ArticlePharmacogenetics and genomics2006
Functional properties of an alternative, tissue-specific promoter for human arylamine N-acetyltransferase 1.
Article in Pharmacogenetics and genomics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- Temporal Modulation of Differential Alternative Splicing in HaCaT Human Keratinocyte Cell Line Chronically Exposed to Arsenic for up to 28 Wk.Environmental health perspectives · 2022Article
- ArylamineFrontiers in pharmacology · 2022Article
- Human arylamine N-acetyltransferase 2 genotype-dependent protein expression in cryopreserved human hepatocytes.Scientific reports · 2020Article
- Population variability of rhesus macaque (Macaca mulatta) NAT1 gene for arylamine N-acetyltransferase 1: Functional effects and comparison with human.Scientific reports · 2019Article
- High N-Acetyltransferase 1 Expression Is Associated with Estrogen Receptor Expression in Breast Tumors, but Is not Under Direct Regulation by Estradiol, 5The Journal of pharmacology and experimental therapeutics · 2018Article
- Arylamine N-acetyltransferases: from drug metabolism and pharmacogenetics to drug discovery.British journal of pharmacology · 2014Review
- Glucocorticoid receptor-mediated transcriptional regulation of N-acetyltransferase 1 gene through distal promoter.The AAPS journal · 2012Article
- NATb/NAT1*4 promotes greater arylamine N-acetyltransferase 1 mediated DNA adducts and mutations than NATa/NAT1*4 following exposure to 4-aminobiphenyl.Molecular carcinogenesis · 2012Article
- Functional analysis of arylamine N-acetyltransferase 1 (NAT1) NAT1*10 haplotypes in a complete NATb mRNA construct.Carcinogenesis · 2012Article
- ATP8B1 gene expression is driven by a housekeeping-like promoter independent of bile acids and farnesoid X receptor.PloS one · 2012Article
- Phenotype of the most common "slow acetylator" arylamine N-acetyltransferase 1 genetic variant (NAT1*14B) is substrate-dependent.Drug metabolism and disposition: the biological fate of chemicals · 2012Article
- Characterization of genetic variation and natural selection at the arylamine N-acetyltransferase genes in global human populations.Pharmacogenomics · 2011Article
- Human N-acetyltransferase 1 *10 and *11 alleles increase protein expression through distinct mechanisms and associate with sulfamethoxazole-induced hypersensitivity.Pharmacogenetics and genomics · 2011Article
- Systemic functional expression of N-acetyltransferase polymorphism in the F344 Nat2 congenic rat.Drug metabolism and disposition: the biological fate of chemicals · 2008Article
- Functional effects of single nucleotide polymorphisms in the coding region of human N-acetyltransferase 1.The pharmacogenomics journal · 2008Article
- Mouse arylamine N-acetyltransferase 2 (Nat2) expression during embryogenesis: a potential marker for the developing neuroendocrine system.Biomarkers : biochemical indicators of exposure, response, and susceptibility to chemicals · 2008Article
- Inflammatory cytokines suppress arylamine N-acetyltransferase 1 in cholangiocarcinoma cells.World journal of gastroenterology · 2007Article
- Tissue expression and genomic sequences of rat N-acetyltransferases rNat1, rNat2, rNat3, and Functional characterization of a novel rNat3*2 genetic variant.Toxicological sciences : an official journal of the Society of Toxicology · 2007Article
- Functional analysis of the human N-acetyltransferase 1 major promoter: quantitation of tissue expression and identification of critical sequence elements.Drug metabolism and disposition: the biological fate of chemicals · 2007Article
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8 authors.
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Abstract
Variable expression of human arylamine N-acetyltransferase 1 (NAT1) due to genetic polymorphism, gene regulation or environmental influences is associated with individual susceptibility to various cancers. Recent studies of NAT1 transcription showed that most mRNAs originate at a promoter, P1, located 11.8 kb upstream of the single open reading frame (ORF) exon. We have now characterized an alternative NAT1 promoter lying 51.5 kb upstream of the NAT1 ORF. In the present study, analysis of human RNAs representing 27 tissue types by reverse transcriptase-polymerase chain reaction (RT-PCR) and quantitative RT-PCR showed the upstream 51.5 kb promoter, designated P3, to be most active in specific tissues, including kidney, liver, lung, and trachea. All NAT1 P3 mRNAs included 5'-untranslated region (5'-UTR) internal exons of 61 and 175 nucleotides in addition to the 79 nucleotide 5'-UTR exon present in P1 mRNA. CAP-dependent amplification of 5'-P3 mRNA termini defined an 84 bp transcription start region in which most start sites are centrally clustered. The hepatoma-derived HepG2 cell line expressed a high level of P3 mRNA with the same spliced structure and start site pattern as found in normal tissues. A 435-bp minimal promoter was defined by transfection of HepG2 with luciferase expression constructs containing genomic fragments from the P3 start region. These findings imply a fundamental role for P3 in NAT1 regulation and define additional regions for genetic polymorphisms associated with enhanced cancer risk.
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