Related Experiment Video
Updated: May 5, 2026

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
Published on: June 29, 2011
Cytochrome c deficiency causes embryonic lethality and attenuates stress-induced apoptosis
K Li1, Y Li, J M Shelton
1Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75390, USA.
Abstract:
Cytochrome c released from mitochondria has been proposed to be an essential component of an apoptotic pathway responsive to DNA damage and other forms of cell stress. Murine embryos devoid of cytochrome c die in utero by midgestation, but cell lines established from early cytochrome c null embryos are viable under conditions that compensate for defective oxidative phosphorylation. As compared to cell lines established from wild-type embryos, cells lacking cytochrome c show reduced caspase-3 activation and are resistant to the proapoptotic effects of UV irradiation, serum withdrawal, or staurosporine. In contrast, cells lacking cytochrome c demonstrate increased sensitivity to cell death signals triggered by TNFalpha. These results define the role of cytochrome c in different apoptotic signaling cascades.
Related Concept Videos
Overview of Cell Death
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the...
Caspases
The Extrinsic Apoptotic Pathway
The Intrinsic Apoptotic Pathway
Cellular Injury I: Introduction
Cellular Injury V: Apoptosis and Autophagy

