Timothy Myles

Summary

Affiliation: University of California
Country: USA

Publications

  1. ncbi Structural requirements for the activation of human factor VIII by thrombin
    Timothy Myles
    Division of Hematology, Stanford University School of Medicine, CA 94305 5156, USA
    Blood 100:2820-6. 2002
  2. pmc Thrombin hydrolysis of human osteopontin is dependent on thrombin anion-binding exosites
    Timothy Myles
    Division of Hematology, Stanford University School of Medicine, Stanford, CA 94305, USA
    J Biol Chem 283:17789-96. 2008
  3. pmc Thrombin-cleaved fragments of osteopontin are overexpressed in malignant glial tumors and provide a molecular niche with survival advantage
    Yasuto Yamaguchi
    Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, California 94305, USA
    J Biol Chem 288:3097-111. 2013
  4. ncbi Thrombin activation of factor XI on activated platelets requires the interaction of factor XI and platelet glycoprotein Ib alpha with thrombin anion-binding exosites I and II, respectively
    Thomas H Yun
    Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, California 94305, USA
    J Biol Chem 278:48112-9. 2003
  5. pmc Thrombin-activatable carboxypeptidase B cleavage of osteopontin regulates neutrophil survival and synoviocyte binding in rheumatoid arthritis
    Shadi A Sharif
    Stanford University School of Medicine, Stanford, California, CA 94305, USA
    Arthritis Rheum 60:2902-12. 2009
  6. ncbi Regulation of tissue inflammation by thrombin-activatable carboxypeptidase B (or TAFI)
    Lawrence L K Leung
    Department of Medicine, Division of Hematology, Stanford University School of Medicine and Veterans Administration Palo Alto Health Care System, Stanford, CA 94305, USA
    Adv Exp Med Biol 632:61-9. 2008
  7. pmc Regulation of chemerin bioactivity by plasma carboxypeptidase N, carboxypeptidase B (activated thrombin-activable fibrinolysis inhibitor), and platelets
    Xiao Yan Du
    Division of Hematology, Stanford University School of Medicine, Stanford, CA 94305, USA
    J Biol Chem 284:751-8. 2009
  8. doi Enhanced abdominal aortic aneurysm formation in thrombin-activatable procarboxypeptidase B-deficient mice
    Geoffrey Schultz
    Department of Vascular Surgery, Stanford University School of Medicine, Veterans Affairs Palo Alto Health Care System, 3801 Miranda Ave, Palo Alto, CA 94304, USA
    Arterioscler Thromb Vasc Biol 30:1363-70. 2010
  9. ncbi Thrombin activatable fibrinolysis inhibitor, a potential regulator of vascular inflammation
    Timothy Myles
    Division of Hematology, Department of Medicine, Stanford University School of Medicine, California 94305, USA
    J Biol Chem 278:51059-67. 2003
  10. ncbi Exosite-interactive regions in the A1 and A2 domains of factor VIII facilitate thrombin-catalyzed cleavage of heavy chain
    Keiji Nogami
    Department of Biochemistry, University of Rochester School of Medicine and Dentistry, Rochester, New York 14642, USA
    J Biol Chem 280:18476-87. 2005

Collaborators

Detail Information

Publications16

  1. ncbi Structural requirements for the activation of human factor VIII by thrombin
    Timothy Myles
    Division of Hematology, Stanford University School of Medicine, CA 94305 5156, USA
    Blood 100:2820-6. 2002
    ..Detailed mutagenic analysis of thrombin can assist in understanding the pathogenesis of bleeding disorders and may lead to the rational design of selective thrombin inhibitors...
  2. pmc Thrombin hydrolysis of human osteopontin is dependent on thrombin anion-binding exosites
    Timothy Myles
    Division of Hematology, Stanford University School of Medicine, Stanford, CA 94305, USA
    J Biol Chem 283:17789-96. 2008
    ..Thus, OPN is a bona fide substrate for thrombin, and generation of thrombin-cleaved OPN with enhanced pro-inflammatory properties provides another molecular link between coagulation and inflammation...
  3. pmc Thrombin-cleaved fragments of osteopontin are overexpressed in malignant glial tumors and provide a molecular niche with survival advantage
    Yasuto Yamaguchi
    Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, California 94305, USA
    J Biol Chem 288:3097-111. 2013
    ..OPN cleavage contributes to GBM development by allowing more cells to bind in niches where they acquire anti-apoptotic properties...
  4. ncbi Thrombin activation of factor XI on activated platelets requires the interaction of factor XI and platelet glycoprotein Ib alpha with thrombin anion-binding exosites I and II, respectively
    Thomas H Yun
    Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, California 94305, USA
    J Biol Chem 278:48112-9. 2003
    ..GPIb alpha plays a critical role in the co-localization of thrombin and FXI and the resultant efficient activation of FXI...
  5. pmc Thrombin-activatable carboxypeptidase B cleavage of osteopontin regulates neutrophil survival and synoviocyte binding in rheumatoid arthritis
    Shadi A Sharif
    Stanford University School of Medicine, Stanford, California, CA 94305, USA
    Arthritis Rheum 60:2902-12. 2009
    ..We undertook this study to investigate the roles of OPN-R and OPN-L in synoviocyte adhesion, which contributes to the formation of invasive pannus, and in neutrophil survival, which affects inflammatory infiltrates in RA...
  6. ncbi Regulation of tissue inflammation by thrombin-activatable carboxypeptidase B (or TAFI)
    Lawrence L K Leung
    Department of Medicine, Division of Hematology, Stanford University School of Medicine and Veterans Administration Palo Alto Health Care System, Stanford, CA 94305, USA
    Adv Exp Med Biol 632:61-9. 2008
    ..Along with the activation of protein C, the activation of proCPB by the endothelial thrombin-thrombomodulin complex represents a homeostatic feedback mechanism in regulating thrombin's pro-inflammatory functions in vivo...
  7. pmc Regulation of chemerin bioactivity by plasma carboxypeptidase N, carboxypeptidase B (activated thrombin-activable fibrinolysis inhibitor), and platelets
    Xiao Yan Du
    Division of Hematology, Stanford University School of Medicine, Stanford, CA 94305, USA
    J Biol Chem 284:751-8. 2009
    ....
  8. doi Enhanced abdominal aortic aneurysm formation in thrombin-activatable procarboxypeptidase B-deficient mice
    Geoffrey Schultz
    Department of Vascular Surgery, Stanford University School of Medicine, Veterans Affairs Palo Alto Health Care System, 3801 Miranda Ave, Palo Alto, CA 94304, USA
    Arterioscler Thromb Vasc Biol 30:1363-70. 2010
    ..To determine whether procarboxypeptidase B (pCPB)(-/-) mice are susceptible to accelerated abdominal aortic aneurysm (AAA) development secondary to unregulated OPN-mediated mural inflammation in the absence of CPB inhibition...
  9. ncbi Thrombin activatable fibrinolysis inhibitor, a potential regulator of vascular inflammation
    Timothy Myles
    Division of Hematology, Department of Medicine, Stanford University School of Medicine, California 94305, USA
    J Biol Chem 278:51059-67. 2003
    ..Our data suggest that TAFIa may have a broad anti-inflammatory role, and its function is not restricted to fibrinolysis...
  10. ncbi Exosite-interactive regions in the A1 and A2 domains of factor VIII facilitate thrombin-catalyzed cleavage of heavy chain
    Keiji Nogami
    Department of Biochemistry, University of Rochester School of Medicine and Dentistry, Rochester, New York 14642, USA
    J Biol Chem 280:18476-87. 2005
    ..These data suggest the acidic region comprising residues 389-394 in factor VIII A2 domain interacts with thrombin via its heparin-binding exosite and facilitates cleavage at Arg(740) during procofactor activation...
  11. ncbi Molecular mapping of the thrombin-heparin cofactor II complex
    Yolanda M Fortenberry
    Department of Pathology, Carolina Cardiovascular Biology Center, University of North Carolina at Chapel Hill, School of Medicine, Chapel Hill, North Carolina 27599 7035, USA
    J Biol Chem 279:43237-44. 2004
    ....
  12. ncbi Crystal structure of anticoagulant thrombin variant E217K provides insights into thrombin allostery
    Wendy J Carter
    University of Cambridge, Department of Haematology, Division of Structural Medicine, Thrombosis Research Unit, Cambridge Institute for Medical Research, Wellcome Trust MRC Building, Hills Road, Cambridge CB2 2XY, United Kingdom
    J Biol Chem 279:26387-94. 2004
    ..We have concluded that the E217K mutation causes the allosteric inactivation of thrombin by destabilizing the Na(+) binding site and that the structure thus may represent the Na(+)-free, catalytically inert "slow" form...
  13. ncbi Glycoprotein Ibalpha-mediated platelet adhesion and aggregation to immobilized thrombin under conditions of flow
    Cees Weeterings
    Department of Haematology, University Medical Centre Utrecht, The Netherlands
    Arterioscler Thromb Vasc Biol 26:670-5. 2006
    ..Recently, it was shown that platelets are able to adhere to immobilized thrombin under static conditions via GPIbalpha...
  14. pmc Regulation of tissue inflammation by thrombin-activatable carboxypeptidase B (or TAFI)
    Lawrence L K Leung
    Department of Medicine, Stanford University School of Medicine and Veterans Administration Palo Alto Health Care System, Palo Alto, CA 94304, USA
    Mol Immunol 45:4080-3. 2008
    ..Along with the activation of protein C, the activation of proCPB by the endothelial thrombin-thrombomodulin complex represents a homeostatic feedback mechanism in regulating thrombin's pro-inflammatory functions in vivo...
  15. ncbi Roles of low specificity and cofactor interaction sites on thrombin during factor XIII activation. Competition for cofactor sites on thrombin determines its fate
    Helen Philippou
    Department of Haematology, Imperial College London, United Kingdom
    J Biol Chem 278:32020-6. 2003
    ..This enables enhanced factor XIII activation to be localized around the fibrin clot. We also conclude that proximity to and competition for cofactor interaction sites primarily directs the fate of thrombin...
  16. pmc Thrombin-activatable procarboxypeptidase B regulates activated complement C5a in vivo
    Toshihiko Nishimura
    Department of Medicine, Stanford University School of Medicine and Veterans Administration Palo Alto Health Care System, Palo Alto, CA 94304, USA
    Blood 109:1992-7. 2007
    ..Its activation, along with protein C, by the endothelial thrombin-TM complex represents a homeostatic response to counteract the inflammatory mediators generated at the site of vascular injury...