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Updated: Sep 20, 2026

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
Published on: June 29, 2011
[Mitochondria and apoptosis]
1Laboratorio de Cultivo de Tejidos y Biología de Tumores, Instituto de Biología Experimental, Facultad de Ciencias, Universidad Central de Venezuela, Apartado 47114, Caracas-Venezuela, 1041.
Abstract:
It is now accepted that mitochondria are endosymbionts, originated in aerobic bacteria which were integrated by the ancestor of eukaryotic cells. A part of the apoptotic machinery could exist in unicellular eukaryotic and some controlling apoptosis components might be present in prokaryotes. It is therefore possible that the mechanism originally involved in the maintenance of the symbiosis between the bacterial ancestor of the mitochondria and the host cell precursor of eukaryotes, provided the basis for the actual mechanism controlling cell survival. Metazoans would have improved this possibility by connecting to the mitochondria as principal effector of cellular death to the pathways of signal transduction. A variety of events appoint to the mitochondria as principal effector of the apoptosis. This including the release caspase activators (cytochrome c), changes in electron transport, loss of mitochondrial transmembrane potential, altered cellular oxidation-reduction, and participation of pro and antiapoptotic Bcl-2 proteins. The different signals that converge on mitochondria for activation or inhibition of these events, delineate several pathways in the physiology of the cellular death.
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