The Inhibitory G Protein Gi Identified as Pertussis Toxin-Catalyzed ADP-Ribosylation
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- Katada Toshiaki
- Department of Physiological Chemistry, Graduate School of Pharmaceutical Sciences, The University of Tokyo
書誌事項
- タイトル別名
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- The Inhibitory G Protein G<sub>i</sub> Identified as Pertussis Toxin-Catalyzed ADP-Ribosylation
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Pertussis toxin (PTX) produced by Bordetella pertussis was first introduced by Ui and his colleagues in research on signal transduction under the name islet-activating protein in 1979, when the mechanism of toxin-induced stimulation of insulin release from pancreatic islets was reported in the rat. The stimulatory effect of PTX in vivo results from the blockage of α2-adrenergic receptor-mediated inhibition of insulin release. The receptor-induced inhibition of cAMP formation was also abolished in pancreatic islets isolated from PTX-treated rats, suggesting that the toxin caused uncoupling of adenylyl cyclase inhibition from receptor stimulation. The action of PTX on isolated membranes required a cytosolic factor, nicotinamide adenine dinucleotide (NAD), and the uncoupling induced by PTX was shown to be due to the toxin-catalyzed ADP-ribosylation of a 41-kDa protein with NAD as another substrate. The 41-kDa PTX substrate was soon identified and purified as the α-subunit of the inhibitory G protein that transmits an inhibitory signal from membrane receptors to adenylyl cyclase. After demonstration of the molecular mechanism of PTX, the toxin was widely utilized as a probe for identifying and analyzing major αβγ-trimeric G proteins. Thus, PTX-sensitive G proteins appeared to carry positive and negative signals from many membrane receptors to a variety of effectors other than adenylyl cyclase.
収録刊行物
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- Biological & Pharmaceutical Bulletin
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Biological & Pharmaceutical Bulletin 35 (12), 2103-2111, 2012
公益社団法人 日本薬学会
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詳細情報 詳細情報について
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- CRID
- 1390001204633734016
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- NII論文ID
- 130002480519
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- NII書誌ID
- AA10885497
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- COI
- 1:STN:280:DC%2BC3s7oslOlsQ%3D%3D
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- ISSN
- 13475215
- 09186158
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- NDL書誌ID
- 024105497
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- PubMed
- 23207763
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可