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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Embryonic lethality and fetal liver apoptosis in mice lacking the c-raf-1 gene.

The Raf kinases play a key role in relaying signals elicited by mitogens or oncogenes. Here, we report that c-raf-1(-/-) embryos are growth retarded and die at midgestation with anomalies in the placenta and in the fetal liver. Although hepatoblast proliferation does not appear to be impaired, c-raf-1(-/-) fetal livers are hypocellular and contain numerous apoptotic cells. Similarly, the poor proliferation of Raf-1(-/-) fibroblasts and hematopoietic cells cultivated in vitro is due to an increase in the apoptotic index of these cultures rather than to a cell cycle defect. Furthermore, Raf-1- deficient fibroblasts are more sensitive than wild- type cells to specific apoptotic stimuli, such as actinomycin D or Fas activation, but not to tumor necrosis factor-alpha. MEK/ERK activation is normal in Raf-1-deficient cells and embryos, and is probably mediated by B-RAF. These results indicate that the essential function of Raf-1 is to counteract apoptosis rather than to promote proliferation, and that effectors distinct from the MEK/ERK cascade must mediate the anti-apoptotic function of Raf-1.[1]

References

  1. Embryonic lethality and fetal liver apoptosis in mice lacking the c-raf-1 gene. Mikula, M., Schreiber, M., Husak, Z., Kucerova, L., Rüth, J., Wieser, R., Zatloukal, K., Beug, H., Wagner, E.F., Baccarini, M. EMBO J. (2001) [Pubmed]
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