抗血栓薬の現状と新薬開発　　トロンビン活性化線溶阻害因子による線溶活性調節機構

• 浦野 哲盟

  浜松医科大学第2生理学教室

書誌事項

タイトル別名

• Research and Development of Novel Anti-thrombotic Agents. Regulatory mechanism of fibrinolysis system by thrombin activatable fibrinolysis inhibitor (TAFI).
• トロンビン カッセイカセンハマ ソガイ インシ ニ ヨル セン ヨウ カッセイ チョウセツ キコウ
• 抗血栓薬の現状と新薬開発

抄録

Thrombin-activatable fibrinolysis inhibitor (TAFI) is a 60-kDa plasma protein that has been shown to be identical to plasma carboxypeptidase B (CPB) and carboxypeptidase U (CPU). TAFI is activated by thrombomodulin (TM)-bound thrombin and specifically removes the C-terminal Lys and Arg by its CPB activity. One of its target substrates is the C-terminal Lys residue in the α-chain of plasmin-digested fibrin, which is critical for plasminogen binding to fibrin. Thus, its removal seems to be the main mechanism through which TAFI inhibits fibrinolysis. In this article, relevance of C-terminal Lys of plasmin-digested fibrin in fibrinolysis is described, and then possible roles of TAFI and TM-bound thrombin in a cross-talk between coagulation and fibrinolysis are discussed.

収録刊行物

• 日本薬理学雑誌

  日本薬理学雑誌 116 (5), 298-303, 2000

  公益社団法人 日本薬理学会

キーワード

• TAFI
• plasma carboxypeptidase B
• リジン結合部位
• トロンボモジュリン
• 線溶

詳細情報

• CRID: 1390282679249717120
• NII論文ID: 10008181289
• NII論文ID: 10010931198
• NII書誌ID: AN00198335
• DOI: 10.1254/fpj.116.298
• COI: 1:CAS:528:DC%2BD3cXotFSrsrk%3D
• ISSN: 13478397
• ISSN: 00155691
• NDL書誌ID: 5539881
• PubMed: 11215380
• Web Site: https://ndlsearch.ndl.go.jp/books/R000000004-I5539881
• Web Site: https://search.jamas.or.jp/link/ui/2001095932
• 本文言語コード: ja
• データソース種別:
  • JaLC
  • NDL
  • Crossref
  • PubMed
  • CiNii Articles
• 抄録ライセンスフラグ: 使用不可