| Project/Area Number |
06670517
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Gastroenterology
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| Research Institution | University of Tsukuba |
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Principal Investigator |
NOMURA Fumio Univ.of Tsukuba, Inst of Clinical Medicine, associate prof, 臨床医学系, 助教授 (80164739)
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| Co-Investigator(Kenkyū-buntansha) |
NAKAI Toshiaki Univ.of Tsukuba, Inst of Clinical Medicine, Professor, 臨床医学系, 教授 (30049192)
NODA Masatoshi Chiba Univ., School of Med Professor, 医学部, 教授 (60164703)
ISOBE Kazumasa Univ.of Tsukuba, Inst of Clinical Medicine, associate prof, 臨床医学系, 講師 (10151440)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1995: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1994: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | GTP-binding protein / ADP-ribosylation / alcohol / ADPリボシル化反応 / GTP結合タン白 |
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| Research Abstract |
Mono-ADP ribosylation, in which the ADP-ribosyl moiety is transferred from NAD to acceptor proteins is one of the important post-translational modifications of cellular proteins. Because mounting evidence suggests significant biological roles of this reaction in transmembrane signal transduction and other cell metabolism, we assessed how long-term alcohol intake alters toxin catalyzed-and endogenous mono-ADP ribosylation in the liver in a rat model. We first found that thiol-preactivated cholera toxin-catalyzed ADP ribosylation of the alpha-subunit of the stimulatory GTP-binding protein was enhanced after long-term alcohol intake. Enexpectedly, but interestingly, this enhancement was not accompanied by a comcomitant increase of cholera toxin catalyzed stimulation of the adenylate cyclase activity. We also found that long-term alcohol intake remarkably enhanced endogenous mono-ADP ribosylation of a 58kDa protein in plasma membrnaes. Thus, long-term alcohol intake stimulated endogenous as well as toxincatalyzed mono-ADP ribosylations. Charcterization of the 58kDa protein will uncover pathophysiological roles of this interesting reaction in alcohol-induced liver damage.
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