<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>27(20)</volume><submitter>Barbier J</submitter><pubmed_abstract>When cells are exposed to a genotoxic stress, a DNA surveillance pathway that involves p53 is activated, allowing DNA repair. Eukaryotic cells have also evolved a mechanism called mRNA surveillance that controls the quality of mRNAs. Indeed, mutant mRNAs carrying premature translation termination codons (PTCs) are selectively degraded by the nonsense-mediated mRNA decay (NMD) pathway. However, in the case of particular genes, such as proto-oncogenes, mutations that do not create PTCs and therefore that do not induce mRNA degradation, can be harmful to cells. In this study, we showed that the H-ras gene in the absence of mutations produces an NMD-target splice variant that is degraded in the cytosol. We observed that a treatment with the genotoxic stress inducer camptothecin for 6 h favored</pubmed_abstract><journal>Molecular and cellular biology</journal><pagination>7315-33</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC2168895</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Regulation of H-ras splice variant expression by cross talk between the p53 and nonsense-mediated mRNA decay pathways.</pubmed_title><pmcid>PMC2168895</pmcid><pubmed_authors>Dutertre M</pubmed_authors><pubmed_authors>Auboeuf D</pubmed_authors><pubmed_authors>de la Grange P</pubmed_authors><pubmed_authors>Bittencourt D</pubmed_authors><pubmed_authors>Sanchez G</pubmed_authors><pubmed_authors>Gratadou L</pubmed_authors><pubmed_authors>Barbier J</pubmed_authors></additional><is_claimable>false</is_claimable><name>Regulation of H-ras splice variant expression by cross talk between the p53 and nonsense-mediated mRNA decay pathways.</name><description>When cells are exposed to a genotoxic stress, a DNA surveillance pathway that involves p53 is activated, allowing DNA repair. Eukaryotic cells have also evolved a mechanism called mRNA surveillance that controls the quality of mRNAs. Indeed, mutant mRNAs carrying premature translation termination codons (PTCs) are selectively degraded by the nonsense-mediated mRNA decay (NMD) pathway. However, in the case of particular genes, such as proto-oncogenes, mutations that do not create PTCs and therefore that do not induce mRNA degradation, can be harmful to cells. In this study, we showed that the H-ras gene in the absence of mutations produces an NMD-target splice variant that is degraded in the cytosol. We observed that a treatment with the genotoxic stress inducer camptothecin for 6 h favored</description><dates><release>2007-01-01T00:00:00Z</release><publication>2007 Oct</publication><modification>2025-04-21T14:52:05.082Z</modification><creation>2019-03-27T02:22:21Z</creation></dates><accession>S-EPMC2168895</accession><cross_references><pubmed>17709397</pubmed><doi>10.1128/mcb.00272-07</doi><doi>10.1128/MCB.00272-07</doi></cross_references></HashMap>