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An Anti-Apoptotic Role for the p53 Family Member, p73, During Developmental Neuron Death

Authors: C D, Pozniak; S, Radinovic; A, Yang; F, McKeon; D R, Kaplan; F D, Miller;

An Anti-Apoptotic Role for the p53 Family Member, p73, During Developmental Neuron Death

Abstract

p53 plays an essential pro-apoptotic role, a function thought to be shared with its family members p73 and p63. Here, we show that p73 is primarily present in developing neurons as a truncated isoform whose levels are dramatically decreased when sympathetic neurons apoptose after nerve growth factor (NGF) withdrawal. Increased expression of truncated p73 rescues these neurons from apoptosis induced by NGF withdrawal or p53 overexpression. In p73–/– mice, all isoforms of p73 are deleted and the apoptosis of developing sympathetic neurons is greatly enhanced. Thus, truncated p73 is an essential anti-apoptotic protein in neurons, serving to counteract the pro-apoptotic function of p53.

Keywords

Neurons, Mice, Inbred BALB C, Sympathetic Nervous System, Tumor Suppressor Proteins, Nuclear Proteins, Apoptosis, Tumor Protein p73, Recombinant Proteins, Adenoviridae, DNA-Binding Proteins, Mice, Nerve Growth Factor, Escherichia coli, Animals, Humans, Protein Isoforms, Genes, Tumor Suppressor, Tumor Suppressor Protein p53, Cells, Cultured

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Powered by OpenAIRE graph
citations
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
451
Top 1%
Top 1%
Top 0.1%