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  • PMID: 25504532 was deleted because it is a duplicate of PMID: 25554796
Aging (Albany NY). 2014 Nov;6(11):921-30.

TAp73 promotes anti-senescence-anabolism not proliferation.

Author information

1
Medical Research Council, Toxicology Unit, Leicester LE1 9HN, UK. Department of Experimental Medicine and Surgery, University of Rome "Tor Vergata", 00133 Rome, Italy.
2
Medical Research Council, Toxicology Unit, Leicester LE1 9HN, UK. Blizard Institute of Cell and Molecular Science, Barts and the London School of Medicine and Dentistry, Queen Mary.
3
Department of Experimental Medicine and Surgery, University of Rome "Tor Vergata", 00133 Rome, Italy.
4
Medical Research Council, Toxicology Unit, Leicester LE1 9HN, UK.
5
Medical Research Council, Toxicology Unit, Leicester LE1 9HN, UK. Department of Experimental Medicine and Surgery, University of Rome "Tor Vergata", 00133 Rome, Italy. Biochemistry Laboratory IDI-IRCC, c/o Department of Experimental Medicine and Surgery, University of Rome "Tor Vergata", 00133 Rome, Italy.
6
Medical Research Council, Toxicology Unit, Leicester LE1 9HN, UK. Department of Cancer Studies and Molecular Medicine, University of Leicester, Leicester UK.

Abstract

TAp73, a member of the p53 family, has been traditionally considered a tumor suppressor gene, but a recent report has claimed that it can promote cellular proliferation. This assumption is based on biochemical evidence of activation of anabolic metabolism, with enhanced pentose phosphate shunt (PPP) and nucleotide biosynthesis. Here, while we confirm that TAp73 expression enhances anabolism, we also substantiate its role in inhibiting proliferation and promoting cell death. Hence, we would like to propose an alternative interpretation of the accumulating data linking p73 to cellular metabolism: we suggest that TAp73 promotes anabolism to counteract cellular senescence rather than to support proliferation.

PMID:
25554796
PMCID:
PMC4276786
DOI:
10.18632/aging.100701
[Indexed for MEDLINE]

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