AI Article Synopsis
- Recent studies reveal that p53, a crucial protein for regulating cell growth and responding to stress, is controlled at the mRNA level through regions that impact its stability and translation.
- A feedback loop between p53 and a protein called PARN helps keep p53 levels low under normal conditions by destabilizing its mRNA, but UV-induced stress boosts p53 levels and activates PARN, affecting gene expression during DNA damage.
- This research offers new insights into how p53 functions and the complex mechanisms governing the processing of mRNA in various cellular environments.
Article Abstract
Although the p53 network has been intensively studied, genetic analyses long hinted at the existence of components that remained elusive. Recent studies have shown regulation of p53 at the mRNA level mediated via both the 5' and the 3' untranslated regions and affecting the stability and translation efficiency of the p53 mRNA. Here, we provide evidence of a feedback loop between p53 and the poly(A)-specific ribonuclease (PARN), in which PARN deadenylase keeps p53 levels low in nonstress conditions by destabilizing p53 mRNA, and the UV-induced increase in p53 activates PARN deadenylase, regulating gene expression during DNA damage response in a transactivation-independent manner. This model is innovative because it provides insights into p53 function and the mechanisms behind the regulation of mRNA 3' end processing in different cellular conditions.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3587245 | PMC |
| http://dx.doi.org/10.1073/pnas.1212533110 | DOI Listing |
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