Complement Component C1Q: C1QB

Complement Component C1Q: C1QB Background

Complement proteins circulate in the blood and are also synthesized locally by fibroblasts, tissue macrophages, and other cells that participate in inflammatory responses. The complement system is a fundamental effector in the natural immunity that appears to have phylogenetitally preceded antigen-specific or acquired immune responses. More than 25 proteins compose the complement system; many are activated proteolytically from inert precursors as a cascade. Complement activation may bemediated by antigen-antibody complexes (classical pathway) or by other macromolecules (classical and/or alternate pathway).

Activated complement components have multiple roles in anaphylactic responses that include enhancement of phagocytosis(opsonization); chemotaxis to guide the migration of inflammatory cells (e.g., neutrophils and mononuclear phagocytes); and cytotoxic effects on target cells by the C5b-9 membrane attack complex (MAC), a heteromeric complex with cytolytic activity. Endogenous inhibitors may block complement activation or deactivate complement components at several steps along the pathway. Cellular responses to complement activation are mediated by various receptors, e.g., CR3, of which the β-subunit is also an integrin-type receptor subunit.

Complement C1q is composed of 18 polypeptide chains: six A-chains, six B-chains, and six C-chains. Southern blot analysis of chromosomal DNA from vertebrate species demonstrated highest similarity between the complement C1qB genes, followed by C1qC and finally C1qA. Sequence comparison of complement C1q from three different species have shown that the B chains have the strongest similarity.

Complement Component C1Q: C1QB Reference

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2. Johnson SA, et al. (1994) Expression of complement C1qB and C4 mRNAs during rat brain development. Brain Res Dev Brain Res. 80(1-2): 163-74.
3. Grewal RP, et al. (1999) C1qB and clusterin mRNA increase in association with neurodegeneration in sporadic amyotrophic lateral sclerosis. Neuroscience letters. 271(1): 65-7.
4. Spielman L, et al. (2002) Induction of the complement component C1qB in brain of transgenic mice with neuronal overexpression of human cyclooxygenase-2. Acta neuropathologica. 103(2): 157-62.