2.3.1.257: N-terminal L-serine Nalpha-acetyltransferase NatD
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For detailed information about N-terminal L-serine Nalpha-acetyltransferase NatD, go to the full flat file.
Reaction
Synonyms
EC 2.3.1.88, hNAA40, hNaa40p/hNatD, N(alpha)-acetyltransferase 40, N-acetyltransferase 11, N-alpha-acetyltransferase 40, Naa40, Naa40p, Nat11, NAT4, NatD, Patt1
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2.3.1.257 N-terminal L-serine Nalpha-acetyltransferase NatDAdvanced search results
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General Information on EC 2.3.1.257 - N-terminal L-serine Nalpha-acetyltransferase NatD
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GENERAL INFORMATION 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
malfunction
metabolism
enzymes N-alpha-acetyltransferase 40 (hNAA40), nicotinamide phosphoribosyltransferase (NAMPT), and NAD-dependent protein deacetylase sirtuin-1 (SIRT-1) have been shown to exert important biological processes, including stress response and aging. The hNAA40, NAMPT, and SIRT-1 pathway might play a role in the determination of the healthy life-span. Metformin modulates this pathway
physiological function
N-alpha-acetyltransferase 40 (NAA40) catalyzes the transfer of an acetyl moiety to the alpha-amino group of serine 1 (S1) on histones H4 and H2A. NAA40 and its corresponding N-terminal acetylation of histone H4 (N-acH4) is linked to colorectal cancer (CRC). NAA40 contributes to colorectal cancer growth by controlling protein arginine methyltransferase 5 (PRMT5) expression. NAA40 stimulates PRMT5 expression in CRC cells
malfunction
depletion of Naa40 in HCT-116 and HT-29 colorectal cancer cells decreases cell survival by enhancing apoptosis. Naa40 knockdown in colon cancer cells activates the mitochondrial caspase-9-mediated apoptotic cascade
malfunction
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enzyme depletion strains show several minor phenotypes, including sensitivity to 3-aminotriazole, benomyl, and thiabendazole
malfunction
depletion of NAA40 inhibits cell proliferation and survival of CRC cell lines and increases their sensitivity to 5-fluorouracil (5-FU) treatment. Moreover, the absence of NAA40 significantly delays the growth of human CRC xenograft tumors. NAA40 knockdown and loss of N-acH4 reduce the levels of symmetric dimethylation of histone H4 (H4R3me2s) through transcriptional downregulation of protein arginine methyltransferase 5 (PRMT5). NAA40 depletion and subsequent repression of PRMT5 results in altered expression of key oncogenes and tumor suppressor genes leading to inhibition of CRC cell growth. NAA40 mRNA levels correlate with those of PRMT5 in CRC patient tissues. H4 arginine 3 symmetric dimethylation (H4R3me2s) levels are notably decreased in the absence of NAA40 and of its mediated N-acH4 compared to the SCR and mock control cells. On the other hand, reduction of NAA40 expression does not influence the total levels of monomethylation (H4R3me1) or asymmetric dimethylation (H4R3me2a) at the third residue of histone H4. Consistently, H4R3me2s levels are reduced upon NAA40 knockdown in SW-480 and SW-620 cells, while H4R3me1 and H4R3me2a levels remain unaffected. PRMT5 upregulation restores viability in NAA40-depleted CRC cells
malfunction
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enzyme depletion strains show several minor phenotypes, including sensitivity to 3-aminotriazole, benomyl, and thiabendazole
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