Evidence map›Paper›PMID 26399478›Full record

ArticleTranscription2015

CTCF regulates NELF, DSIF and P-TEFb recruitment during transcription.

Clélia Laitem, Justyna Zaborowska, Michael Tellier, Yuki Yamaguchi, Qingfu Cao, Sylvain Egloff, Hiroshi Handa, Shona Murphy

Open access · bronzeAbstract read
In one paragraph

Article in Transcription, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

18 citing papers in PubMed, 24 citations in OpenAlex.

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  18. Cajal body function in genome organization and transcriptome diversity.BioEssays : news and reviews in molecular, cellular and developmental biology · 2016
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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

8 authors at 5 institutions in 4 countries.

Clélia Laitema Sir William Dunn School of Pathology; University of Oxford ; Oxford , UK.
Justyna Zaborowskaa Sir William Dunn School of Pathology; University of Oxford ; Oxford , UK.
Michael Telliera Sir William Dunn School of Pathology; University of Oxford ; Oxford , UK.
Yuki Yamaguchib Graduate School of Bioscience and Biotechnology; Tokyo Institute of Technology ; Yokohama , Japan.
Qingfu Caob Graduate School of Bioscience and Biotechnology; Tokyo Institute of Technology ; Yokohama , Japan.
Sylvain Egloffc Université de Toulouse; UPS; Laboratoire de Biologie Moléculaire Eucaryote ; Toulouse , France.
Hiroshi Handad Department of Nanoparticle Translational Research ; Tokyo Medical University ; Tokyo , Japan.
Shona Murphya Sir William Dunn School of Pathology; University of Oxford ; Oxford , UK.
Science Oxford · GBLaboratoire de Biologie Moléculaire des Eucaryotes · FRResearch Institute for Bioscience and Biotechnology · NPTokyo Institute of Technology · JPTokyo Medical University · JP

Funding

Medical Research Council G0400653Medical Research Council MR/M010716/1Wellcome Trust 106134
6 · The paper itself

Abstract

CTCF is a versatile transcription factor with well-established roles in chromatin organization and insulator function. Recent findings also implicate CTCF in the control of elongation by RNA polymerase (RNAP) II. Here we show that CTCF knockdown abrogates RNAP II pausing at the early elongation checkpoint of c-myc by affecting recruitment of DRB-sensitivity-inducing factor (DSIF). CTCF knockdown also causes a termination defect on the U2 snRNA genes (U2), by affecting recruitment of negative elongation factor (NELF). In addition, CTCF is required for recruitment of positive elongation factor b (P-TEFb), which phosphorylates NELF, DSIF, and Ser2 of the RNAP II CTD to activate elongation of transcription of c-myc and recognition of the snRNA gene-specific 3' box RNA processing signal. These findings implicate CTCF in a complex network of protein:protein/protein:DNA interactions and assign a key role to CTCF in controlling RNAP II transcription through the elongation checkpoint of the protein-coding c-myc and the termination site of the non-coding U2, by regulating the recruitment and/or activity of key players in these processes.

Indexed as

Transcription, GeneticCCCTC-Binding FactorGene Knockdown TechniquesHeLa CellsHumansNuclear ProteinsPhosphorylationPositive Transcriptional Elongation Factor BProto-Oncogene Proteins c-mycRepressor ProteinsRNA Polymerase IIRNA, Small NuclearTranscriptional Elongation FactorsTranscription FactorsCCCTC-Binding FactorCTCF protein, humanMYC protein, humanNSMF protein, humanNuclear ProteinsPositive Transcriptional Elongation Factor BProto-Oncogene Proteins c-mycRepressor ProteinsRNA Polymerase IIRNA, Small NuclearSUPT5H protein, humanTranscriptional Elongation FactorsTranscription FactorsU2 small nuclear RNACTCFelongation checkpointP-TEFbRNA Polymerase II pausingsnRNA genetranscription

Identifiers

PMID26399478
PMCPMC4802788
OpenAlexW2227674067

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.