1989
DOI: 10.1016/0163-7258(89)90036-3
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N-acetyltransferase

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Cited by 240 publications
(20 citation statements)
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“…Detections were separately duplicated for quality control of genotyping. In brief, the three mutations 481C to T, 590 G to A and 857 G to A were detected by a PCR-RFLP (restriction fragment length polymorphism) method as described previously [17]. After PCR amplification using specific primers, the PCR products were digested with the restriction enzymes Kpn I, Taq I, and Bam HI to determine the nucleotide substitution at 481, 590, and 857, respectively.…”
Section: Methodsmentioning
confidence: 99%
“…Detections were separately duplicated for quality control of genotyping. In brief, the three mutations 481C to T, 590 G to A and 857 G to A were detected by a PCR-RFLP (restriction fragment length polymorphism) method as described previously [17]. After PCR amplification using specific primers, the PCR products were digested with the restriction enzymes Kpn I, Taq I, and Bam HI to determine the nucleotide substitution at 481, 590, and 857, respectively.…”
Section: Methodsmentioning
confidence: 99%
“…These include activation of a lupus diathesis (Alarcon-Segovia et al 1967) or a latent viral infection (Lerner et al 1974); immune response to drug (metabolite) or to drugaltered nucleoprotein-conjugate (Allison 1971;Cornacchia et al 1988;Rubin 1988;Weigle 1973;Wheeler et al 1991;Yamauchi et al 1975); loss of tolerance following drug-protein conjugation (hapten-carrier complex) via bioactivation Park & Kitteringham 1990;Roberts et al 1989;Uetrecht et al 1984;Wheeler et al 1991); drugs acting as polyclonal activators or adjuvants in vivo Ochi et al 1983;Rubin 1988;Yu & Ziff 1985); effects on macrophage antigen recognition and processing; pharmacokinetic -a direct role of acetylation phenotype (Foad et al 1977;Freemen et al 1979;Price-Evans 1989;Price-Evans et al 1960;Reidenberg et al 1975;Weber & Hein 1985); and immunogenetic -a unique class II antigen encoded by the major histocompatibility complex which would control response to complement or account for the restricted antibody responses seen in DRL (Batchelor et al 1980;Fielder et al 1983;Fronek et al 1991;Hess 1988;Mitchell et al 1987Mitchell et al , 1990Schur et al 1990;Sim & Gill 1984;Totoritis et al 1988;Welch et al 1988). Frequently, studies of this nature in humans have attempted to focus on the expression of autoimmunity as an end result of exposure to punitive environmental chemicals or drugs without an appreciation or knowledge of other predisposing factors · such as age, sex, preexistent pathology, abnormal renal or liver metabolism and genetic polymorphism of the patient population.…”
Section: Mechanism(s) Of Induction Of Drlmentioning
confidence: 99%
“…Proteins that catalyze the transacetylation of acetyl coenzyme A (Acetyl-CoA) to arylamines and arylalkylamines are commonly referred to as arylamine N -acetyltransferases and arylalkylamine N -acetyltransferases (aaNAT), respectively (Evans, 1989). In mammals, aaNAT is primarily involved in the synthesis of N -acetylserotonin.…”
Section: Introductionmentioning
confidence: 99%