• Produktbild: Thrombin
  • Produktbild: Thrombin

Thrombin Physiology and Disease

Fr. 137.00

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Beschreibung

Produktdetails

Einband

Taschenbuch

Erscheinungsdatum

23.11.2010

Herausgeber

Michael E. Maragoudakis + weitere

Verlag

Springer Us

Seitenzahl

266

Maße (L/B/H)

23.5/15.5/1.6 cm

Gewicht

439 g

Auflage

Softcover reprint of hardcover 1st edition 2009

Sprache

Englisch

ISBN

978-1-4419-1877-2

Beschreibung

Produktdetails

Einband

Taschenbuch

Erscheinungsdatum

23.11.2010

Herausgeber

Verlag

Springer Us

Seitenzahl

266

Maße (L/B/H)

23.5/15.5/1.6 cm

Gewicht

439 g

Auflage

Softcover reprint of hardcover 1st edition 2009

Sprache

Englisch

ISBN

978-1-4419-1877-2

Herstelleradresse

Springer-Verlag KG
Sachsenplatz 4-6
1201 Wien
AT

Email: GPSR Kontakt

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  • Produktbild: Thrombin
  • Produktbild: Thrombin
  • 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