Sci. STKE, 18 July 2000
Apoptosis A Kinder Cut of p73
In the brain of very young mammals, a vast oversupply of neurons is pruned back as the neuronal interconnections become increasingly refined. The pruning process relies on p53-promoted apoptosis. Pozniak et al. now find that the actions of p53 are counterbalanced by the actions of a truncated form of p73 lacking its transactivation domain. In its full-length form, p73 also promotes apoptosis, but its truncated form blocks apoptosis. The decision to produce truncated or full-length p73 is made at the point of transcription, which suggests a potential mechanism for a very rapid response to changing cell-death or cell-survival needs. A healthy supply of truncated p73, and thus cell survival, is promoted by the presence of nerve growth factor (NGF). Thus, p73, whose function depends on the particular isoform produced, is a mediator of the NGF cell-survival signal.
Pozniak, C.D., Radinovic, S., Yang, A., McKeon, F., Kaplan, D.R., and Miller, F.D. (2000) An anti-apoptotic role for the p53 family member, p73, during developmental neuron death. Science 289: 304-306. [Abstract] [Full Text]
Citation: A Kinder Cut of p73. Sci. STKE 2000, tw3 (2000).
Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882