Evidence map›Paper›PMID 32805052›Full record

ArticleNucleic acids research2020

CDK12 globally stimulates RNA polymerase II transcription elongation and carboxyl-terminal domain phosphorylation.

Michael Tellier, Justyna Zaborowska, Livia Caizzi, Eusra Mohammad, Taras Velychko, Björn Schwalb, Ivan Ferrer-Vicens, Daniel Blears, Takayuki Nojima, Patrick Cramer and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
4.9field-weighted citation impact, top 4% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

64 citing papers in PubMed, 100 citations in OpenAlex.

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  11. Direct roles of long non-coding RNAs in transcription activation.Nature structural & molecular biology · 2026
    Review
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  19. Dual Modes of Gene Regulation by CDK12.bioRxiv : the preprint server for biology · 2025
    Article
  20. Article

4 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 2 countries.

Michael TellierSir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, UK.
Justyna ZaborowskaSir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, UK.
Livia CaizziMax Planck Institute for Biophysical Chemistry, Department of Molecular Biology, Am Fassberg 11, 37077 Göttingen, Germany.
Eusra MohammadMax Planck Institute for Biophysical Chemistry, Department of Molecular Biology, Am Fassberg 11, 37077 Göttingen, Germany.
Taras VelychkoMax Planck Institute for Biophysical Chemistry, Department of Molecular Biology, Am Fassberg 11, 37077 Göttingen, Germany.
Björn SchwalbMax Planck Institute for Biophysical Chemistry, Department of Molecular Biology, Am Fassberg 11, 37077 Göttingen, Germany.
Ivan Ferrer-VicensSir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, UK.
Daniel BlearsMechanisms of Transcription Laboratory, The Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.
Takayuki NojimaSir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, UK.
Patrick CramerMax Planck Institute for Biophysical Chemistry, Department of Molecular Biology, Am Fassberg 11, 37077 Göttingen, Germany.
Shona MurphySir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, UK.
Max Planck Institute for Biophysical Chemistry · DEUniversity of Oxford · GBThe Francis Crick Institute · GB

Funding

European Research Council 693023Medical Research Council G0400653Wellcome Trust 210641/Z/18/ZWellcome Trust WT106134AIAWellcome Trust WT210641/Z/18/Z
6 · The paper itself

Abstract

Cyclin-dependent kinase 12 (CDK12) phosphorylates the carboxyl-terminal domain (CTD) of RNA polymerase II (pol II) but its roles in transcription beyond the expression of DNA damage response genes remain unclear. Here, we have used TT-seq and mNET-seq to monitor the direct effects of rapid CDK12 inhibition on transcription activity and CTD phosphorylation in human cells. CDK12 inhibition causes a genome-wide defect in transcription elongation and a global reduction of CTD Ser2 and Ser5 phosphorylation. The elongation defect is explained by the loss of the elongation factors LEO1 and CDC73, part of PAF1 complex, and SPT6 from the newly-elongating pol II. Our results indicate that CDK12 is a general activator of pol II transcription elongation and indicate that it targets both Ser2 and Ser5 residues of the pol II CTD.

Indexed as

Transcription Elongation, GeneticChromatinCyclin-Dependent KinasesHEK293 CellsHumansMutationPhosphorylationRNARNA Polymerase IISequence Analysis, RNASerineTranscriptional Elongation FactorsCDK12 protein, humanChromatinCyclin-Dependent KinasesRNARNA Polymerase IISerineTranscriptional Elongation Factors

Identifiers

PMID32805052
PMCPMC7641311
OpenAlexW3036643926

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.