EC Number   |
General Information |
Reference |
|---|
   2.3.1.255 | malfunction |
knockdown of Naa10 in HeLa cells leads to apoptosis and sensitizes cells for daunorubicin-induced apoptosis |
740508 |
| 2.3.1.255 | malfunction |
measuring the different time points of gene expression upon Naa10 siRNA treatment, NTN1 and its receptor UNC5B are found to be the most dramatically overexpressed among the genes involved in morphogenesis |
-, 758388 |
| 2.3.1.255 | malfunction |
measuring the different time points of gene expression upon Naa10 siRNA treatment, NTN1 and its receptor UNC5B are found to be the most dramatically overexpressed among the genes involved in morphogenesis. Analysis of upregulated genes in Naa10 stably knocked down H1299 cell line, overview |
758388 |
| 2.3.1.255 | malfunction |
mutation ard1::HIS3 leads to a defect in transcription of a-specific genes, but permits expression of the information resident at HML. The mutant shows a phenotypes with reduced viability and sensitivity to heat shock and salt, it fails to enter stationay phase, it shows a lack of glycogen accumulation, a sporulation defect, poor mating, and fails to undergo meiosis. The mutant nat1-5::LEU;ard1 is inable to sporulate, has slow growth, reduced mating, inhibited sporulation, and impaired resistance to heat shock. It fails G1 arrest, shows a partial depression of HML, and fails to accumulate storage. yNaa10 deficiency leads to a growth defect, sensitivity to caffeine and cycloheximide, impaired resistance to heat shock, and decreased mating efficiency |
-, 756675 |
| 2.3.1.255 | malfunction |
mutations in N-terminal acetyltransferase Naa10 are the cause of Ogden Syndrome |
741085 |
| 2.3.1.255 | malfunction |
mutations in the X-linked gene NAA10 cause Ogden Syndrome (also known as NAA10-related syndrome), which affects numerous aspects of development. Wide-ranging developmental defects are observed in humans with mutations in NAA10 and NAA15 |
-, 758492 |
| 2.3.1.255 | malfunction |
NAA10 germline variants are found in patients with the X-linked lethal Ogden syndrome, and in other familial or de novo cases with variable degrees of developmental delay, intellectual disability (ID) and cardiac anomalies. A R83H missense variant in NAA10 is detected by whole exome sequencing in two unrelated boys with intellectual disability, developmental delay, ADHD like behaviour, very limited speech and cardiac abnormalities. Phenotypes, overview. Mutant NAA10-R83H has a reduced monomeric catalytic activity, likely due to impaired enzyme-acetyl-CoA binding |
756298 |
| 2.3.1.255 | malfunction |
naa10 morphants display increased lethality, growth retardation and developmental abnormalities like bent axis, abnormal eyes and bent tails |
735797 |
| 2.3.1.255 | malfunction |
NAA10 variants have been found in patients with an X-linked developmental disorder called Ogden syndrome in its most severe form and, in other familial or de novo cases, with variable degrees of syndromic intellectual disability (ID) affecting both sexes. The mutant NAA10-V111G has a reduced stability and 85% reduced monomeric catalytic activity, while catalytic NatA function remains unaltered. The syndromic cases may also require a degree of compromised NatA function. The Naa10-V111G phenotype shows mild/moderate non-syndromic intellectual disability, and delayed motor and language development, but normal behavior without autistic traits. The blood leukocyte X-inactivation pattern is within normal range (80/20) |
756297 |
| 2.3.1.255 | malfunction |
oligomerization results in the loss of KAT activity |
757723 |
