cytochrome c

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Related to cytochrome c: Cytochrome c oxidase

cy·to·chrome c

(sī'tō-krōm), [MIM*123970]
The mobile cytochrome that transports electrons from Complex III to Complex IV of the respiratory chain.


A gene on chromosome 7p15.3 that encodes cytochrome c, an electron carrier protein, which transfers electrons from the heme group of the cytochrome c1 subunit of cytochrome reductase to the cytochrome oxidase complex, the final protein carrier in the mitochondrial electron-transport chain. CYCS plays a role in apoptosis by suppressing anti-apoptotic members or by activating pro-apoptotic members of the Bcl-2 family, leading to altered mitochondrial membrane permeability and the release of cytochrome c into the cytosol. Binding of cytochrome c to Apaf-1 activates caspase-9, which then accelerates apoptosis by activating other caspases.

Molecular pathology
Defects in CYCS cause thrombocytopaenia type 4.
References in periodicals archive ?
Polymorphisms were identified in cytochrome b, cytochrome c gene and d-loopregion (Table IV).
After single gene based analysis, collectively sequences of three genes (cytochrome b, cytochrome c and d-loop) based multidimensional scaling plot was generated.
Cytochrome b, cytochrome c and d-loop region (collectively) based Evolutionary analysis of Axis porcinus.
After the confirmation of the activated caspase-3, a marker of apoptosis development, and the elevated levels of active caspase-8 and Fas protein, we did not observe increased levels of active caspase-9 or released cytochrome c in SHS-exposed rat hearts.
Further evidence confirming which of them is involved in the activation of caspase-3 is provided by the findings of elevated levels of caspase-8 and Fas, coupled with no alteration or even reduced levels of caspase-9 activity and cytosolic cytochrome c in ventricles of rats exposed to SHS (Figures 3 and 4).
2], which might counterbalance the action of elevated pro-apoptotic protein Bad and prohibit the release of cytochrome c from the mitochondria.
Cytochrome C and dATP-dependent formation of Apaf-1/Caspase-9 complex initiates an apoptotic protease cascade.
NADPH-dependent reductase activity was determined by the measurement of the increasing absorbance of the preparation, corresponding to the reduction of the cytochrome C.