ArticleNucleic acids research2008
Induction of PPM1D following DNA-damaging treatments through a conserved p53 response element coincides with a shift in the use of transcription initiation sites.
Article in Nucleic acids research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 57 citations in OpenAlex.
- Decoding the Central Dogma: Quantitative Insights into Transcription and Translation Dynamics in the p53-Mediated DNA Damage Response.Journal of molecular biology · 2026Review
- Clonal hematopoiesis and hematological malignancy.The Journal of clinical investigation · 2024Review
- p53 rapidly restructures 3D chromatin organization to trigger a transcriptional response.Nature communications · 2024Article
- The transcriptomic revolution and radiation biology.International journal of radiation biology · 2022Article
- High Expression ofCancers · 2021Article
- Inhibition of the DNA damage response phosphatase PPM1D reprograms neutrophils to enhance anti-tumor immune responses.Nature communications · 2021Article
- In Vivo Validation of Alternative FDXR Transcripts in Human Blood in Response to Ionizing Radiation.International journal of molecular sciences · 2020Article
- Census and evaluation of p53 target genes.Oncogene · 2017Review
- A novel mathematical model of ATM/p53/NF- κB pathways points to the importance of the DDR switch-off mechanisms.BMC systems biology · 2016Article
- Wip1 phosphatase: between p53 and MAPK kinases pathways.Oncotarget · 2016Review
- Feedbacks, Bifurcations, and Cell Fate Decision-Making in the p53 System.PLoS computational biology · 2016Article
- WIP1 stimulates migration and invasion of salivary adenoid cystic carcinoma by inducing MMP-9 and VEGF-C.Oncotarget · 2015Article
- Targeting PPM1D by lentivirus-mediated RNA interference inhibits the tumorigenicity of bladder cancer cells.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2014Article
- The transcription factor p53: not a repressor, solely an activator.Cell cycle (Georgetown, Tex.) · 2014Article
- Wip1 suppresses apoptotic cell death through direct dephosphorylation of BAX in response to γ-radiation.Cell death & disease · 2013Article
- Activation of WIP1 phosphatase by HTLV-1 Tax mitigates the cellular response to DNA damage.PloS one · 2013Article
- Molecular determinants of ovarian cancer chemoresistance: new insights into an old conundrum.Annals of the New York Academy of Sciences · 2012Review
- Wip1 sensitizes p53-negative tumors to apoptosis by regulating the Bax/Bcl-xL ratio.Cell cycle (Georgetown, Tex.) · 2012Article
- Regulation of the Wip1 phosphatase and its effects on the stress response.Frontiers in bioscience (Landmark edition) · 2012Review
- A bioinformatics filtering strategy for identifying radiation response biomarker candidates.PloS one · 2012Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
PPM1D (Wip1), a type PP2C phosphatase, is expressed at low levels in most normal tissues but is overexpressed in several types of cancers. In cells containing wild-type p53, the levels of PPM1D mRNA and protein increase following exposure to genotoxic stress, but the mechanism of regulation by p53 was unknown. PPM1D also has been identified as a CREB-regulated gene due to the presence of a cyclic AMP response element (CRE) in the promoter. Transient transfection and chromatin immunoprecipitation experiments in HCT116 cells were used to characterize a conserved p53 response element located in the 5' untranslated region (UTR) of the PPM1D gene that is required for the p53-dependent induction of transcription from the human PPM1D promoter. CREB binding to the CRE contributes to the regulation of basal expression of PPM1D and directs transcription initiation at upstream sites. Following exposure to ultraviolet (UV) or ionizing radiation, the abundance of transcripts with short 5' UTRs increased in cells containing wild-type p53, indicating increased utilization of downstream transcription initiation sites. In cells containing wild-type p53, exposure to UV resulted in increased PPM1D protein levels even when PPM1D mRNA levels remained constant, indicating post-transcriptional regulation of PPM1D protein levels.
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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.