E I Peerschke

Summary

Affiliation: Cornell University
Country: USA

Publications

  1. ncbi request reprint The soluble recombinant form of a binding protein/receptor for the globular domain of C1q (gC1qR) enhances blood coagulation
    E I Peerschke
    New York Hospital Cornell Medical College, New York 10021, USA
    Blood Coagul Fibrinolysis 9:29-37. 1998
  2. ncbi request reprint Expression of gC1q-R/p33 and its major ligands in human atherosclerotic lesions
    Ellinor I B Peerschke
    Department of Pathology, Weill Medical College of Cornell University, 525 East 68th Street, Room F715, New York, NY 10021, USA
    Mol Immunol 41:759-66. 2004
  3. ncbi request reprint Human blood platelet gC1qR/p33
    E I Peerschke
    Department of Pathology, Weill Medical College of Cornell University, New York, USA
    Immunol Rev 180:56-64. 2001
  4. ncbi request reprint Platelet activation by sustained exposure to low-dose plasmin
    A L Ervin
    Department of Pediatric Oncology, Memorial Sloan Kettering Cancer Center, New York, New York, USA
    Blood Coagul Fibrinolysis 12:415-25. 2001
  5. ncbi request reprint Anagrelide metabolite induces thrombocytopenia in mice by inhibiting megakaryocyte maturation without inducing platelet aggregation
    W J Lane
    Division of Hematology-Oncology, Weill Medical College of Cornell University, New York, NY 10021, USA
    Exp Hematol 29:1417-24. 2001
  6. ncbi request reprint Ex vivo evaluation of erythrocytosis-enhanced platelet thrombus formation using the cone and plate(let) analyzer: effect of platelet antagonists
    Ellinor I B Peerschke
    Department of Pathology, Weill Medical College of Cornell University, New York, NY, USA
    Br J Haematol 127:195-203. 2004
  7. ncbi request reprint Tissue factor pathway inhibitor-2 (TFPI-2) recognizes the complement and kininogen binding protein gC1qR/p33 (gC1qR): implications for vascular inflammation
    Ellinor I B Peerschke
    New York Presbyterian Hospital, Weill Cornell Center, 525 East 68th Street, Room F715, New York 10021, USA
    Thromb Haemost 92:811-9. 2004
  8. pmc gC1qR/p33 blockade reduces Staphylococcus aureus colonization of target tissues in an animal model of infective endocarditis
    Ellinor I B Peerschke
    Department of Pathology and Laboratory Medicine, Weill Medical College of Cornell University, New York, New York, USA
    Infect Immun 74:4418-23. 2006
  9. ncbi request reprint gC1qR/p33 serves as a molecular bridge between the complement and contact activation systems and is an important catalyst in inflammation
    Berhane Ghebrehiwet
    Department of Medicine, SUNY at Stony Brook, Stony Brook, NY 11794, USA
    Adv Exp Med Biol 586:95-105. 2006
  10. pmc The contribution of gC1qR/p33 in infection and inflammation
    Ellinor I B Peerschke
    Department of Pathology, Weill Medical College of Cornell University, New York Presbyterian Hospital, 525 East 68th Street, Room F715, NY 10021, USA
    Immunobiology 212:333-42. 2007

Collaborators

Detail Information

Publications22

  1. ncbi request reprint The soluble recombinant form of a binding protein/receptor for the globular domain of C1q (gC1qR) enhances blood coagulation
    E I Peerschke
    New York Hospital Cornell Medical College, New York 10021, USA
    Blood Coagul Fibrinolysis 9:29-37. 1998
    ..Although the mechanism of action of gC1qR on blood coagulation remains obscure, the data suggest a potential role for this protein in hemostatic and thrombotic events...
  2. ncbi request reprint Expression of gC1q-R/p33 and its major ligands in human atherosclerotic lesions
    Ellinor I B Peerschke
    Department of Pathology, Weill Medical College of Cornell University, 525 East 68th Street, Room F715, New York, NY 10021, USA
    Mol Immunol 41:759-66. 2004
    ....
  3. ncbi request reprint Human blood platelet gC1qR/p33
    E I Peerschke
    Department of Pathology, Weill Medical College of Cornell University, New York, USA
    Immunol Rev 180:56-64. 2001
    ..Here we focus on the structure and function of platelet gC1qR and its emerging role in modulating platelet function at sites of vascular injury and inflammation...
  4. ncbi request reprint Platelet activation by sustained exposure to low-dose plasmin
    A L Ervin
    Department of Pediatric Oncology, Memorial Sloan Kettering Cancer Center, New York, New York, USA
    Blood Coagul Fibrinolysis 12:415-25. 2001
    ..Taken together, these data suggest that sustained exposure of platelets to very low plasmin doses leads to platelet activation and thus may contribute to thrombotic complications in vivo...
  5. ncbi request reprint Anagrelide metabolite induces thrombocytopenia in mice by inhibiting megakaryocyte maturation without inducing platelet aggregation
    W J Lane
    Division of Hematology-Oncology, Weill Medical College of Cornell University, New York, NY 10021, USA
    Exp Hematol 29:1417-24. 2001
    ..CONCLUSIONS: We describe a cross-species reactive anagrelide metabolite that selectively inhibits MK maturation and migration, lowering platelet levels without influencing platelet aggregation...
  6. ncbi request reprint Ex vivo evaluation of erythrocytosis-enhanced platelet thrombus formation using the cone and plate(let) analyzer: effect of platelet antagonists
    Ellinor I B Peerschke
    Department of Pathology, Weill Medical College of Cornell University, New York, NY, USA
    Br J Haematol 127:195-203. 2004
    ..These findings support the use of CPA for ex vivo evaluation of the contribution of RBC to platelet function and its inhibition under physiological shear conditions...
  7. ncbi request reprint Tissue factor pathway inhibitor-2 (TFPI-2) recognizes the complement and kininogen binding protein gC1qR/p33 (gC1qR): implications for vascular inflammation
    Ellinor I B Peerschke
    New York Presbyterian Hospital, Weill Cornell Center, 525 East 68th Street, Room F715, New York 10021, USA
    Thromb Haemost 92:811-9. 2004
    ..Taken together, these data suggest that gC1qR may participate in tissue remodeling and inflammation by localizing TFPI-2 to the pericellular environment to modulate local protease activity and regulate HK activation...
  8. pmc gC1qR/p33 blockade reduces Staphylococcus aureus colonization of target tissues in an animal model of infective endocarditis
    Ellinor I B Peerschke
    Department of Pathology and Laboratory Medicine, Weill Medical College of Cornell University, New York, New York, USA
    Infect Immun 74:4418-23. 2006
    ..aureus binding to fibrinogen. Such impacts may include direct modulation of complement (MAb 60.11) and kinin cascades (MAb 74.5.2) and/or activation of immune and inflammatory responses via localized immune complex formation...
  9. ncbi request reprint gC1qR/p33 serves as a molecular bridge between the complement and contact activation systems and is an important catalyst in inflammation
    Berhane Ghebrehiwet
    Department of Medicine, SUNY at Stony Brook, Stony Brook, NY 11794, USA
    Adv Exp Med Biol 586:95-105. 2006
    ....
  10. pmc The contribution of gC1qR/p33 in infection and inflammation
    Ellinor I B Peerschke
    Department of Pathology, Weill Medical College of Cornell University, New York Presbyterian Hospital, 525 East 68th Street, Room F715, NY 10021, USA
    Immunobiology 212:333-42. 2007
    ....
  11. ncbi request reprint Proposed research training guidelines for residents in laboratory medicine
    Ellinor I B Peerschke
    Department of Pathology and Laboratory Medicine, Weill Medical College of Cornell University, New York, NY 10021, USA
    Clin Lab Med 27:241-53; abstract v-vi. 2007
    ..The proposed curricula are purposely unstructured to allow maximum flexibility for training programs to meet the needs and career goals of individual residents...
  12. ncbi request reprint cC1q-R (calreticulin) and gC1q-R/p33: ubiquitously expressed multi-ligand binding cellular proteins involved in inflammation and infection
    Berhane Ghebrehiwet
    Department of Medicine, State University of New York, Health Sciences Center, T 16040 State University of New York, Stony Brook, NY 11794 8161, USA
    Mol Immunol 41:173-83. 2004
    ....
  13. ncbi request reprint Receptor for the globular heads of C1q (gC1q-R, p33, hyaluronan-binding protein) is preferentially expressed by adenocarcinoma cells
    Daniel B Rubinstein
    Section of Hematology Oncology, Boston University School of Medicine, Boston, MA 02118, USA
    Int J Cancer 110:741-50. 2004
    ....
  14. ncbi request reprint Cooperation of C1q receptors and integrins in C1q-mediated endothelial cell adhesion and spreading
    Xiaodong Feng
    Department of Dermatology, State University of New York, Health Sciences Center T 16 040, Stony Brook, NY 11794, USA
    J Immunol 168:2441-8. 2002
    ..Taken together these results suggest that endothelial cell adhesion and spreading require the cooperation of both C1qRs and beta(1) integrins and possibly other membrane-spanning molecules...
  15. ncbi request reprint The laboratory evaluation of platelet dysfunction
    Ellinor I B Peerschke
    Department of Pathology, New York Presbyterian Hospital, Weill Medical College, Cornell University, 525 East 68th Street, Room F 715, New York, NY 10021, USA
    Clin Lab Med 22:405-20. 2002
    ..It remains to be seen whether such screening tests will better predict clinical bleeding or thrombotic risk...
  16. ncbi request reprint Zinc induces exposure of hydrophobic sites in the C-terminal domain of gC1q-R/p33
    Rajeev Kumar
    Department of Medicine, State University of New York, Stony Brook, NY 11794 8161, USA
    Mol Immunol 39:69-75. 2002
    ..Taken together, our data suggest that zinc can induce the exposure of hydrophobic sites in the C-terminal domain of gC1q-R involved in binding to HK/FXII...
  17. pmc Expression of complement components and inhibitors on platelet microparticles
    Wei Yin
    Department of Pathology and Laboratory Medicine, Weill Medical College of Cornell University, New York, NY, USA
    Platelets 19:225-33. 2008
    ..Complement activation contributes to a variety of vascular and inflammatory disease states including atherosclerosis and ischemia/reperfusion injury...
  18. ncbi request reprint gC1q-R/p33: structure-function predictions from the crystal structure
    Berhane Ghebrehiwet
    Department of Medicine, State University of New York, Stony Brook 11794 8161, USA
    Immunobiology 205:421-32. 2002
    ....
  19. ncbi request reprint Activation-dependent surface expression of gC1qR/p33 on human blood platelets
    Ellinor I B Peerschke
    Department of Pathology, Weill Medical College of Cornell University, New York, New York 10021, USA
    Thromb Haemost 89:331-9. 2003
    ..aureus protein A, supports the hypothesis that gC1qR expressed on activated platelets may contribute directly to thrombosis, inflammation, and endovascular infections...
  20. ncbi request reprint Complement component C1q induces endothelial cell adhesion and spreading through a docking/signaling partnership of C1q receptors and integrins
    Berhane Ghebrehiwet
    Department of Medicine, Health Sciences Center, Division of Rheumatology, State University of New York, Stony Brook, NY 11794, USA
    Int Immunopharmacol 3:299-310. 2003
    ..5.2 and HK...
  21. ncbi request reprint Protein S assays: an analysis of North American Specialized Coagulation Laboratory Association proficiency testing
    Elizabeth M Van Cott
    Division of Clinical Laboratories, Department of Pathology, Massachusetts General Hospital, Boston 02114, USA
    Am J Clin Pathol 123:778-85. 2005
    ..Many total protein S antigen assays do not add to the diagnosis and can be unreliable for protein S deficiency subtyping. Better standardization of functional and antigenic assays is needed...
  22. ncbi request reprint Rituximab in the treatment of acquired factor VIII inhibitors
    Adrian Wiestner
    Hematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA
    Blood 100:3426-8. 2002
    ..Responses continue off treatment from more than 7 to more than 12 months. This report adds to the growing evidence that rituximab has efficacy in immune disorders resulting from autoantibody formation...