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Gene Review

Nat1  -  N-acetyltransferase 1 (arylamine N...

Rattus norvegicus

Synonyms: AT-1, Aac1, Arylamide acetylase 1, Arylamine N-acetyltransferase 1, N-acetyltransferase type 1, ...
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Disease relevance of Nat1

  • Genes for the 290 amino acid, 33-34 kDa cytosolic acetyltransferases (NAT1* and NAT2*) from rat and hamster were cloned and expressed in Escherichia coli [1].
  • Cells were aspirated from tumors with low metastatic potential (following subcutaneous inoculation of 10(6) tumor cells the H, G and AT-1 variants had less than 5% metastases; AT-2 had 5-20%) and were compared to the electrophoretic mobility of cells aspirated from highly metastatic tumors (MAT-LyLu, MAT-Lu, AT-3 had greater than 90% metastases) [2].
  • In this study, we reported the effects of vitamin C on arylamine N-acetyltransferase (NAT) activity and DNA adduct formation in rat glial tumor cell line (C6 glioma) [3].

High impact information on Nat1

  • A complementary DNA (cDNA) library from the anaplastic nonmetastasizing subline AT-1 was used for a differential hybridization analysis, using probes derived from mRNAs of the AT-1 and the metastasizing MAT-LyLu subline [4].
  • In 2 weakly metastatic cell lines (AT-1 and AT-2), p9Ka transcript amounts were, respectively, 6.29 +/- 0.74 and 5.55 +/- 1.11 times that detected in the G cells [5].
  • The data also indicate that at low substrate concentrations, NAT1 would apparently play the predominant role in vivo in N-acetylation and N,O-acyltransfer of aromatic amine derivatives, including their metabolic activation to DNA-reactive agents [1].
  • These data suggest that steroidogenesis may be modulated by angiotensin peptides that act in part through intracellular AT1 receptors [6].
  • Quinapril, ZPP, PCMS, and PMSF, as well as losartan and PD-123319, the angiotensin receptor type 1 (AT1) and type 2 (AT2) receptor antagonists, were used in progesterone production studies [6].

Chemical compound and disease context of Nat1


Biological context of Nat1

  • This result is consistent with substrate specificity data indicating that N-OH-AAF is a much better acetyl donor for hamster NAT1 than NAT2 [8].
  • The low metastatic sublines G, AT-1, and AT-2 had 0.32 +/- standard deviation 0.10, 0.38 +/- 0.12, and 0.14 +/- 0.05 sister chromatid exchanges per chromosome, respectively [9].
  • Pinocytosis failed to distinguish sublines of high (AT-3 63.5 +/- standard error 4.1 mean channel number, MAT-LyLu 63.2 +/- 6.3, MAT-Lu 64.3 +/- 5.6) and low (G 33.5 +/- 1.2, AT-1 63.5 +/- 4.1, AT-2 58.4 +/- 3.6) (rank p = 0.38) metastatic potential but correlated strongly with visually graded membrane ruffling (r = 0.95, p = 0.003) [10].
  • None of the phosphorylation modulators led to a significant change in NAT1 or NAT2 activities [11].
  • The effect of SLO pretreatment of rats on cytochrome P-450-catalyzed tolbutamide hydroxylation and NAT activities toward PA (a substrate for NAT1), and p-aminobenzoic acid (a substrate for NAT2) was examined ex vivo [12].

Anatomical context of Nat1


Associations of Nat1 with chemical compounds

  • In most of the sublines with a more advanced state of progression (i.e., the moderately differentiated, moderately fast growing HI-M; the poorly differentiated, faster growing HI-F; and the anaplastic, very fast growing AT-1, AT-2, and MAT-Lu tumors), however, no expression of keratin specific for luminal cells was detected [17].
  • Monomorphic (NAT1) and polymorphic (NAT2) activities were determined using N-acetylprocainamide and N-acetamidobenzoic acid formation, respectively [18].
  • Serum melatonin levels reflected the circadian pattern of the NAT1 activity, without, however, showing any quantitative differences between the two strains [19].
  • However, while levels of Ang II type 1 (AT1) receptor increased over time after LPS injection, those of Ang II type 2 (AT2) receptor were downregulated, (3) data of NO system (NO-NOS), the key vasodilator, were the most intriguing [20].
  • Effect of streptolysin-O-on rat hepatic acetyl coenzyme-A: arylamine N-acetyltransferase and cytochrome P-450 2B 1/2 activities ex vivo [12].

Physical interactions of Nat1


Other interactions of Nat1

  • Cloning, sequencing and expression of NAT1 and NAT2 encoding genes from rapid and slow acetylator inbred rats [21].
  • To investigate melatonin synthesis and secretion in LEW/N and F344/N rats, we examined the diurnal activity of pineal arylalkylamine N-acetyltransferase (NAT1), the rate-limiting enzyme in melatonin biosynthesis, which demonstrates circadian rhythmicity, as well as the diurnal levels of serum melatonin, in both strains [19].
  • The inducers led to the expected increases in CYP1A1 and CYP1A2 but the NAT1 and NAT2 activities remained unchanged [11].

Analytical, diagnostic and therapeutic context of Nat1

  • The nonmetastatic G, occasionally metastatic AT-1 and AT-2, and highly metastatic AT-3 and MAT-Lu Dunning sublines, and normal dorsal prostate were grown in culture and filmed by time-lapse videomicroscopy [22].
  • Size-exclusion HPLC chromatograms of NAT1 activity revealed similar patterns in both rat strains.(ABSTRACT TRUNCATED AT 250 WORDS)[19]
  • Our study shows that the N-acetyl transferases NAT1 or NAT2, the catalysts responsible for the formation of the highly reactive N-acetoxy derivatives of N-hydroxylated aromatic amines, are not responsible for the drastic decrease in arylamine genotoxicity after treatment of the metabolizing system with protein phosphatase inhibitors [11].
  • Angiotensin II (Ang II) receptor binding was localized in rat adrenal gland, kidney, and brain by in vitro autoradiography using the antagonist analogue 125I-[Sar1, Ile8]Ang II and differentiated into type I (AT-1) and type II (AT-2) subtypes using unlabelled non-peptide antagonists specific for Ang II subtypes [14].
  • Northern blot analysis was carried out to measure the cerebral tissue content of a novel translational repressor (NAT-1) and another thyroid hormone-responsive (THR) mRNA [23].


  1. Recombinant rat and hamster N-acetyltransferases-1 and -2: relative rates of N-acetylation of arylamines and N,O-acyltransfer with arylhydroxamic acids. Jones, R.F., Land, S.J., King, C.M. Carcinogenesis (1996) [Pubmed]
  2. Cell surface charge in predicting metastatic potential of aspirated cells from the Dunning rat prostatic adenocarcinoma model. Carter, H.B., Coffey, D.S. J. Urol. (1988) [Pubmed]
  3. Vitamin C inhibited DNA adduct formation and arylamine N-acetyltransferase activity and gene expression in rat glial tumor cells. Hung, C.F., Lu, K.H. Neurochem. Res. (2001) [Pubmed]
  4. Down modulation of fibronectin messenger RNA in metastasizing rat prostatic cancer cells revealed by differential hybridization analysis. Schalken, J.A., Ebeling, S.B., Isaacs, J.T., Treiger, B., Bussemakers, M.J., de Jong, M.E., Van de Ven, W.J. Cancer Res. (1988) [Pubmed]
  5. Elevated expression of calcium-binding protein p9Ka is associated with increasing malignant characteristics of rat prostate carcinoma cells. Ke, Y., Jing, C., Barraclough, R., Smith, P., Davies, M.P., Foster, C.S. Int. J. Cancer (1997) [Pubmed]
  6. Localized accumulation of angiotensin II and production of angiotensin-(1-7) in rat luteal cells and effects on steroidogenesis. Pepperell, J.R., Nemeth, G., Yamada, Y., Naftolin, F., Merino, M. Am. J. Physiol. Endocrinol. Metab. (2006) [Pubmed]
  7. Effects of carmustine and lomustine on arylamine N-acetyltransferase activity and 2-aminofluorene-DNA adducts in rat glial tumor cells. Hung, C.F. Neurochem. Res. (2000) [Pubmed]
  8. Characterization of hamster recombinant monomorphic and polymorphic arylamine N-acetyltransferases: bioactivation and mechanism-based inactivation studies with N-hydroxy-2-acetylaminofluorene. Sticha, K.R., Bergstrom, C.P., Wagner, C.R., Hanna, P.E. Biochem. Pharmacol. (1998) [Pubmed]
  9. Genetic instability assessed by sister chromatid exchange analysis in the Dunning R-3327 rat prostatic adenocarcinoma model and its relationship to metastatic potential. Sharief, Y., Mohler, J.L. Prostate (1995) [Pubmed]
  10. Flow cytometric assay of pinocytosis: correlation with membrane ruffling and metastatic potential in the Dunning R-3327 rat prostatic adenocarcinoma model. Mohler, J.L., Sharief, Y. Cytometry. (1993) [Pubmed]
  11. Control of the mutagenicity of arylamines by protein kinases and phosphatases: II. Lack of response of rat liver N-acetyl transferases to phosphorylation modulators. Padma, P.R., Oesch-Bartlomowicz, B., Hengstler, J.G., Oesch, F. Arch. Toxicol. (1997) [Pubmed]
  12. Effect of streptolysin-O-on rat hepatic acetyl coenzyme-A: arylamine N-acetyltransferase and cytochrome P-450 2B 1/2 activities ex vivo. Drobitch, R.K., Divakaruni, P., Svensson, C.K. Immunopharmacology and immunotoxicology. (1998) [Pubmed]
  13. Regulation of cGMP synthesis in cultured podocytes by vasoactive hormones. Lewko, B., Gołos, M., Latawiec, E., Angielski, S., Stepinski, J. J. Physiol. Pharmacol. (2006) [Pubmed]
  14. Angiotensin II receptor subtypes in rat brain and peripheral tissues. Song, K., Zhuo, J., Allen, A.M., Paxinos, G., Mendelsohn, F.A. Cardiology (1991) [Pubmed]
  15. Translocation of AT1- and AT2-Receptors by Higher Concentrations of Angiotensin II in the Smooth Muscle Cells of Rat Internal Anal Sphincter. de Godoy, M.A., Rattan, S. J. Pharmacol. Exp. Ther. (2006) [Pubmed]
  16. Intracerebroventricular administration of betacytotoxics alters expression of brain monoamine transporter genes. Salković-Petrisić, M., Lacković, Z. Journal of neural transmission (Vienna, Austria : 1996) (2003) [Pubmed]
  17. Intermediate filament expression and the progression of prostatic cancer as studied in the Dunning R-3327 rat prostatic carcinoma system. Ramaekers, F.C., Verhagen, A.P., Isaacs, J.T., Feitz, W.F., Moesker, O., Schaart, G., Schalken, J.A., Vooijs, G.P. Prostate (1989) [Pubmed]
  18. Cellular distribution of N-acetyltransferase activity in the rat small intestine. Ware, J.A., Reilly, T.P., Svensson, C.K. Biochem. Pharmacol. (1998) [Pubmed]
  19. Differences in arylalkylamine N-acetyltransferase activity between inflammatory disease-susceptible Lewis and -resistant Fischer rats. Mastorakos, G., Patchev, V.K., Chader, G.J., Chrousos, G.P., Gaudet, S.J. Neuroendocrinology (1995) [Pubmed]
  20. Time-dependent expression of renal vaso-regulatory molecules in LPS-induced endotoxemia in rat. Yamaguchi, N., Jesmin, S., Zaedi, S., Shimojo, N., Maeda, S., Gando, S., Koyama, A., Miyauchi, T. Peptides (2006) [Pubmed]
  21. Cloning, sequencing and expression of NAT1 and NAT2 encoding genes from rapid and slow acetylator inbred rats. Doll, M.A., Hein, D.W. Pharmacogenetics (1995) [Pubmed]
  22. Time lapse videomicroscopic identification of Dunning R-3327 adenocarcinoma and normal rat prostate cells. Mohler, J.L., Partin, A.W., Isaacs, W.B., Coffey, D.S. J. Urol. (1987) [Pubmed]
  23. Effect of amitriptyline on the messenger RNA of thyroid hormone-responsive genes in rat cerebral tissue. Mooradian, A.D., Li, J.P. Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale. (2000) [Pubmed]
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