ArticleMolecular and cellular biology2007
Regulation of H-ras splice variant expression by cross talk between the p53 and nonsense-mediated mRNA decay pathways.
Article in Molecular and cellular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 41 citations in OpenAlex.
- The Role of Splicing Machinery as a Promising Potential Therapeutic Target for Pituitary Neuroendocrine Tumors (PitNETs).Cancers · 2026Review
- Human introns contain conserved tissue-specific cryptic poison exons.NAR genomics and bioinformatics · 2024Article
- mRNA 3'UTR lengthening by alternative polyadenylation attenuates inflammatory responses and correlates with virulence of Influenza A virus.Nature communications · 2023Article
- The RNA-binding proteins hnRNP H and F regulate splicing of a MYC-dependent HRAS exon in prostate cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Tissue-specific regulation of gene expression via unproductive splicing.Nucleic acids research · 2023Article
- Modulation of alternative splicing during early infection of human primary B lymphocytes with Epstein-Barr virus (EBV): a novel function for the viral EBNA-LP protein.Nucleic acids research · 2021Article
- Suppression of Heterogeneous Nuclear Ribonucleoprotein C Inhibit Hepatocellular Carcinoma Proliferation, Migration, and InvasionFrontiers in oncology · 2021Article
- Murine Long Noncoding RNA Morrbid Contributes in the Regulation of NRAS Splicing in Hepatocytes In Vitro.International journal of molecular sciences · 2020Article
- Rotavirus Infection Alters Splicing of the Stress-Related Transcription Factor XBP1.Journal of virology · 2019Article
- Role of epigenetic factors in the selection of the alternative splicing isoforms of humanOncotarget · 2018Article
- mRNAs containing NMD-competent premature termination codons are stabilized and translated under UPF1 depletion.Scientific reports · 2017Article
- The BRCA1-Δ11q Alternative Splice Isoform Bypasses Germline Mutations and Promotes Therapeutic Resistance to PARP Inhibition and Cisplatin.Cancer research · 2016Article
- mRNA export through an additional cap-binding complex consisting of NCBP1 and NCBP3.Nature communications · 2015Article
- Alternative RNA structure-coupled gene regulations in tumorigenesis.International journal of molecular sciences · 2014Review
- The Ddx5 and Ddx17 RNA helicases are cornerstones in the complex regulatory array of steroid hormone-signaling pathways.Nucleic acids research · 2014Article
- The RNA helicase DDX5/p68 is a key factor promoting c-fos expression at different levels from transcription to mRNA export.Nucleic acids research · 2013Article
- Dual role of the ddx5/ddx17 RNA helicases in the control of the pro-migratory NFAT5 transcription factor.Oncogene · 2012Article
- The human T-lymphotropic virus type 1 tax protein inhibits nonsense-mediated mRNA decay by interacting with INT6/EIF3E and UPF1.Journal of virology · 2012Article
- IGF-1 deficiency resists cardiac hypertrophy and myocardial contractile dysfunction: role of microRNA-1 and microRNA-133a.Journal of cellular and molecular medicine · 2012Article
- Distinct p53 genomic binding patterns in normal and cancer-derived human cells.Cell cycle (Georgetown, Tex.) · 2011Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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 the production of the H-ras NMD-target transcript degraded in the cytosol by the NMD process. Our data indicated that the NMD process allowed the elimination of transcripts produced in response to a short-term treatment with camptothecin from the major proto-oncogene H-ras, independently of PTCs induced by mutations. The camptothecin effects on H-ras gene expression were p53 dependent and involved in part modulation of the SC35 splicing factor. Interestingly, a long-term treatment with camptothecin as well as p53 overexpression for 24 h resulted in the accumulation of the H-ras NMD target in the cytosol, although the NMD process was not completely inhibited as other NMD targets are not stabilized. Finally, Upf1, a major NMD effector, was necessary for optimal p53 activation by camptothecin, which is consistent with recent data showing that NMD effectors are required for genome stability. In conclusion, we identified cross talk between the p53 and NMD pathways that regulates the expression levels of H-ras splice variants.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.