ArticleThe Biochemical journal2005
Genomic organization of human arylamine N-acetyltransferase Type I reveals alternative promoters that generate different 5'-UTR splice variants with altered translational activities.
Article in The Biochemical journal, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Population variability of rhesus macaque (Macaca mulatta) NAT1 gene for arylamine N-acetyltransferase 1: Functional effects and comparison with human.Scientific reports · 2019Article
- Functional expression of human arylamine N-acetyltransferase NAT1*10 and NAT1*11 alleles: a mini review.Pharmacogenetics and genomics · 2018Review
- PharmGKB summary: very important pharmacogene information for N-acetyltransferase 2.Pharmacogenetics and genomics · 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
- mRNA transcript diversity creates new opportunities for pharmacological intervention.Molecular pharmacology · 2012Review
- 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
- Identification of a novel, tissue-specific ABCG2 promoter expressed in pediatric acute megakaryoblastic leukemia.Leukemia research · 2011Article
- Eukaryotic initiation factor 2B epsilon induces cap-dependent translation and skeletal muscle hypertrophy.The Journal of physiology · 2011Article
- 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
- Identification of N-acetyltransferase 2 (NAT2) transcription start sites and quantitation of NAT2-specific mRNA in human tissues.Drug metabolism and disposition: the biological fate of chemicals · 2007Article
- Loss of function polymorphisms in NAT1 protect against spina bifida.Human genetics · 2006Article
- Functional properties of an alternative, tissue-specific promoter for human arylamine N-acetyltransferase 1.Pharmacogenetics and genomics · 2006Article
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5 authors.
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No grant is acknowledged in the PubMed record.
Abstract
In humans, a polymorphic gene encodes the drug-metabolizing enzyme NAT1 (arylamine N-acetyltransferase Type 1), which is widely expressed throughout the body. While the protein-coding region of NAT1 is contained within a single exon, examination of the human EST (expressed sequence tag) database at the NCBI revealed the presence of nine separate exons, eight of which were located in the 5' non-coding region of NAT1. Differential splicing produced at least eight unique mRNA isoforms that could be grouped according to the location of the first exon, which suggested that NAT1 expression occurs from three alternative promoters. Using RT (reverse transcriptase)-PCR, we identified one major transcript in various epithelial cells derived from different tissues. In contrast, multiple transcripts were observed in blood-derived cell lines (CEM, THP-1 and Jurkat), with a novel variant, not identified in the EST database, found in CEM cells only. The major splice variant increased gene expression 9-11-fold in a luciferase reporter assay, while the other isoforms were similar or slightly greater than the control. We examined the upstream region of the most active splice variant in a promoter-reporter assay, and isolated a 257 bp sequence that produced maximal promoter activity. This sequence lacked a TATA box, but contained a consensus Sp1 site and a CAAT box, as well as several other putative transcription-factor-binding sites. Cell-specific expression of the different NAT1 transcripts may contribute to the variation in NAT1 activity in vivo.
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