2.3.1.5: arylamine N-acetyltransferase
This is an abbreviated version!
For detailed information about arylamine N-acetyltransferase, go to the full flat file.
Word Map on EC 2.3.1.5
-
2.3.1.5
-
pineal
-
melatonin
-
rhythm
-
circadian
-
n-acetylation
-
retina
-
2-aminofluorene
-
night
-
p-aminobenzoic
-
nocturnal
-
arylalkylamine
-
n-acetylserotonin
-
hydrazine
-
medicine
-
diurnal
-
isoniazid
-
light-dark
-
aa-nat
-
paba
-
pinealocytes
-
nighttime
-
hydroxyindole-o-methyltransferase
-
sulfamethazine
-
hiomt
-
accoa
-
xenobiotic-metabolizing
-
monomorphic
-
daytime
-
quinpirole
-
tryptamine
-
anti-tubercular
-
pharmacology
-
sulpiride
-
light-exposed
-
analysis
-
molecular biology
-
n-hydroxylated
-
drug development
-
midnight
-
p-aminosalicylic
-
o-acetyltransferase
-
n-hydroxyarylamine
-
spiroperidol
- 2.3.1.5
-
pineal
- melatonin
-
rhythm
-
circadian
-
n-acetylation
- retina
- 2-aminofluorene
-
night
-
p-aminobenzoic
-
nocturnal
- arylalkylamine
- n-acetylserotonin
- hydrazine
- medicine
-
diurnal
- isoniazid
-
light-dark
- aa-nat
- paba
- pinealocytes
-
nighttime
- hydroxyindole-o-methyltransferase
- sulfamethazine
- hiomt
- accoa
-
xenobiotic-metabolizing
-
monomorphic
-
daytime
- quinpirole
- tryptamine
-
anti-tubercular
- pharmacology
- sulpiride
-
light-exposed
- analysis
- molecular biology
-
n-hydroxylated
- drug development
-
midnight
-
p-aminosalicylic
- o-acetyltransferase
- n-hydroxyarylamine
-
spiroperidol
Reaction
Synonyms
(BACAN)NAT3, (MYCAB)NAT1, 2-naphthylamine N-acetyltransferase, 4-aminobiphenyl N-acetyltransferase, ABW01_24350, acetyl CoA-arylamine N-acetyltransferase, acetyltransferase, 2-naphthylamine N-, acetyltransferase, 4-aminobiphenyl, acetyltransferase, arylamine, acetyltransferase, p-aminosalicylate N-, acetyltransferase, procainamide N-, acetyltransferase, serotonin N-, arylamine acetylase, arylamine acetyltransferase, arylamine N-acetyl transferase, arylamine N-acetyltransferase, arylamine N-acetyltransferase 1, arylamine N-acetyltransferase 2, arylamine N-acetyltransferase C, arylamine N-acetyltransferase I, arylamine N-acetyltransferase type 1, arylamine N-acetyltransferase type 2, arylamine N-acetyltransferase type I, arylamine-N-acetyltransferase 1, BanatA, BanatB, BanatC, beta-naphthylamine N-acetyltransferase, indoleamine N-acetyltransferase, MlNAT1, MMNAT, More, MSNAT, N-acetyltransferase, N-acetyltransferase a, N-acetyltransferase b, N-acetyltransferase type 2, N-hydroxyarylamine O-acetyltransferase, NAT, NAT 1, NAT-a, NAT-b, NAT1, NAT2, NAT2*1, NAT2*2, NAT3, NAT31, NfNAT, p-aminosalicylate N-acetyltransferase, PANAT, rhesus NAT2, serotonin acetyltransferase, serotonin N-acetyltransferase, STNAT, TBNAT, Tpau_4046, UDP-2-acetamido-3-amino-2,3-dideoxy-D-glucuronic acid 3-N-acetyltransferase, UDP-D-Glc(2NAc3N)A 3-N-acetyltransferase, WbpD
ECTree
2.3.1.5 arylamine N-acetyltransferaseAdvanced search results
results (
results (Inhibitors
Inhibitors on EC 2.3.1.5 - arylamine N-acetyltransferase
Please wait a moment until all data is loaded. This message will disappear when all data is loaded.
top
INHIBITOR 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
IMAGE
(5E)-5-[(4-hydroxy-3,5-diiodophenyl)methylidene]-2-sulfanylidene-1,3-thiazolidin-4-one
25fold more selective towards the inhibition of recombinant human NAT1 than N-acetyltransferase 2. Incubation of MDA-MB-231 cell line with (5E)-5-[(4-hydroxy-3,5-diiodophenyl)methylidene]-2-sulfanylidene-1,3-thiazolidin-4-one results in 60% reduction in NAT1 activity and significant decreases in cell growth, anchorage-dependent growth, and anchorage-independent growth
(5Z)-3-amino-5-(3-hydroxy-2,4-diiodobenzylidene)-2-thioxo-1,3-thiazolidin-4-one
-
inhibition of both recombinant enzyme and native enzyme in ZR-75 cell lysate, competitive
(5Z)-5-(2-methylbenzylidene)-2-thioxo-1,3-thiazolidin-4-one
-
inhibition of both recombinant enzyme and native enzyme in ZR-75 cell lysate, competitive
(5Z)-5-(3,4-dichlorobenzylidene)-2-thioxo-1,3-thiazolidin-4-one
-
inhibition of both recombinant enzyme and native enzyme in ZR-75 cell lysate, competitive
(5Z)-5-(3-hydroxy-2,4-diiodobenzylidene)-2-thioxo-1,3-thiazolidin-4-one
-
inhibition of both recombinant enzyme and native enzyme in ZR-75 cell lysate, competitive
(5Z)-5-(3-hydroxybenzylidene)-2-thioxo-1,3-thiazolidin-4-one
-
inhibition of both recombinant enzyme and native enzyme in ZR-75 cell lysate, competitive
(5Z)-5-(4-chlorobenzylidene)-2-thioxo-1,3-thiazolidin-4-one
-
inhibition of both recombinant enzyme and native enzyme in ZR-75 cell lysate, competitive
2,3-Dihydroxybiphenyl
-
the growth of strain BCG is retarded when the cultures are incubated either in the presence of 2,3-dihydroxybiphenyl on both solid and liquid media
2-nitrosofluorene
-
potent inactivator, incubation with 2-nitrosofluorene causes 91% inactivation. In the presence of a 500fold excess of glutathione (0.5 mM), inhibition is reduced to 28%
2-nitrosotoluene
-
less potent inactivator of NAT1, NAT1 with 2-nitrosotoluene causes 46% inhibition of the enzyme, whereas the presence of AcCoA lowers the extent of inhibition to 5%
3-chlorocatechol
-
the growth of strain BCG is retarded when the cultures are incubated either in the presence of 3-chlorocatechol on both solid and liquid media
4-nitrosobenzene
-
less potent inactivator of NAT1, NAT1 with nitrosobenzene causes 59% inhibition of the enzyme, whereas the presence of AcCoA lowers the extent of inhibition to 13%
4-nitrosobiphenyl
-
potent inactivator, incubation with 4-nitrosobiphenyl causes 71% inactivation. In the presence of a 500fold excess of glutathione (0.5 mM), inhibition is reduced to 35%
5-aminosalicylic acid
-
substrate inhibition; substrate inhibition, in which the substrate binds both to the free form of the enzyme and the acetyl coenzyme A-enzyme complex in non-productive reaction pathways; substrate inhibition through 5-aminosalicylic acid in which the substrate binds both to the free form of the enzyme and the acetyl coenzyme A-enzyme complex
5-methoxypsoralen
-
i.e. 5-MOP, activates the enzyme at 50 mM in Colo 205 cells, inhibitory at lower dosage of 0.05-0.5 mM, concentrations of 5-25 mM have no effect in Colo 205 cells
Ag+
-
26% remaining activity isoenzyme Nat-b; 30% remaining activity isoenzyme NAT-a
alpha-solanine
noncompetitive, alpha-solanine can significantly decrease NAT activity in intact Hep-G2 cells or the cytoplasm. Km does not differ either for intact HepG2 cells or for the cytoplasm, while Vmax is significantly different
ATP
non-competitive inhibitor with respect to the acetyl acceptor, competitive inhibitor with respect to acetyl-coenzyme A. There is no effect by presence or absence of Mg2+
Berberine
-
berberine affects kinetic constants of NAT, 24 h berberine treatment decreases bacterial growth and amounts of 2-acetylaminofluorene in Salmonella typhimurium by downregulation of the NAT enzyme expression
cytokine
-
mixture of proinflammatory cytokines, interferon-gamma, interleukin-1beta, tumor necrosis factor-alpha
-
H2O2
-
NAT1 is reversibly inactivated by physiological aoncentrations of hydrogen peroxide. Inactivation of NAT1 is fully reversed by physiological concentrations of GSH
Hg2+
-
11% remaining activity isoenzyme Nat-b; 36% remaining activity isoenzyme NAT-a
N-(3-((2''-methoxyethyl)amino)-1,4-dioxo-1,4-dihydronaphthalen-2-yl)benzenesulfonamide
-
-
-
N-(3-(2''-chlorophenyl)-1,4-dioxo-1,4-dihydronaphthalen-2-yl)benzenesulfonamide
-
-
-
N-(3-(3'',5''-dimethylphenoxy)-1,4-dioxo-1,4-dihydronaphthalen-2-yl)benzenesulfonamide
-
-
-
N-(3-(3'',5''-dimethylphenylamino)-1,4-dioxo-1,4-dihydronaphthalen-2-yl)benzenesulfonamide
-
-
-
N-(3-(3'',5''-dimethylphenylamino)-5-nitro-1,4-dioxo-1,4-dihydronaphthalen-2-yl)benzenesulfonamide
-
-
-
N-(3-(3'',5''-dimethylphenylamino)-6-nitro-1,4-dioxo-1,4-dihydronaphthalen-2-yl)benzenesulfonamide
-
-
-
N-(3-(3'',5''-dimethylphenylamino)-7-nitro-1,4-dioxo-1,4-dihydronaphthalen-2-yl)benzenesulfonamide
-
-
-
N-(3-(3'',5''-dimethylphenylamino)-8-nitro-1,4-dioxo-1,4-dihydronaphthalen-2-yl)benzenesulfonamide
-
-
-
N-(3-(3''-chlorophenyl)-1,4-dioxo-1,4-dihydronaphthalen-2-yl)benzenesulfonamide
-
-
-
N-(3-(3''-formylphenyl)-1,4-dioxo-1,4-dihydronaphthalen-2-yl)benzenesulfonamide
-
-
-
N-(3-(3''-formylphenyl)-1,4-dioxo-1,4-dihydronaphthalen-2-yl)phenylacetamide
-
-
-
N-(3-(4''-bromophenoxy)-1,4-dioxo-1,4-dihydronaphthalen-2-yl)benzenesulfonamide
-
-
-
N-(3-(4''-bromophenylamino)-1,4-dioxo-1,4-dihydronaphthalen-2-yl)benzenesulfonamide
-
-
-
N-(3-(4''-chlorophenyl)-1,4-dioxo-1,4-dihydronaphthalen-2-yl)benzenesulfonamide
-
-
-
N-(3-(4''-formylphenyl)-1,4-dioxo-1,4-dihydronaphthalen-2-yl)benzenesulfonamide
-
-
-
N-(3-(benzylamino)-1,4-dioxo-1,4-dihydronaphthalen-2-yl)benzenesulfonamide
-
-
-
N-(3-(cyclopentylamino)-1,4-dioxo-1,4-dihydronaphthalen-2-yl)benzenesulfonamide
-
-
-
N-(3-(furan-2''-yl)-1,4-dioxo-1,4-dihydronaphthalen-2-yl)-benzenesulfonamide
-
-
-
N-(3-(furan-3''-yl)-1,4-dioxo-1,4-dihydronaphthalen-2-yl)-benzenesulfonamide
-
-
-
N-(5-amino-3-(3'',5''-dimethylphenylamino)-1,4-dioxo-1,4-dihydronaphthalen-2-yl)benzenesulfonamide
-
-
-
N-(6-amino-3-(3'',5''-dimethylphenylamino)-1,4-dioxo-1,4-dihydronaphthalen-2-yl)benzenesulfonamide
-
-
-
N-(7-amino-3-(3'',5''-dimethylphenylamino)-1,4-dioxo-1,4-dihydronaphthalen-2-yl)benzenesulfonamide
-
-
-
N-(8-amino-1,4-dioxo-3-(phenylamino)-1,4-dihydronaphthalen-2-yl)benzenesulfonamide
-
-
-
N-(8-amino-3-(3'',5''-dimethylphenylamino)-1,4-dioxo-1,4-dihydronaphthalen-2-yl)benzenesulfonamide
-
-
-
N-(8-nitro-1,4-dioxo-3-(phenylamino)-1,4-dihydronaphthalen-2-yl)benzenesulfonamide
-
-
-
N-[3-(3,5-dimethylanilino)-1,4-dioxo-1,4-dihydronaphthalen-2-yl]-N-methylbenzenesulfonamide
-
-
proinflammatory cytokine
-
treatment of cholangiocarcinoma KKU-100 cells with cytokines (interferon-gamma, interleukin-1beta and tumor necrosis factor-alpha) suppresses NAT1 activity, reducing the Vmax without affecting the Km
-
S-nitroso-glutathione
-
treatment of cholangiocarcinoma KKU-100 cells S-nitroso-glutathione results in reduced NAT1 activity as early as 2 h, and the suppression persists for 48 h
S-nitroso-N-acetyl-DL-penicillamine
-
reversible inactivation due to direct atteck of the highly reactive cysteine residue in the enzyme active site on the sulfur of S-nitrosothiols to form a mixed disulfide between these NO-derived oxidants and NAT1
thiram
irreversible inhibitor, modification of NAT1 catalytic cysteine residue
(5Z)-5-(2-hydroxybenzylidene)-2-thioxo-1,3-thiazolidin-4-one
-
i.e. Rhod-o-hp. Significant reduction of cell growth by increasing the percent of MDA-MB-231 cells in G2/M phase of the cell cycle, and reduction of the ability of cells to grow in soft agar
(5Z)-5-(2-hydroxybenzylidene)-2-thioxo-1,3-thiazolidin-4-one
-
inhibition of both recombinant enzyme and native enzyme in ZR-75 cell lysate, competitive
11alpha-hydroxycinnamosmolide
-
a drimane sesquiterpenoid lactone from Warburgia salutaris inhibits the purified mycobacterial enzyme and contributes to the anti-mycobacterial activity of Warburgia salutaris
11alpha-hydroxycinnamosmolide
-
a drimane sesquiterpenoid lactone from Warburgia salutaris inhibits the purified mycobacterial enzyme and contributes to the anti-mycobacterial activity of Warburgia salutaris, the component or extract has no effect on a Nat-deficient Mycobacterium bovis strain; a drimane sesquiterpenoid lactone isolated from Warburgia salutaris. Compound inhibits the growth of Mycobacterium bovis BCG wild-type in a dose-dependent fashion, while it had little effect of the growth of Mycobacterium bovis BCG nat deleted mutant
11alpha-hydroxycinnamosmolide
-
a drimane sesquiterpenoid lactone from Warburgia salutaris inhibits the purified mycobacterial enzyme and contributes to the anti-mycobacterial activity of Warburgia salutaris, 35% inhibition of the recombinant enzyme at 0.5 mg/ml; a novel drimane sesquiterpenoid lactone isolated from Warburgia salutaris. Compound inhibits recombinant NAT activity of Mycobacterium smegmatis (35% inhibition of acetylation at 0.5 mg/mL). Compound exhibits anti-mycobacterial activity against Mycobacterium tuberculosis H37Rv and Mycobacterium bovis BCG Pasteur. Compound does not inhibit growth of Escherichia coli and is not toxic to cultured mammalian macrophage cells at the concentrations at which anti-mycobacterial activity is observed; isolated from the bark of Warburgia salutaris
caffeic acid
-
4 mM, 65.3% suppression. Dose-dependent enzyme inhibition in cytosolic and intact cell examinations
caffeic acid
-
4 mM, 37.6% suppression. Dose-dependent enzyme inhibition in cytosolic and intact cell examinations
caffeic acid
-
4 mM, 37.9% suppression. Dose-dependent enzyme inhibition in cytosolic and intact cell examinations
caffeic acid
-
4 mM, 39.7% suppression. Dose-dependent enzyme inhibition in cytosolic and intact cell examinations
caffeic acid
-
4 mM, 83.7% suppression. Dose-dependent enzyme inhibition in cytosolic and intact cell examinations
chlorogenic acid
-
dose-dependent enzyme inhibition in cytosolic and intact cell examinations
chlorogenic acid
-
4mM, significant inhibitory effect for 4 hours. Dose-dependent enzyme inhibition in cytosolic and intact cell examinations
chlorogenic acid
-
dose-dependent enzyme inhibition in cytosolic and intact cell examinations
chlorogenic acid
-
dose-dependent enzyme inhibition in cytosolic and intact cell examinations
chlorogenic acid
-
dose-dependent enzyme inhibition in cytosolic and intact cell examinations
cisplatin
-
exposure of MCF-7 breast cancer cells to cisplatin at clinically relevant concentrations (below 0.4 nM) causes significant dose-dependent inhibition of the endogenous NAT1 enzyme. The incubation of NAT1 with various concentrations of cisplatin results in the dose-dependent modification of cysteine residues, as indicated by the disappearance of fluorescein-conjugated iodoacetamide labeling
cisplatin
-
treating C57BL/6J mice with cisplatin significantly decreases murine Nat2 (murine counterpart of human NAT1) enzymatic function in the liver (25% inhibition), kidney (40% inhibition), and blood cells (50% inhibition)
ellagic acid
-
48.9% to 80.3% inhibition of the enzyme activity in the intact cell, time- and dose-dependent inhibition, ellagic acid suppresses enzyme activity in six clinically isolated Pseudomonas aeruginosa strains
ferulic acid
-
4 mM, 46.5% suppression. Dose-dependent enzyme inhibition in cytosolic and intact cell examinations
ferulic acid
-
4 mM, 35.8% suppression. Dose-dependent enzyme inhibition in cytosolic and intact cell examinations
ferulic acid
-
4 mM, 41.4% suppression. Dose-dependent enzyme inhibition in cytosolic and intact cell examinations
ferulic acid
-
4 mM, 39.7% suppression. Dose-dependent enzyme inhibition in cytosolic and intact cell examinations
ferulic acid
-
4 mM, 75.1% suppression. Dose-dependent enzyme inhibition in cytosolic and intact cell examinations
hydrogen peroxide
inactivates isozyme NAT1, in vivo effect, overview
hydrogen peroxide
-
inhibition is caused by oxidation at the active site cysteine
iodoacetamide
-
incubation of TBNAT with iodoacetamide results in a time-dependentloss of enzymatic activity
methotrexate
-
inhibits reaction with 4-aminobenzoic acid, but with sulfamethazine, possibly due to two different enzymes
N-[3-(3,5-dimethylanilino)-1,4-dioxo-1,4-dihydronaphthalen-2-yl]benzenesulfonamide
-
selective competitive inhibitor
N-[3-(3,5-dimethylanilino)-1,4-dioxo-1,4-dihydronaphthalen-2-yl]benzenesulfonamide
-
93.3% inhibition of isoform NAT1 at 0.03 mM and 10.6% inhibition of isoform NAT2
N-[3-(3,5-dimethylanilino)-1,4-dioxo-1,4-dihydronaphthalen-2-yl]benzenesulfonamide
-
selective competitive inhibitor
N-[3-(3,5-dimethylanilino)-1,4-dioxo-1,4-dihydronaphthalen-2-yl]benzenesulfonamide
-
37.6% inhibition of isoform Nat1 at 0.03 mM and 92.4% inhibition of isoform Nat2
Zn2+
-
39% remaining activity isoenzyme Nat-b; 41% remaining activity isoenzyme NAT-a
additional information
inhibitory potency of flavonoids on isozyme NAT1, no inhibition by curcumin, silymarin, and scopoletin, overview; inhibitory potency of flavonoids on isozyme NAT2, no inhibition by ()epigallocatechin gallate, gallic acid, caffeic acid, and ferulic acid, overview
-
additional information
inhibitory potency of flavonoids on isozyme NAT1, no inhibition by curcumin, silymarin, and scopoletin, overview; inhibitory potency of flavonoids on isozyme NAT2, no inhibition by ()epigallocatechin gallate, gallic acid, caffeic acid, and ferulic acid, overview
-
additional information
-
inhibitory potency of flavonoids on isozyme NAT1, no inhibition by curcumin, silymarin, and scopoletin, overview; inhibitory potency of flavonoids on isozyme NAT2, no inhibition by ()epigallocatechin gallate, gallic acid, caffeic acid, and ferulic acid, overview
-
additional information
-
inhibition profile by polyphenol compounds is different between NAT1 and NAT2. The small polyphenol of cinnamic acid derivates shows some inhibitory activity toward NAT1 , but it has very low activity toward NAT2
-
additional information
not inhibited by N-(3-(3,5-dimethylphenylamino)-1,4-dioxo-1,4-dihydronaphthalen-2-yl)benzenesulfonamide
-
additional information
-
not inhibited by N-(3-(3,5-dimethylphenylamino)-1,4-dioxo-1,4-dihydronaphthalen-2-yl)benzenesulfonamide
-
additional information
-
the enzyme is inhibited by layered silicate nanoparticles and layered double hydroxide clays
-
additional information
-
not inhibited by N-methylphenethylamine. GSH or dithiothreitol are unable to reactivate significantly inhibited isoform NAT1
-
additional information
the activity of NAT1 in cell culture does not change when cells are stimulated with different concentrations of sirtuin agonist resveratrol; the activity of NAT1 in cell culture does not change when cells are stimulated with different concentrations of sirtuin agonist resveratrol, compared to cells in culture medium. No effect on NAT1 activity is observed when sirtuins are inhibited with different concentrations of nicotinamide for 24 h
-
additional information
the activity of NAT1 in cell culture does not change when cells are stimulated with different concentrations of sirtuin agonist resveratrol; the activity of NAT1 in cell culture does not change when cells are stimulated with different concentrations of sirtuin agonist resveratrol, compared to cells in culture medium. No effect on NAT1 activity is observed when sirtuins are inhibited with different concentrations of nicotinamide for 24 h
-
additional information
-
no significant inactivation with either iodoacetic acid or bromoacetic acid, NAT2
-
additional information
-
no inhibition by CdCl2, arsenite, diisopropylfluorophosphate
-
additional information
-
no inhibition by CdCl2, arsenite, diisopropylfluorophosphate; no inhibition by paraoxon
-
additional information
-
no inhibition by acetylated products and 2-mercaptoethanol
-
