Sulfating-Activity and Stability of cDNA-Expressed Allozymes of Human Phenol Sulfotransferase, ST1A3*1 (213Arg) and ST1A3*2 (213His), Both of Which Exist in Japanese as Well as Caucasians.
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概要
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We recently found single amino acid substitutions (213Arg/His and 223Met/Val) in polymorphic human phenol-sulfating phenol sulfotransferase (SULT: cDNAs encoding ST1A3, P PST or HAST1/2) among Caucasians and African-Americans. In a Japanese population (n=143), allele frequencies of 213Arg and 213His were 83.2 and 16.8%, respectively, but the 223Val allele was not found. 213His homozygosity was reportedly associated with both very low (>7-fold) sulfating activities of p-nitrophenol (at 4μM) and low thermostability in platelets. Sulfating-activity determinations using recombinant 213Arg- and 213His-forms (ST1A3*1 and ST1A3*2, respectively) did not, however, reveal appreciable deficiency in [35S] 3'-phosphoadenosine 5'-phosphosulfate (PADS)-dependent sulfation of p-nitrophenol (4μM) by ST1A3*2 (7.5vs. 10.2 nmol/min/nmol SULT for ST1A3). Kinetic parameters for p-nitrophenol for p-nitrophenol sulfation supported the slight decrease in sulfating activities at 4μM (Km, 0.82xs. 1.75μM; Vmax, 13.2vs. 13.1 nmol/min/nmol SULT, respec-tively, for ST1A3*1 and *2). p-Nitrophenyl sulfate-dependent 2-naphthol sulfation by ST1A3*2 was 69% of that by ST1A3*1 (p<0.05). However, ST1A3*2 was remarkably unstable at 45 and 37°C as compared to ST1A3*1. The lower p-nitrophenol sulfating activity of ST1A3*2 may explain the lower platelet p-nitrophenol sulfation in ST1A3*2 homozygotes. Protein instability and ST1A3 gene regulation may be both involved in the polymorphism of p-nitrophenol sulfation in human tissues.
- 社団法人 日本生化学会の論文
著者
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SHIMIZU Makiko
Division of Pharmacology, National Institute of Health Sciences
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LANG Nicholas
Arkansas Cancer Research Center
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Ozawa Shogo
Division Of Pharmacology National Institute Of Health Sciences
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KADLUBAR Fred
National Center for Toxicological Research
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Miyajima Atsuko
Division Of Pharmacology Biological Safety Research Center National Institute Of Health Sciences
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Katoh Takahiko
Department Of Biochemistry School Of Medicine University Of Occupational And Environmental Health
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Fukuoka Masamichi
Department Of Clinical Pharmacology And Toxicology Showa Pharmaceutical University
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Ohno Yasuo
Division Of Internal Medicine And Thoracic Oncology National Cancer Center Hospital
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Matsumoto Yoshiaki
Department Of Clinical Pharmacokinetics College Of Pharmacy Nihon University
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Tang Yong-Ming
National Center fro Toxicological Research
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