pathway Info Card

Complement-dependent Cytotoxicity

Information about Complement-dependent Cytotoxicity: characteristics, related genes and pathways, plus antibodies you can use for research. This page is being enriched constantly, if you see some information you would like this page to include please send your suggestions to us.

Overview of Complement-dependent Cytotoxicity

Most recent studies have shown that Complement-dependent Cytotoxicity shares some biological mechanisms with antibody-dependent-cellular-cytotoxicity, cell-adhesion, cell-cycle, cell-death, cell-growth, cell-killing, cell-proliferation, complement-activation, cytolysis, drug-resistance, glycosylation, humoral-immune-response, hypersensitivity, immune-response, induction-of-apoptosis, localization, pathogenesis, phagocytosis, secretion, sensitization.

Among the many pathways, these few ones have gauged particular interests from scientists studying Complement-dependent Cytotoxicity, and have been seen in publications frequently: antibody-dependent-cellular-cytotoxicity, cell-adhesion, cell-cycle, cell-death, cell-growth, cell-killing, cell-proliferation, complement-activation, cytolysis, drug-resistance, glycosylation, humoral-immune-response, hypersensitivity, immune-response, induction-of-apoptosis, localization, pathogenesis, phagocytosis, secretion, sensitization

Quite a number of genes have been found to play important roles in Complement-dependent Cytotoxicity, such as C3, CD46, CD55, CD59, CTLA4, EGFR, ERBB2, FCGR3A, HLA-A, HLA-B, HLA-DQA1, HLA-DRB4, IGHG3, IL2, KRT20, MS4A1, NOD2, S100A6, TNF. See what Boster has to offer for the research of these genes by clicking the gene name links below and view a more detailed info card/product listing for that gene.

In a later update, we will include information such as current drugs and therapy solutions as well as on-going and past clinical trials for this pathway. Plesae stay updated.