Y14 governs p53 expression and modulates DNA damage sensitivity View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-03-31

AUTHORS

Chia-Chen Lu, Chi-Chieh Lee, Ching-Tzu Tseng, Woan-Yuh Tarn

ABSTRACT

Y14 is a core component of the exon junction complex (EJC), while it also exerts cellular functions independent of the EJC. Depletion of Y14 causes G2/M arrest, DNA damage and apoptosis. Here we show that knockdown of Y14 induces the expression of an alternative spliced isoform of p53, namely p53β, in human cells. Y14, in the context of the EJC, inhibited aberrant exon inclusion during the splicing of p53 pre-mRNA, and thus prevent p53β expression. The anti-cancer agent camptothecin specifically suppressed p53β induction. Intriguingly, both depletion and overexpression of Y14 increased overall p53 protein levels, suggesting that Y14 governs the quality and quantity control of p53. Moreover, Y14 depletion unexpectedly reduced p21 protein levels, which in conjunction with aberrant p53 expression accordingly increased cell sensitivity to genotoxic agents. This study establishes a direct link between Y14 and p53 expression and suggests a function for Y14 in DNA damage signaling. More... »

PAGES

45558

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/srep45558

DOI

http://dx.doi.org/10.1038/srep45558

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1084133294

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/28361991


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