Editors' ChoiceApoptosis

A Kinder Cut of p73

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Science's STKE  18 Jul 2000:
Vol. 2000, Issue 41, pp. tw3
DOI: 10.1126/stke.2000.41.tw3

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]

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