Cytochrome c deficiency causes embryonic lethality and attenuates stress-induced apoptosis.

Published

Journal Article

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.

Full Text

Duke Authors

Cited Authors

  • Li, K; Li, Y; Shelton, JM; Richardson, JA; Spencer, E; Chen, ZJ; Wang, X; Williams, RS

Published Date

  • May 12, 2000

Published In

Volume / Issue

  • 101 / 4

Start / End Page

  • 389 - 399

PubMed ID

  • 10830166

Pubmed Central ID

  • 10830166

International Standard Serial Number (ISSN)

  • 0092-8674

Digital Object Identifier (DOI)

  • 10.1016/s0092-8674(00)80849-1

Language

  • eng

Conference Location

  • United States