Thrombin : physiology and disease
著者
書誌事項
Thrombin : physiology and disease
Springer, c2009
- : hbk
大学図書館所蔵 全1件
  青森
  岩手
  宮城
  秋田
  山形
  福島
  茨城
  栃木
  群馬
  埼玉
  千葉
  東京
  神奈川
  新潟
  富山
  石川
  福井
  山梨
  長野
  岐阜
  静岡
  愛知
  三重
  滋賀
  京都
  大阪
  兵庫
  奈良
  和歌山
  鳥取
  島根
  岡山
  広島
  山口
  徳島
  香川
  愛媛
  高知
  福岡
  佐賀
  長崎
  熊本
  大分
  宮崎
  鹿児島
  沖縄
  韓国
  中国
  タイ
  イギリス
  ドイツ
  スイス
  フランス
  ベルギー
  オランダ
  スウェーデン
  ノルウェー
  アメリカ
注記
Includes bibliographical references and index
内容説明・目次
内容説明
In addition to its central role in blood coagulation, it has become increasingly apparent that thrombin and thrombin receptors are involved in many other physiological processes and can contribute to a variety of disease states such as tumor progression and metastasis, inflammation, neurological disorders and cardiovascular complications. This book is a collection of reviews of up-to-date information on the above topics by leaders in these fields.
This book will be of value to researchers and academic professionals both in basic and clinical science who are interested in the fields of biochemistry, biophysics, cell biology, pharmacology, cancer, inflammation, angiogenesis, cardiovascular system and neuronal system. These areas of research are prime target areas for drug development by many pharmaceutical and biotechnology companies.
目次
Table of contents 1. Thrombin: structure, functions and regulation 1.1. Introduction 1.2. Thrombin and Na+ 1.3. Thrombin structure 1.4. Kinetics of Na+ activation 1.5. Structures of E*, E and E:Na+ 1.6. Thrombin interaction with protein C 1.7. Thrombin interaction with the PARs 1.8. Dissociating procoagulant and anticoagulant activities 1.9. WE: a prototypic anticoagulant/antithrombotic thrombin 1.10. References 2. Thrombin: to PAR or not to PAR, and the regulation of inflammation 2.1. Introduction 2.2. Thrombin and the search for its receptor 2.3. Enzymes other than thrombin that are potential physiological regulators of PARs 2.3.1. Enzymes of the coagulation pathway 2.3.2. Proteinases of the gastrointestinal tract 2.3.3. PAR-regulating proteinases in the central nervous system 2.3.4. Immune cell-derived proteinases and PARs 2.3.5. Tumor-derived proteinases and a possible physiological role for kallikrein-related peptidases (KLKs) as PAR regulators 2.3.6. Pathogen-derived proteinases and PAR activation 2.4. Receptor dynamics and cell signaling: enzyme versus peptide-mediated activation 2.4.1. PAR-mediated signaling 2.4.2. PAR activation by enzyme versus peptide 2.5. PAR activation and the inflammation actions of thrombin 2.6. Non-PAR mechanisms of cell regulation mediated by thrombin and other proteinases 2.6.1. Signaling targets that are not 'classical' receptors 2.6.2. Non-catalytic mechanisms for proteinase-mediated signaling 2.6.3. Thrombin-mediated generation of agonists from fibrin and other substrates 2.7. Therapeutic implications of thrombin action via PAR and non-PAR mechanisms 2.7.1. Targeting thrombin and other serine proteinases 2.7.2. Targeting the PARs 2.8. Summary 2.9. Acknowledgements 2.10. References 3. Regulation of thrombin receptor signaling 3.1. Introduction 3.2. Cell type specific expression of thrombin receptors 3.3. Thrombin receptor activation and signaling 3.3.1. Proteolytic mechanism of thrombin receptor activation 3.3.2. Thrombin receptor signaling to heterotrimeric G-proteins 3.3.3. Cell type specific thrombin receptor signaling 3.4. Regulation of thrombin receptor signaling 3.4.1. Thrombin receptor desensitization 3.4.2. Thrombin receptor internalization 3.4.3. Thrombin receptor down-regulation 3.5. PAR activation and signaling by other proteases 3.6. Conclusions 3.7. Acknowledgements 3.8. References 4. Thrombin-activated protein C: integrated to regulate vascular physiology 4.1. The protein C pathway is localized to the endothelial cell surface and limits thrombin generation through negative feedback 4.2. APC has protective effects in systemic inflammation that are independent of its anticoagulant function 4.3. The thrombin receptor PAR1 mediates APC signaling in tissues culture 4.4. APC and thrombin can mediate opposite cellular responses in endothelial cells through PAR1 activation 4.4.1. Barrier integrity 4.4.2. Adhesion molecule expression 4.4.3. Apoptosis 4.5. Role of the sphingosine-1 phosphate pathway in mediating protective signaling by PAR1. 4.6. Protective PAR1 signaling by APC is mechanistically coupled to PC activation by thrombin 4.7. Not PAR1- or EPCR-dependent mechanisms for signaling by the PC pathway? 4.8. Thrombin-PAR1 and APC-PAR1 signaling in in vivo models of inflammation 4.9. How can activation of the thrombin receptor PAR1 by the PC pathway be of physi
「Nielsen BookData」 より