Recombinant Mouse Complement factor I (Cfi)

Function

Trypsin-like serine protease that plays an essential role in regulating the immune response by controlling all complement pathways. Inhibits these pathways by cleaving three peptide bonds in the alpha-chain of C3b and two bonds in the alpha-chain of C4b thereby inactivating these proteins. Essential cofactors for these reactions include factor H and C4BP in the fluid phase and membrane cofactor protein/CD46 and CR1 on cell surfaces. The presence of these cofactors on healthy cells allows degradation of deposited C3b by CFI in order to prevent undesired complement activation, while in apoptotic cells or microbes, the absence of such cofactors leads to C3b-mediated complement activation and subsequent opsonization

Subcellular Location

Secreted, extracellular space

Tissue Specificity

Expressed in the liver by hepatocytes. Also present in other cells such as monocytes, fibroblasts or keratinocytes

Subunit

Heterodimer of a light and heavy chains; disulfide-linked. The fully processed and mature protein circulates as a zymogen, and is allosterically activated by substrate-induced remodeling of the active site. Interacts with C3b. Interacts with complement factor H

• Minta J.O. et al. cDNA cloning, sequencing and chromosomal assignment of the gene for mouse complement factor I (C3b/C4b inactivator): identification of a species specific divergent segment in factor I. — Mol. Immunol. (1996)
• The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC). — Genome Res. (2004)
• Yun Y.-S. et al. Cloning and characterization of the non-catalytic heavy chain of mouse complement factor I gene: structure comparison with the human homologue. — Biochem. Mol. Biol. Int. (1999)
• Ghesquiere B. et al. Proteome-wide characterization of N-glycosylation events by diagonal chromatography. — J. Proteome Res. (2006)
• Bernhard O.K. et al. Enhanced analysis of the mouse plasma proteome using cysteine-containing tryptic glycopeptides. — J. Proteome Res. (2007)
• Rose K.L. et al. Factor I is required for the development of membranoproliferative glomerulonephritis in factor H-deficient mice. — J. Clin. Invest. (2008)
• Huttlin E.L. et al. A tissue-specific atlas of mouse protein phosphorylation and expression. — Cell (2010)