=6&db=m Variants in NAA15 cause pediatric hypertrophic cardiomyopathy. causal interaction,diagnostic usage,unassigned 3,1,0 2.3.1.255 Heart Defects, Congenital http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29621621&form=6&db=m Phenotypic consequences of gene disruption by a balanced de novo translocation involving SLC6A1 and NAA15. causal interaction,unassigned 4,0 2.3.1.255 Heart Defects, Congenital http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33557580&form=6&db=m Mechanisms of Congenital Heart Disease Caused by NAA15 Haploinsufficiency. causal interaction,therapeutic application,unassigned 4,1,0 2.3.1.255 Infertility http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32461302&form=6&db=m NAA50 Is an Enzymatically Active N?-Acetyltransferase That Is Crucial for Development and Regulation of Stress Responses. unassigned - 2.3.1.255 Insulin Resistance http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33296651&form=6&db=m Reduction of mNAT1/hNAT2 Contributes to Cerebral Endothelial Necroptosis and A? Accumulation in Alzheimer's Disease. causal interaction,ongoing research,unassigned 1,2,0 2.3.1.255 Intellectual Disability http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28990276&form=6&db=m Exome sequencing reveals NAA15 and PUF60 as candidate genes associated with intellectual disability. causal interaction,unassigned 2,0 2.3.1.255 Intellectual Disability http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29656860&form=6&db=m Truncating Variants in NAA15 Are Associated with Variable Levels of Intellectual Disability, Autism Spectrum Disorder, and Congenital Anomalies. causal interaction,unassigned 3,0 2.3.1.255 Intellectual Disability http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33103328&form=6&db=m Variants in NAA15 cause pediatric hypertrophic cardiomyopathy. causal interaction,diagnostic usage,unassigned 3,1,0 2.3.1.255 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19716809&form=6&db=m Phosphorylation of ARD1 by IKKbeta contributes to its destabilization and degradation. ongoing research,unassigned 4,0 2.3.1.255 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23557624&form=6&db=m Design, Synthesis, and Kinetic Characterization of Protein N-Terminal Acetyltransferase Inhibitors. causal interaction,diagnostic usage,unassigned 4,1,0 2.3.1.255 Prostatic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27659526&form=6&db=m Acetylation of androgen receptor by ARD1 promotes dissociation from HSP90 complex and prostate tumorigenesis. causal interaction,ongoing research,unassigned 3,2,0 2.3.1.255 Thyroid Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20178098&form=6&db=m Depletion of the human N(alpha)-terminal acetyltransferase A (hNatA) induces p53-dependent apoptosis and p53-independent growth inhibition. ongoing research,therapeutic application,unassigned 2,1,0 2.3.1.255 Thyroid Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21351257&form=6&db=m Depletion of the human N?-terminal acetyltransferase A induces p53-dependent apoptosis and p53-independent growth inhibition. ongoing research,therapeutic application,unassigned 3,1,0 2.3.1.255 Tuberculosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27353550&form=6&db=m Biochemical evidence for relaxed substrate specificity of N?-acetyltransferase (Rv3420c/rimI) of Mycobacterium tuberculosis. unassigned - 2.3.1.255 Tuberculosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31389995&form=6&db=m Biophysical and functional characterizations of recombinant RimI acetyltransferase from Mycobacterium tuberculosis. causal interaction,ongoing research,therapeutic application,unassigned 3,4,1,0