Disease relevance of CYC1

• This results in damage to the mitochondria, with initiation of a membrane permeability transition and a decline in membrane potential, followed by release of cytochrome c, caspase 3 activation, and cellular toxicity [1].

High impact information on CYC1

• There was release of mitochondrial cytochrome c into the cytosol and activation of caspase 3, which were prevented by cyclosporine, diallylsulfide, and Trolox [1].
• Caspase cascades in apoptosis induced by G418 were initiated by at least two pathways: the release of cytochrome c from mitochondria, which was observed under confocal microscopy, and endoplasmic reticulum stress, demonstrated by the increase in Ca2+ concentration and the cleavage of m-calpain and procaspase-12 [2].
• No significant release of cytochrome c from mitochondria was detected suggesting that the intrinsic mitochondrial pathway is not predominant in the apoptotic process [3].

Biological context of CYC1

• Despite the release of cytochrome C from the mitochondrial fraction there was no inhibition of apoptosis with the pan caspase inhibitor, ZVAD-FMK [4].

Analytical, diagnostic and therapeutic context of CYC1

• Cytochrome C was assessed by western blotting of mitochondrial and cytoplasmic fractions [4].

References