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acetyl-CoA + an N-terminal-L-seryl-[histone H2A]
an N-terminal-Nalpha-acetyl-L-seryl-[histone H2A] + CoA
acetyl-CoA + an N-terminal-L-seryl-[histone H4]
an N-terminal-Nalpha-acetyl-L-seryl-[histone H4] + CoA
acetyl-CoA + histone H2A
CoA + Nalpha-acetyl-histone H2A
Saccharomyces cerevisiae histone H2A, 2SGGKGGKAGSAAKASQSR19 N-terminal sequence
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-
?
acetyl-CoA + histone H4
CoA + Nalpha-acetyl-histone H4
Saccharomyces cerevisiae histone H4, 2SGRGKGGKGLGKGGAKR18 N-terminal sequence. hNaa40p catalyzes H4 Nalpha-acetylation and not H4 lysine Nepsilon-acetylation, immunoprecipitated hNaa40p specifically Nt-acetylates H4 in vitro
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-
?
acetyl-CoA + N-terminal-L-seryl1-[histone H2A]
N-terminal-Nalpha-acetyl-L-seryl1-[histone H2A] + CoA
acetyl-CoA + N-terminal-L-seryl1-[histone H4]
N-terminal-Nalpha-acetyl-L-seryl1-[histone H4] + CoA
acetyl-CoA + peptide
CoA + Nalpha-acetylpeptide
acetyl-CoA + Ser-Gly-Arg-Gly
acetyl-CoA + Nalpha-acetyl-Ser-Gly-Arg-Lys
acetyl-CoA + Ser-Gly-Gly-Lys
acetyl-CoA + Nalpha-acetyl-Ser-Gly-Gly-Lys
additional information
?
-
acetyl-CoA + an N-terminal-L-seryl-[histone H2A]
an N-terminal-Nalpha-acetyl-L-seryl-[histone H2A] + CoA
-
-
-
?
acetyl-CoA + an N-terminal-L-seryl-[histone H2A]
an N-terminal-Nalpha-acetyl-L-seryl-[histone H2A] + CoA
-
-
-
?
acetyl-CoA + an N-terminal-L-seryl-[histone H2A]
an N-terminal-Nalpha-acetyl-L-seryl-[histone H2A] + CoA
-
-
-
-
?
acetyl-CoA + an N-terminal-L-seryl-[histone H2A]
an N-terminal-Nalpha-acetyl-L-seryl-[histone H2A] + CoA
-
-
-
-
?
acetyl-CoA + an N-terminal-L-seryl-[histone H4]
an N-terminal-Nalpha-acetyl-L-seryl-[histone H4] + CoA
-
-
-
?
acetyl-CoA + an N-terminal-L-seryl-[histone H4]
an N-terminal-Nalpha-acetyl-L-seryl-[histone H4] + CoA
-
-
-
?
acetyl-CoA + an N-terminal-L-seryl-[histone H4]
an N-terminal-Nalpha-acetyl-L-seryl-[histone H4] + CoA
-
-
-
-
?
acetyl-CoA + an N-terminal-L-seryl-[histone H4]
an N-terminal-Nalpha-acetyl-L-seryl-[histone H4] + CoA
-
efficient acetylation requires at least 30 to 50 amino acid residues of the N terminus of histone H4
-
-
?
acetyl-CoA + an N-terminal-L-seryl-[histone H4]
an N-terminal-Nalpha-acetyl-L-seryl-[histone H4] + CoA
-
efficient acetylation requires at least 30 to 50 amino acid residues of the N terminus of histone H4
-
-
?
acetyl-CoA + N-terminal-L-seryl1-[histone H2A]
N-terminal-Nalpha-acetyl-L-seryl1-[histone H2A] + CoA
-
-
-
?
acetyl-CoA + N-terminal-L-seryl1-[histone H2A]
N-terminal-Nalpha-acetyl-L-seryl1-[histone H2A] + CoA
-
-
-
-
?
acetyl-CoA + N-terminal-L-seryl1-[histone H4]
N-terminal-Nalpha-acetyl-L-seryl1-[histone H4] + CoA
-
-
-
?
acetyl-CoA + N-terminal-L-seryl1-[histone H4]
N-terminal-Nalpha-acetyl-L-seryl1-[histone H4] + CoA
-
-
-
-
?
acetyl-CoA + peptide
CoA + Nalpha-acetylpeptide
-
-
-
?
acetyl-CoA + peptide
CoA + Nalpha-acetylpeptide
hNaa40p preferentially acetylates Ser-Gly-Gly-Gly-Lys- starting peptides
-
-
?
acetyl-CoA + Ser-Gly-Arg-Gly
acetyl-CoA + Nalpha-acetyl-Ser-Gly-Arg-Lys
-
-
-
-
?
acetyl-CoA + Ser-Gly-Arg-Gly
acetyl-CoA + Nalpha-acetyl-Ser-Gly-Arg-Lys
-
-
-
-
?
acetyl-CoA + Ser-Gly-Gly-Lys
acetyl-CoA + Nalpha-acetyl-Ser-Gly-Gly-Lys
-
-
-
-
?
acetyl-CoA + Ser-Gly-Gly-Lys
acetyl-CoA + Nalpha-acetyl-Ser-Gly-Gly-Lys
-
-
-
-
?
additional information
?
-
hNaa40p is a NAT selectively acetylating Ser-Gly or Gly-Gly starting peptides. NatD also is defined as the catalytic unit Naa40p (Nat4) which co-translationally Nt-acetylates histones H2A and H4. Recombinant hNaa40p Nt-acetylates the oligopeptides derived from the N-termini of both histones
-
-
?
additional information
?
-
-
hNaa40p is a NAT selectively acetylating Ser-Gly or Gly-Gly starting peptides. NatD also is defined as the catalytic unit Naa40p (Nat4) which co-translationally Nt-acetylates histones H2A and H4. Recombinant hNaa40p Nt-acetylates the oligopeptides derived from the N-termini of both histones
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?
additional information
?
-
specificity determination using an in vitro proteome-derived peptide library Nt-acetylation assay, in vitro acetylation using synthetic oligopeptides as substrates, overview
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?
additional information
?
-
-
specificity determination using an in vitro proteome-derived peptide library Nt-acetylation assay, in vitro acetylation using synthetic oligopeptides as substrates, overview
-
-
?
additional information
?
-
the enzyme does not catalyze H4 lysine Nepsilon-acetylation
-
-
?
additional information
?
-
-
the enzyme does not catalyze H4 lysine Nepsilon-acetylation
-
-
?
additional information
?
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-
does not acetylate histone H3 or adrenocorticotropin
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-
?
additional information
?
-
-
the enzyme does not acetylate histone H3, adrenocorticotropin, and an altered iso-1-cytochrome c protein with short NatD type N termini (SGGKGGKA)
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-
?
additional information
?
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-
the enzyme does not acetylate histone H3, adrenocorticotropin, and an altered iso-1-cytochrome c protein with short NatD type N termini (SGGKGGKA)
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?
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acetyl-CoA + an N-terminal-L-seryl-[histone H2A]
an N-terminal-Nalpha-acetyl-L-seryl-[histone H2A] + CoA
acetyl-CoA + an N-terminal-L-seryl-[histone H4]
an N-terminal-Nalpha-acetyl-L-seryl-[histone H4] + CoA
acetyl-CoA + N-terminal-L-seryl1-[histone H2A]
N-terminal-Nalpha-acetyl-L-seryl1-[histone H2A] + CoA
acetyl-CoA + N-terminal-L-seryl1-[histone H4]
N-terminal-Nalpha-acetyl-L-seryl1-[histone H4] + CoA
acetyl-CoA + peptide
CoA + Nalpha-acetylpeptide
hNaa40p preferentially acetylates Ser-Gly-Gly-Gly-Lys- starting peptides
-
-
?
acetyl-CoA + Ser-Gly-Arg-Gly
acetyl-CoA + Nalpha-acetyl-Ser-Gly-Arg-Lys
acetyl-CoA + Ser-Gly-Gly-Lys
acetyl-CoA + Nalpha-acetyl-Ser-Gly-Gly-Lys
additional information
?
-
acetyl-CoA + an N-terminal-L-seryl-[histone H2A]
an N-terminal-Nalpha-acetyl-L-seryl-[histone H2A] + CoA
-
-
-
?
acetyl-CoA + an N-terminal-L-seryl-[histone H2A]
an N-terminal-Nalpha-acetyl-L-seryl-[histone H2A] + CoA
-
-
-
?
acetyl-CoA + an N-terminal-L-seryl-[histone H2A]
an N-terminal-Nalpha-acetyl-L-seryl-[histone H2A] + CoA
-
-
-
-
?
acetyl-CoA + an N-terminal-L-seryl-[histone H2A]
an N-terminal-Nalpha-acetyl-L-seryl-[histone H2A] + CoA
-
-
-
-
?
acetyl-CoA + an N-terminal-L-seryl-[histone H4]
an N-terminal-Nalpha-acetyl-L-seryl-[histone H4] + CoA
-
-
-
?
acetyl-CoA + an N-terminal-L-seryl-[histone H4]
an N-terminal-Nalpha-acetyl-L-seryl-[histone H4] + CoA
-
-
-
?
acetyl-CoA + an N-terminal-L-seryl-[histone H4]
an N-terminal-Nalpha-acetyl-L-seryl-[histone H4] + CoA
-
-
-
-
?
acetyl-CoA + an N-terminal-L-seryl-[histone H4]
an N-terminal-Nalpha-acetyl-L-seryl-[histone H4] + CoA
-
efficient acetylation requires at least 30 to 50 amino acid residues of the N terminus of histone H4
-
-
?
acetyl-CoA + an N-terminal-L-seryl-[histone H4]
an N-terminal-Nalpha-acetyl-L-seryl-[histone H4] + CoA
-
efficient acetylation requires at least 30 to 50 amino acid residues of the N terminus of histone H4
-
-
?
acetyl-CoA + N-terminal-L-seryl1-[histone H2A]
N-terminal-Nalpha-acetyl-L-seryl1-[histone H2A] + CoA
-
-
-
?
acetyl-CoA + N-terminal-L-seryl1-[histone H2A]
N-terminal-Nalpha-acetyl-L-seryl1-[histone H2A] + CoA
-
-
-
-
?
acetyl-CoA + N-terminal-L-seryl1-[histone H4]
N-terminal-Nalpha-acetyl-L-seryl1-[histone H4] + CoA
-
-
-
?
acetyl-CoA + N-terminal-L-seryl1-[histone H4]
N-terminal-Nalpha-acetyl-L-seryl1-[histone H4] + CoA
-
-
-
-
?
acetyl-CoA + Ser-Gly-Arg-Gly
acetyl-CoA + Nalpha-acetyl-Ser-Gly-Arg-Lys
-
-
-
-
?
acetyl-CoA + Ser-Gly-Arg-Gly
acetyl-CoA + Nalpha-acetyl-Ser-Gly-Arg-Lys
-
-
-
-
?
acetyl-CoA + Ser-Gly-Gly-Lys
acetyl-CoA + Nalpha-acetyl-Ser-Gly-Gly-Lys
-
-
-
-
?
acetyl-CoA + Ser-Gly-Gly-Lys
acetyl-CoA + Nalpha-acetyl-Ser-Gly-Gly-Lys
-
-
-
-
?
additional information
?
-
hNaa40p is a NAT selectively acetylating Ser-Gly or Gly-Gly starting peptides. NatD also is defined as the catalytic unit Naa40p (Nat4) which co-translationally Nt-acetylates histones H2A and H4. Recombinant hNaa40p Nt-acetylates the oligopeptides derived from the N-termini of both histones
-
-
?
additional information
?
-
-
hNaa40p is a NAT selectively acetylating Ser-Gly or Gly-Gly starting peptides. NatD also is defined as the catalytic unit Naa40p (Nat4) which co-translationally Nt-acetylates histones H2A and H4. Recombinant hNaa40p Nt-acetylates the oligopeptides derived from the N-termini of both histones
-
-
?
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Carcinoma, Hepatocellular
Patt1, a novel protein acetyltransferase that is highly expressed in liver and downregulated in hepatocellular carcinoma, enhances apoptosis of hepatoma cells.
Colonic Neoplasms
Depletion of histone N-terminal-acetyltransferase Naa40 induces p53-independent apoptosis in colorectal cancer cells via the mitochondrial pathway.
Colonic Neoplasms
NAA40 contributes to colorectal cancer growth by controlling PRMT5 expression.
Colorectal Neoplasms
Depletion of histone N-terminal-acetyltransferase Naa40 induces p53-independent apoptosis in colorectal cancer cells via the mitochondrial pathway.
Colorectal Neoplasms
NAA40 contributes to colorectal cancer growth by controlling PRMT5 expression.
Diabetes Mellitus
Differential Expression of Human N-Alpha-Acetyltransferase 40 (hNAA40), Nicotinamide Phosphoribosyltransferase (NAMPT) and Sirtuin-1 (SIRT-1) Pathway in Obesity and T2DM: Modulation by Metformin and Macronutrient Intake.
Diabetes Mellitus, Type 2
Differential Expression of Human N-Alpha-Acetyltransferase 40 (hNAA40), Nicotinamide Phosphoribosyltransferase (NAMPT) and Sirtuin-1 (SIRT-1) Pathway in Obesity and T2DM: Modulation by Metformin and Macronutrient Intake.
Liver Neoplasms
Identification of NAA40 as a Potential Prognostic Marker for Aggressive Liver Cancer Subtypes.
Liver Neoplasms
N-Terminal Acetyltransferases Are Cancer-Essential Genes Prevalently Upregulated in Tumours.
n-terminal l-serine nalpha-acetyltransferase natd deficiency
Liver Patt1 deficiency protects male mice from age-associated but not high-fat diet-induced hepatic steatosis.
Neoplasms
Depletion of histone N-terminal-acetyltransferase Naa40 induces p53-independent apoptosis in colorectal cancer cells via the mitochondrial pathway.
Neoplasms
Identification of NAA40 as a Potential Prognostic Marker for Aggressive Liver Cancer Subtypes.
Neoplasms
N-Terminal Acetyltransferases Are Cancer-Essential Genes Prevalently Upregulated in Tumours.
Neoplasms
NAA40 contributes to colorectal cancer growth by controlling PRMT5 expression.
Obesity
Differential Expression of Human N-Alpha-Acetyltransferase 40 (hNAA40), Nicotinamide Phosphoribosyltransferase (NAMPT) and Sirtuin-1 (SIRT-1) Pathway in Obesity and T2DM: Modulation by Metformin and Macronutrient Intake.
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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
-
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
-
enzyme depletion strains show several minor phenotypes, including sensitivity to 3-aminotriazole, benomyl, and thiabendazole
-
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D127A/E129A
the mutant shows significantly decreased catalytic efficiency (1.6-18fold) compared to the wild type enzyme
T174A
the mutant shows wild type catalytic efficiency
W90A
the mutant exhibits markedly decreased catalytic efficiency (2.8fold) compared to the wild type enzyme
Y136A
the mutant shows significantly decreased catalytic efficiency (1.6-1.8fold) compared to the wild type enzyme
Y136F
the catalytic efficiency of the mutant is modestly affected compared to the wild type enzyme
Y138A
the mutant shows significantly decreased catalytic efficiency (1.6-1.8fold) compared to the wild type enzyme
Y211A
the mutant shows wild type catalytic efficiency
Y85A
the mutant exhibits markedly decreased catalytic efficiency (5.8fold) compared to the wild type enzyme
additional information
enzyme silencing by lentivirus-based shRNA sequences (NAA40-KD1 and NAA40-KD2) targeting two distinct sites of NAA40 mRNA in HCT-116, HT-29, SW-480, and SW-620 cells. Depletion of NAA40 impedes cell proliferation and results in morphological alterations, such as cellular rounding. NAA40 depletion impairs CRC xenograft tumor growth
additional information
-
enzyme silencing by lentivirus-based shRNA sequences (NAA40-KD1 and NAA40-KD2) targeting two distinct sites of NAA40 mRNA in HCT-116, HT-29, SW-480, and SW-620 cells. Depletion of NAA40 impedes cell proliferation and results in morphological alterations, such as cellular rounding. NAA40 depletion impairs CRC xenograft tumor growth
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Song, O.k.; Wang, X.; Waterborg, J.H.; Sternglanz, R.
An Nalpha-acetyltransferase responsible for acetylation of the N-terminal residues of histones H4 and H2A
J. Biol. Chem.
278
38109-38112
2003
Saccharomyces cerevisiae
brenda
Hole, K.; van Damme, P.; Dalva, M.; Aksnes, H.; Glomnes, N.; Varhaug, J.; Lillehaug, J.; Gevaert, K.; Arnesen, T.
The human N-alpha-acetyltransferase 40 (hNaa40p/hNatD) is conserved from yeast and N-terminally acetylates histones H2A and H4
PLoS ONE
6
e24713
2011
Homo sapiens (Q86UY6), Homo sapiens
brenda
Pavlou, D.; Kirmizis, A.
Depletion of histone N-terminal-acetyltransferase Naa40 induces p53-independent apoptosis in colorectal cancer cells via the mitochondrial pathway
Apoptosis
21
298-311
2015
Homo sapiens, Homo sapiens (Q86UY6)
brenda
Polevoda, B.; Hoskins, J.; Sherman, F.
Properties of Nat4, an Nalpha-acetyltransferase of Saccharomyces cerevisiae that modifies N termini of histones H2A and H4
Mol. Cell. Biol.
29
2913-2924
2009
Saccharomyces cerevisiae, Saccharomyces cerevisiae B-15329
brenda
Magin, R.; Liszczak, G.; Marmorstein, R.
The molecular basis for histone H4- and H2A-specific amino-terminal acetylation by NatD
Structure
23
332-341
2015
Homo sapiens (Q86UY6)
brenda
Demetriadou, C.; Pavlou, D.; Mpekris, F.; Achilleos, C.; Stylianopoulos, T.; Zaravinos, A.; Papageorgis, P.; Kirmizis, A.
NAA40 contributes to colorectal cancer growth by controlling PRMT5 expression
Cell Death Dis.
10
236
2019
Homo sapiens (Q86UY6), Homo sapiens
brenda
Alshahrani, A.; AlDubayee, M.; Zahra, M.; Alsebayel, F.M.; Alammari, N.; Alsudairy, F.; Almajed, M.; Aljada, A.
Differential expression of human N-alpha-acetyltransferase 40 (hNAA40), nicotinamide phosphoribosyltransferase (NAMPT) and sirtuin-1 (SIRT-1) pathway in obesity and T2DM modulation by Mmetformin and macronutrient intake
Diabetes
12
2765-2774
2019
Homo sapiens (Q86UY6), Homo sapiens
brenda