Cytochrome C in Apoptosis, Immune Response and Cancer

Mon, 01/27/2014 - 12:22

Cytochrome C is an electron carrier protein that localizes in mitochondrion intermembrane space and has been identified as one of the key signaling molecules of apoptosis or programmed cell death. Suppression of the anti-apoptotic members or activation of the pro-apoptotic members of the Bcl2 family leads to altered mitochondrial membrane permeability resulting in release of cytochrome c into the cytosol. Binding of cytochrome C to Apaf1 triggers the activation of Caspase 9, which then accelerates apoptosis by activating other caspases.

This protein has been involved in the following super pathways: TWEAK Pathway; Respiratory electron transport, ATP synthesis by chemiosmotic coupling, and heat production by uncoupling proteins; Apoptosis and survival Caspase cascade; Apoptosis and survival Lymphotoxin-beta receptor signaling; and Development Dopamine D2 receptor transactivation of EGFR pathways. Cytochrome C has been associated with over 150 diseases and disorders including    thrombocytopenia 4, acute T cell leukemia, bladder transitional cell papilloma, amelanotic melanoma, tyrosinemia, mitochondrial encephalomyopathy, Antley-Bixler syndrome, optic atrophy, macroglobulinemia, hyperthyroidism, breast adenocarcinoma, and brain ischemia.

A study using Novus cytochrome C antibody (NB100-56503) showed that a monoclonal antibody specific for a cytochrome C T cell stimulatory peptide inhibits T cell responses and affects the way the peptide associates with antigen-presenting cells. It does so by blocking the formation of peptide-MHC class II molecule complexes at the cell surface and by interfering with uptake of the peptide into endosomes (1).

Western Blot: Cytochrome C Antibody (7H8.2C12) [NB100-56503] Western Blot: Cytochrome C Antibody (7H8.2C12) [NB100-56503]

Another study using the same antibody revealed that cytochrome C-related Caspase 3 activation determines treatment response and relapse in childhood precursor B-cell acute lymphoblastic leukemia. Deficient activation of apoptosis signaling pathways may be responsible for treatment failure in acute leukemia. By combining both parameters, caspase-3 activation and cytochrome c release, they identified a novel indicator, cytochrome C-related activation of caspase-3 (CRAC), which may serve as a functionally defined risk factor for treatment stratification (2).

(1)   PMID: 1846813

(2)   PMID: 16467206

Novus Biologicals offers the following Cytochrome C reagents for your research needs:

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