ArticleOncogene1999
Cyclin C/CDK8 and cyclin H/CDK7/p36 are biochemically distinct CTD kinases.
Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
58 citing papers in PubMed, 119 citations in OpenAlex.
- 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
- Role of Cyclins and Cytoskeletal Proteins in Endometriosis: Insights into Pathophysiology.Cancers · 2024Review
- Cyclin-dependent kinases: Masters of the eukaryotic universe.Wiley interdisciplinary reviews. RNA · 2023Review
- CDK8 and CDK19 act redundantly to control the CFTR pathway in the intestinal epithelium.EMBO reports · 2023Article
- Unveiling the noncanonical activation mechanism of CDKs: insights from recent structural studies.Frontiers in molecular biosciences · 2023Review
- Exploitation of the Mediator complex by viruses.PLoS pathogens · 2022Article
- Cyclin-dependent kinase inhibitors in brain cancer: current state and future directions.Cancer drug resistance (Alhambra, Calif.) · 2020Review
- Article
- The Emerging Role of Cyclin-Dependent Kinases (CDKs) in Pancreatic Ductal Adenocarcinoma.International journal of molecular sciences · 2018Review
- Development of Highly Potent and Selective Steroidal Inhibitors and Degraders of CDK8.ACS medicinal chemistry letters · 2018Article
- Retroviral cyclin controls cyclin-dependent kinase 8-mediated transcription elongation and reinitiation.Journal of virology · 2015Article
- Genome-wide targeting of the epigenetic regulatory protein CTCF to gene promoters by the transcription factor TFII-I.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Promoter occupancy of STAT1 in interferon responses is regulated by processive transcription.Molecular and cellular biology · 2015Article
- CYCLIN-DEPENDENT KINASE8 differentially regulates plant immunity to fungal pathogens through kinase-dependent and -independent functions in Arabidopsis.The Plant cell · 2014Article
- Cyclin-dependent kinase 7 controls mRNA synthesis by affecting stability of preinitiation complexes, leading to altered gene expression, cell cycle progression, and survival of tumor cells.Molecular and cellular biology · 2014Article
- The basal transcription machinery as a target for cancer therapy.Cancer cell international · 2014Article
- Cross-talk of phosphorylation and prolyl isomerization of the C-terminal domain of RNA Polymerase II.Molecules (Basel, Switzerland) · 2014Review
- Article
- RNA polymerase II C-terminal domain: Tethering transcription to transcript and template.Chemical reviews · 2013Review
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Phosphorylation of the carboxyl-terminal domain (CTD) of RNA polymerase II is important for basal transcriptional processes in vivo and for cell viability. Several kinases, including certain cyclin-dependent kinases, can phosphorylate this substrate in vitro. It has been proposed that differential CTD phosphorylation by different kinases may regulate distinct transcriptional processes. We have found that two of these kinases, cyclin C/CDK8 and cyclin H/CDK7/p36, can specifically phosphorylate distinct residues in recombinant CTD substrates. This difference in specificity may be largely due to their varying ability to phosphorylate lysine-substituted heptapeptide repeats within the CTD, since they phosphorylate the same residue in CTD consensus heptapeptide repeats. Furthermore, this substrate specificity is reflected in vivo where cyclin C/ CDK8 and cyclin H/CDK7/p36 can differentially phosphorylate an endogenous RNA polymerase II substrate. Several small-molecule kinase inhibitors have different specificities for these related kinases, indicating that these enzymes have diverse active-site conformations. These results suggest that cyclin C/CDK8 and cyclin H/CDK7/p36 are physically distinct enzymes that may have unique roles in transcriptional regulation mediated by their phosphorylation of specific sites on RNA polymerase II.
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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.