Human blood platelet gC1qR/p33

Platelets are involved in the development of many types of vascular lesions. In addition to their role in primary hemostasis, they participate in inflammatory processes that may contribute to the development of thrombosis, atherosclerosis and vasculitis. In this regard, we have been interested in pl...

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Bibliographic Details
Published in:Immunological reviews 2001-04, Vol.180 (1), p.56-64
Main Authors: Peerschke, Ellinor I. B., Ghebrehiwet, Berhane
Format: Article
Language:English
Subjects:
Bacterial Adhesion
Biotinylation
Blood Coagulation Factors - metabolism
Blood Platelets - immunology
Carrier Proteins
Complement C1q - metabolism
complement component C1
complement component C1q
Humans
Hyaluronan Receptors
Kinins - metabolism
Ligands
Membrane Glycoproteins
Mitochondrial Proteins
Platelet Aggregation
Protein Binding
Receptors, Complement - blood
Receptors, Complement - chemistry
Receptors, Complement - physiology
Recombinant Fusion Proteins - metabolism
Staphylococcal Infections - immunology
Staphylococcal Protein A - metabolism
Staphylococcus aureus - immunology
Staphylococcus aureus - pathogenicity
Staphylococcus aureus - physiology
Virulence
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Summary:Platelets are involved in the development of many types of vascular lesions. In addition to their role in primary hemostasis, they participate in inflammatory processes that may contribute to the development of thrombosis, atherosclerosis and vasculitis. In this regard, we have been interested in platelet interactions with the complement subcomponent C1q. C1q has been shown to modulate platelet interactions with collagen and immune complexes, and has been identified at sites of vascular injury and inflammation, as well as in atherosclerotic lesions. Platelets express a variety of C1q binding sites, including gC1qR/p33 (gC1qR), a multifunctional, multicompartment cellular protein. 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. The authors are grateful to Wei‐Xing Guo M.D. for construction of the Exon 2 expression vector and GST‐E2 fusion protein expression, and to Yan Fang and Tara K. Murphy for technical assistance. This research was supported in part by grant HL50291 from the National Heart Lung and Blood Institute (EIBP, BG) and grant IM771 (BG) from the American Cancer Society.
ISSN:0105-2896
1600-065X
DOI:10.1034/j.1600-065X.2001.1800105.x