EC Number   |
General Information  |
Reference |
|---|
   2.3.1.255 | evolution |
RimI belongs to the general control non-repressible (GCN5)-related N-acetyltransferase (GNAT) family that carries a conserved Q/RxxGxG/A Ac-CoA-binding motif |
-, 755712 |
| 2.3.1.255 | evolution |
there are seven known NAT types (NatA through NatG), each composed of one or more specific subunits and having specific substrates defined by the very first amino acid residue (serine, alanine, etc.) |
-, 758492 |
| 2.3.1.255 | malfunction |
Aenzyme knockdown significantly reduces dendritic extension in cultured Purkinje cells |
703852 |
| 2.3.1.255 | malfunction |
enzyme knockdown causes a phenotype with lethality, growth retardation, bent axis and tails, abnormal eyes, and less pigmentation |
756675 |
| 2.3.1.255 | malfunction |
enzyme mutants show phenotypes with pleiotropic oogenesis, aberrant mitosis, egg chamber encapsulation defects, and nurse cell chromatin dispersion defects |
756675 |
| 2.3.1.255 | malfunction |
HYPK is a negative regulator for hNatA acetylation activity |
757754 |
| 2.3.1.255 | malfunction |
inactive Naa10 mutant S37Pw shows a phenotype with perinatal lethal disorder, hypotonia, global developmental delay, cryptorchidism, cardiac arrhythmias, skin laxity, dysmorphic features, hernias, and large fontanels. Naa10 mutant Y43S shows a phenotype with intellectual disability, facial dysmorphism, scoliosis, and long QT. Mutant R83C shows a phenootype with hypotonia, global developmental delay, dysmorphic features, autism spectrum disorder, epileptic encephalopathy, extrapyramidal signs, hypertension with left ventricular hypertrophy, thin corpus callosum, and progressive white matter loss. Mutations V107F and R116W cause phenotypes with severe global developmental delay with postnatal growth, skeletal anomalies, truncal hypotonia with hypertonia of the extremities, minor facial features, and behavioral anomalies. Mutation of residue F128 causes moderate to severe intellectually disability, feeding difficulties, eye anomalies, hypotonia, and developmental delay |
756675 |
| 2.3.1.255 | malfunction |
inhibition of hARD1/NAA10 autoacetylation by K136R mutation induces the drop of KAT activity, but not NAT activity |
757723 |
| 2.3.1.255 | malfunction |
knockdown and overexpression of Naa10p in osteosarcoma cells respectively leads to decreased and increased cell migratory/invasive abilities. Re-expression of Naa10p, but not of an enzymatically inactive mutant, relieves suppression of the invasive ability in vitro and metastasis in vivo imposed by Naa10p-knockdown. The matrix metalloproteinase (MMP)-2 is responsible for the Naa10p-induced invasive phenotype |
756332 |
| 2.3.1.255 | malfunction |
knockdown of acetyltransferase ARD1 significantly reduces the growth rate of human cancer cell lines. Furthermore, ARD1 knockdown induces apoptosis or sensitizes cells to drug induced apoptosis. Enzyme knockdown reduces the transcriptional activity of the beta-Catenin/TCF4 complex, downregulating cyclin D1 and thereby promoting G1-arrest and inhibition of cell proliferation of lung cancer cells |
740340 |
