Results 171 to 180 of about 113,435 (208)
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Factor I-dependent inactivation of human complement C4b of the classical pathway by C3b/C4b receptor (CR1, CD35) and membrane cofactor protein (MCP, CD46).

Journal of biochemistry, 1992
Proteolytic inactivation of C4b is a crucial step for regulation of the classical complement pathway. A plasma protease factor I and membrane cofactors, C3b/C4b receptor (CR1) and membrane cofactor protein (MCP), participate in the regulation of cell-bound C4b although the physiological potency of these cofactors remains unknown.
T, Masaki   +4 more
openaire   +2 more sources

Limited Proteolysis of Complement Protein C3b by Regulatory Enzyme C3b Inactivator: Isolation and Characterization of a Biologically Active Fragment, C3d,g

The Journal of Biochemistry, 1985
Limited proteolysis of C3b by C3b inactivator (factor I) consists of a two-step reaction; rapid cleavage of C3b to yield a nicked C3b derivative, iC3b, and followed by slow cleavage of iC3b to yield two antigenically distinct fragments, C3c and C3d,g.
T, Seya, S, Nagasawa
openaire   +2 more sources

The fourth component of human complement treated with amines or chaotropes or frozen-thawed (C4b-like C4): interaction with C4 binding protein and cleavage by C3b/C4b inactivator.

The Journal of Immunology, 1982
Abstract We have shown previously that C4 treated with amines or chaotropes, although uncleaved, exhibits properties that are similar to C4b. Studies by other groups suggest that this C4b-like form of C4 is characterized by the lack of an internal thiolester bond that is present in native C4. We report here that C4 treated
I, von Zabern   +3 more
openaire   +2 more sources

Glycation inactivation of the complement regulatory protein CD59: a possible role in the pathogenesis of the vascular complications of human diabetes.

Diabetes, 2004
Micro- and macrovascular diseases are major causes of morbidity and mortality in the diabetic population, but the cellular and molecular mechanisms that link hyperglycemia to these complications remain incompletely understood. We proposed that in human diabetes, inhibition by glycation of the complement regulatory protein CD59 increases deposition of ...
Xuebin, Qin   +7 more
openaire   +1 more source

The IgA‐Binding Lectin Jacalin Induces Complement Activation by Inhibition of ‐Inactivator Function

Scandinavian Journal of Immunology, 1987
P. Hiemstra   +4 more
semanticscholar   +1 more source

Acute-phase reactant proteins and complement components and inhibitors in patients with ovarian cancer.

Gynecologic Oncology, 1981
B. Lukomska   +3 more
semanticscholar   +1 more source

CD46: expanding beyond complement regulation.

Trends in immunology, 2004
Rebecca C. Riley-Vargas   +4 more
semanticscholar   +1 more source

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