ArticleOncogene2013
CDK8 regulates E2F1 transcriptional activity through S375 phosphorylation.
Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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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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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
38 citing papers in PubMed, 74 citations in OpenAlex.
- CDK8 Inhibition Increases E2F1 Transcriptional Activity and Promotes STAT3-Dependent Suppression of Mcl-1 in Triple-Negative Breast Cancer Cell Line MDA-MB-468.International journal of molecular sciences · 2026Article
- Mediator Kinase Inhibitor Selectivity and Activity in Colorectal Cancer.ACS chemical biology · 2025Article
- Cyclin-dependent protein kinases and cell cycle regulation in biology and disease.Signal transduction and targeted therapy · 2025Review
- Transcriptional coupling of telomeric retrotransposons with the cell cycle.Science advances · 2025Article
- Article
- Distinct effects of CDK8 module subunits on cellular growth and proliferation in Drosophila.Development (Cambridge, England) · 2024Article
- Article
- A Selective and Orally Bioavailable Quinoline-6-Carbonitrile-Based Inhibitor of CDK8/19 Mediator Kinase with Tumor-Enriched Pharmacokinetics.Journal of medicinal chemistry · 2022Article
- Targeting transcription cycles in cancer.Nature reviews. Cancer · 2022Review
- Cdk8 Kinase Module: A Mediator of Life and Death Decisions in Times of Stress.Microorganisms · 2021Review
- Gene Transcription as a Therapeutic Target in Leukemia.International journal of molecular sciences · 2021Review
- Interplay between cofactors and transcription factors in hematopoiesis and hematological malignancies.Signal transduction and targeted therapy · 2021Review
- Pharmacological Inhibition of CDK8 in Triple-Negative Breast Cancer Cell Line MDA-MB-468 Increases E2F1 Protein, Induces Phosphorylation of STAT3 and Apoptosis.Molecules (Basel, Switzerland) · 2020Article
- All-Atomic Molecular Dynamic Studies of Human andInternational journal of molecular sciences · 2020Article
- Review
- The Mediator CDK8-Cyclin C complex modulates Dpp signaling in Drosophila by stimulating Mad-dependent transcription.PLoS genetics · 2020Article
- Antagonizing CDK8 Sensitizes Colorectal Cancer to Radiation Through Potentiating the Transcription of e2f1 Target Gene apaf1.Frontiers in cell and developmental biology · 2020Article
- Regulation of E2F1 activity via PKA-mediated phosphorylations.Turkish journal of biology = Turk biyoloji dergisi · 2020Article
- Cyclin C: The Story of a Non-Cycling Cyclin.Biology · 2019Review
- Understanding Obesity as a Risk Factor for Uterine Tumors Using Drosophila.Advances in experimental medicine and biology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation of the Wnt/β-catenin pathway is a critical step in the development of colorectal cancers. A key mediator of this activation is the recently described oncogene CDK8, which is amplified in a large number of colorectal tumors. CDK8 affects β-catenin activation by interaction of the CDK8 submodule of the mediator complex with β-catenin/TCF transcriptional complex, and by CDK8 interacting with and phosphorylating E2F1, which acts as a repressor of β-catenin/TCF transcriptional activity. The amino-acid residue in E2F1 that CDK8 phosphorylates and how this phosphorylation impacts E2F1 activity in general is not known. Here, we describe that CDK8 phosphorylates serine 375 in E2F1 both in vitro and in cells, and that phosphorylation of this residue is required for E2F1 interaction with CDK8, and that the phosphorylation is dependent on CDK8 kinase activity. The phosphorylation of S375 by CDK8 regulates E2F1 ability to repress transcription of β-catenin/TCF-dependent genes, as well as activation of E2F1-dependent genes. This regulation is due to inactivation of E2F1 transcriptional activation, and not to the interference of E2F1's ability to bind to E2F1-binding sites in various promoters or to interact with DP1.
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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.