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Results 1 - 10 of 16 > >>
EC Number
General Information
Commentary
Reference
malfunction
Aenzyme knockdown significantly reduces dendritic extension in cultured Purkinje cells
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
malfunction
knockdown of Naa10 in HeLa cells leads to apoptosis and sensitizes cells for daunorubicin-induced apoptosis
malfunction
mutations in N-terminal acetyltransferase Naa10 are the cause of Ogden Syndrome
malfunction
naa10 morphants display increased lethality, growth retardation and developmental abnormalities like bent axis, abnormal eyes and bent tails
malfunction
reduced enzyme levels result in pleiotropic oogenesis defects including abnormal cyst encapsulation, desynchronized cystocyte division, disrupted nurse cell chromosome dispersion, and abnormal chorion patterning. Loss of Ard1 affects cell survival/proliferation and is lethal for the animal
metabolism
ARD1 variants have different effects on hypoxia-inducible factor-1alpha stability and acetylation
metabolism
Naa10 activates and/or amplifies the transcriptional activity of beta-catenin/TCF transcriptional activity thereby stimulating cyclin D1 and c-Myc expression leading to inhibition of p21WAF1/CIP1 and promoting the G1/S cell cycle transition. Naa10 is essential for the activation of caspase-2/-3/-7 and -9 in HeLa cells after doxorubicin stimulation
metabolism
NAT1 and ARD1 proteins function together to catalyze the N-terminal acetylation of a subset of yeast proteins
physiological function
ARD1 is essential for viability in mammalian and insect-stage Trypanosoma brucei cells
Results 1 - 10 of 16 > >>