ArticleOncogene2013
The RNA helicase p68 (DDX5) is selectively required for the induction of p53-dependent p21 expression and cell-cycle arrest after DNA damage.
Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
64 citing papers in PubMed, 95 citations in OpenAlex.
- DDX5 orchestrates RNA homeostasis to ensure oocyte developmental competence.Nature communications · 2026Article
- Investigating Metabolically Altered Pathways in Small Cell Lung Cancer: From RNA Sequencing Analysis to Seahorse-Based Functional Validation.Methods and protocols · 2026Article
- Evaluating the Impact of Two Different Diets on the Protein Profile of the Brain, Liver, and Intestine of the Barramundi.Proteomes · 2026Article
- Targeting R-loops: diverse RNA helicases in R-loop resolution and their potential as targets for cancer therapy.Frontiers in cell and developmental biology · 2026Review
- The Transcriptional CoactivatorGenes · 2025Article
- RNA helicases, DDX5 and DDX17, facilitate lytic reactivation of gammaherpesviruses.PLoS pathogens · 2025Article
- Unwinding new therapeutic opportunities in rhabdomyosarcoma: the role of RNA helicase DDX5.Frontiers in cell and developmental biology · 2025Review
- Diverse functions of DEAD-box proteins in oligodendrocyte development, differentiation, and homeostasis.Journal of neurochemistry · 2025Review
- DEAD/H Box 5 (DDX5) Augments E2F1-Induced Cell Death Independent of the Tumor Suppressor p53.International journal of molecular sciences · 2024Article
- DDX5 promotes esophageal squamous cell carcinoma growth through sustaining VAV3 mRNA stability.Oncogene · 2024Article
- METTL1-modulated LSM14A facilitates proliferation and migration in glioblastoma via the stabilization of DDX5.iScience · 2024Article
- Fragile X Messenger Ribonucleoprotein Protein and Its Multifunctionality: From Cytosol to Nucleolus and Back.Biomolecules · 2024Review
- Role of the DEAD-box RNA helicase DDX5 (p68) in cancer DNA repair, immune suppression, cancer metabolic control, virus infection promotion, and human microbiome (microbiota) negative influence.Journal of experimental & clinical cancer research : CR · 2023Review
- DEAD-box RNA helicases with special reference to p68: Unwinding their biology, versatility, and therapeutic opportunity in cancer.Genes & diseases · 2023Review
- Hypoxia-mediated regulation of DDX5 through decreased chromatin accessibility and post-translational targeting restricts R-loop accumulation.Molecular oncology · 2023Article
- RNA binding protein DDX5 restricts RORγtScience advances · 2023Article
- DDX5 mRNA-targeting antisense oligonucleotide as a new promising therapeutic in combating castration-resistant prostate cancer.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Positive allosteric GABAFrontiers in physiology · 2023Article
- Article
- Where all the Roads Meet? A Crossover Perspective on Host Factors Regulating SARS-CoV-2 infection.Journal of molecular biology · 2022Review
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
The RNA helicase p68 (DDX5) is an established co-activator of the p53 tumour suppressor that itself has a pivotal role in orchestrating the cellular response to DNA damage. Although several factors influence the biological outcome of p53 activation, the mechanisms governing the choice between cell-cycle arrest and apoptosis remain to be elucidated. In the present study, we show that, while p68 is critical for p53-mediated transactivation of the cell-cycle arrest gene p21(WAF1/CIP1), it is dispensable for induction of several pro-apoptotic genes in response to DNA damage. Moreover, p68 depletion results in a striking inhibition of recruitment of p53 and RNA Pol II to the p21 promoter but not to the Bax or PUMA promoters, providing an explanation for the selective effect on p21 induction. Importantly, these findings are mirrored in a novel inducible p68 knockout mouse model in which p68 depletion results in a selective inhibition of p21 induction in several tissues. Moreover, in the bone marrow, p68 depletion results in an increased sensitivity to γ-irradiation, consistent with an increased level of apoptosis. These data highlight a novel function of p68 as a modulator of the decision between p53-mediated growth arrest and apoptosis in vitro and in vivo.
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Registered trials
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.