نتایج جستجو برای: c4 complement

تعداد نتایج: 80191  

Journal: :Infection and immunity 1982
F Clas M Loos

Killing of Salmonella minnesota and Salmonella typhimurium S and R strains in serum of nonimmune humans and guinea pigs was drastically reduced in the selective absence of C1q, C1r, Ca2+, C4, or C2, the components of the classical complement pathway. Binding of C1 and C1q to the S form and six different core-deficient R mutant strains became stronger the shorter the lipopolysaccharide molecule....

2014
Lakshmi Carmel Wijeyewickrema Renee Charlene Duncan Robert Neil Pike

The C1s protease of the classical complement pathway propagates the initial activation of this pathway of the system by cleaving and thereby activating the C4 and C2 complement components. This facilitates the formation of the classical pathway C3 convertase (C4bC2a). C1s has a Lys residue located at position 628 (192 in chymotrypsin numbering) of the SP domain that has the potential to partial...

Journal: :Cancer research 1975
M Segerling S H Ohanian T Borsos

Metabolic inhibitors commonly used in the treatment of cancer increase the ability of antibody and complement to kill guinea pig tumor cells in vitro. No correlation was found between increased killing and changes in cell surface antigen concentration or binding of complement components C4 and C3.

Journal: :The Journal of Experimental Medicine 1996
M R Weiser J P Williams F D Moore L Kobzik M Ma H B Hechtman M C Carroll

Reperfusion of ischemic tissue induces an acute inflammatory response that can result in necrosis and irreversible cell injury to both local vascular endothelium and parenchyma. To examine the pathogenesis of ischemia/reperfusion injury, we have used mice deficient in complement components C3, C4, or serum immunoglobulin in a hindlimb model of ischemia. We found that mice homozygous deficient i...

2003
C. Carrol

Reperfusion ofischemic tissue induces an acute inflammatory response that can result in necrosis and irreversible cell injury to both local vascular endothelium and parenchyma. To examine the pathogenesis of ischemia/reperfusion injury, we have used mice deficient in complement components C3, C4, or serum immunoglobulin in a hindlimb model of ischemia. We found that mice homozygous deficient in...

2016
Jill Buyon Richard Furie Chaim Putterman Rosalind Ramsey-Goldman Kenneth Kalunian Derren Barken John Conklin Thierry Dervieux

BACKGROUND The relationship between cell-bound complement activation products (CB-CAPs: EC4d, EC3d), anti-C1q, soluble complement C3/C4 and disease activity in systemic lupus erythematosus (SLE) was evaluated. METHODS Per protocol, at baseline all SLE subjects enrolled in this longitudinal study presented with active disease and elevated CB-CAPs. At each monthly visit, the non-serological (ns...

Journal: :The Biochemical journal 2005
Kwok-Min Hui George L Orriss Tilman Schirmer Bergljót Magnadóttir Jürg A Schifferli Jameel M Inal

CRIT (complement C2 receptor inhibitor trispanning) is a newly described transmembrane molecule that is capable of binding C2 via its first extracellular domain (ed1). CRIT competes with C4b for the binding of C2. Previous experiments have suggested that a major binding site for C2 is located on short, almost identical peptide sequences of CRIT-ed1 and the beta-chain of C4. The C2 domains invol...

Journal: :Molecular immunology 2008
Amelia Clark Alexander Weymann Eric Hartman Yumirle Turmelle Michael Carroll Joshua M Thurman V Michael Holers Dennis E Hourcade David A Rudnick

UNLABELLED Complement signaling has been implicated as important for normal hepatic regeneration. However, the specific mechanism by which complement is activated during liver regeneration remains undefined. To address this question, we investigated the hepatic regenerative response to partial hepatectomy in wildtype mice, C3-, C4-, and factor B-null mice, and C4-null mice treated with a factor...

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