Background: Electron carrier protein. The oxidized form of the cytochrome c heme group can accept an electron from the heme group of the cytochrome c1 subunit of cytochrome reductase. Cytochrome c then transfers this electron to the cytochrome oxidase complex, the final protein carrier in the mitochondrial electron-transport chain.
Plays a role in apoptosis. Suppression of the anti-apoptotic members or activation of the pro-apoptotic members of the Bcl-2 family leads to altered mitochondrial membrane permeability resulting in release of cytochrome c into the cytosol. Binding of cytochrome c to Apaf-1 triggers the activation of caspase-9, which then accelerates apoptosis by activating other caspases.
Defects in CYCS are the cause of thrombocytopenia type 4 (THC4) also known as autosomal dominant thrombocytopenia type 4. Thrombocytopenia is the presence of relatively few platelets in blood. THC4 is a non-syndromic form of thrombocytopenia. Clinical manifestations of thrombocytopenia are absent or mild. THC4 may be caused by dysregulated platelet formation.
Positive Control: Rat1 cell line; Mitochondrion matrix.
Immunogen: Full length recombinant Cytochrome C.
Purification Method: Ammonium Sulfate Precipitation.
Formulation: Provided as solution in phosphate buffered saline with 0.08% sodium azide.
References: 1. Morison, I.M., et al. 'A mutation of human cytochrome c enhances the intrinsic apoptotic pathway but causes only thrombocytopenia.' Nat. Genet. 2008, 40, 387-389
2. Skulachev, V.P. 'Cytochrome c is the apoptotic and antioxidant cascades.’ FEBS Lett 1998, 423, 275-280.
UniProt: P99999 (Human)
P62898 (Rat)
P00008 (Rabbit)
P00011 (Dog).
Caution: This product is intended FOR RESEARCH USE ONLY, and FOR TESTS IN VITRO, not for use in diagnostic or therapeutic procedures involving humans or animals.
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