InVivoMAb anti-human GC1q R (C1QBP)

About InVivoMAb anti-human GC1q R (C1QBP)

The 60.11 monoclonal antibody reacts with the mature form of gClq R from human, mouse, and rat species. This antibody detects the monomeric and dimeric forms of gClq R, but it does not bind gClq-R’s truncated form which lacks residues 74-95. gClq R, also called p32 or HABP1, has been identified as the major cellular binding site for complement component 1q (C1q). gClq R has a molecular weight of 33 kDa, and is a highly anionic protein that shows ubiquitous expression with predominant localization to the mitochondrial matrix of cells. gClq R has also been shown to localize to the cell surface as well as some cellular organelles, such as the endoplasmic reticulum and nucleus. The expression of gClq-R has been reported to be upregulated in epithelial cancers (e.g., mammary cancer, colorectal cancer, and pulmonary cancers). In tumors, the gC1q R protein has been shown to be released into the tumor microenvironment, where it regulates cancer cell proliferation and metastasis through activation of the complement and the kinin-kallikrein system (KKS) signaling pathways. In vitro studies have shown an induction in the expression of gClq R in normal cells (e.g., blood platelets, endothelial cells) responding to reparative and inflammatory stimuli. In vitro pretreatment with the 60.11 antibody has been shown to inhibit the complement component C1q-induced adhesion and spreading of endothelial cells. In vivo blockade of gC1q R with the 60.11 antibody has been shown to reduce Staphylococcus aureus colonization of target tissues in a rat model of infective endocarditis. In experiments involving a mouse model of orthotropic triple-negative breast cancer xenograft, in vivo blockade of gC1q R with a 60.11 antibody is shown to decrease the growth of the tumors. Like PD-1 and PD-L1 signaling, studies involving the interaction between cancer cells expressed C1q and cytotoxic T cells positive for gC1qR have suggested the C1q and gC1qR axis as a checkpoint inhibitor in cancer immunotherapy.