Evidence map›Paper›PMID 19487575›Full record

ArticleGenes & development2009

A role for Chk1 in blocking transcriptional elongation of p21 RNA during the S-phase checkpoint.

Rachel Beckerman, Aaron J Donner, Melissa Mattia, Melissa J Peart, James L Manley, Joaquin M Espinosa, Carol Prives

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
–field-weighted citation impact
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

42 citing papers in PubMed, 68 citations in OpenAlex.

  1. Trial
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  3. Epigenetics · 2022
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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

7 authors at 2 institutions in 1 country.

Rachel BeckermanDepartment of Biological Sciences, Columbia University, New York, New York 10027, USA.
Aaron J Donner
Melissa Mattia
Melissa J Peart
James L Manley
Joaquin M Espinosa
Carol Prives
Columbia University · USUniversity of Colorado Boulder · US

Funding

Scientific ReagentsP01CA087497 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI PRIVES, CAROL · 2000 to 2021
$35.4M
MRNA SYTHESIS IN ANIMAL CELLS--3END FORMATIONR01GM028983 · NIGMS · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI MANLEY, JAMES L. · 1985 to 2014
$6.4M
Stress- and Promoter-Specific Mechanisms of Transcritpional Activation by p53R01CA117907 · NCI · UNIVERSITY OF COLORADO DENVER · PI ESPINOSA, JOAQUIN M. · 2006 to 2022
$4.4M
PROPERTIES AND REGULATION OF P53 IN TUMOR CELLSR01CA077742 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI PRIVES, CAROL · 1999 to 2014
$3.8M
NCI NIH HHS CA117907NCI NIH HHS CA77742NCI NIH HHS CA87497NCI NIH HHS P01 CA087497NCI NIH HHS R01 CA077742NCI NIH HHS R01 CA117907NIGMS NIH HHS R01 GM028983
6 · The paper itself

Abstract

We reported previously that when cells are arrested in S phase, a subset of p53 target genes fails to be strongly induced despite the presence of high levels of p53. When DNA replication is inhibited, reduced p21 mRNA accumulation is correlated with a marked reduction in transcription elongation. Here we show that ablation of the protein kinase Chk1 rescues the p21 transcription elongation defect when cells are blocked in S phase, as measured by increases in both p21 mRNA levels and the presence of the elongating form of RNA polymerase II (RNAPII) toward the 3' end of the p21 gene. Recruitment of specific elongation and 3' processing factors (DSIF, CstF-64, and CPSF-100) is also restored. While additional components of the RNAPII transcriptional machinery, such as TFIIB and CDK7, are recruited more extensively to the p21 locus after DNA damage than after replication stress, their recruitment is not enhanced by ablation of Chk1. Significantly, ablating Chk2, a kinase closely related in substrate specificity to Chk1, does not rescue p21 mRNA levels during S-phase arrest. Thus, Chk1 has a direct and selective role in the elongation block to p21 observed during S-phase arrest. These findings demonstrate for the first time a link between the replication checkpoint mediated by ATR/Chk1 and the transcription elongation/3' processing machinery.

Indexed as

Gene Expression Regulation, NeoplasticAtaxia Telangiectasia Mutated ProteinsCaffeineCell Cycle ProteinsCheckpoint Kinase 1Checkpoint Kinase 2Cyclin-Dependent Kinase Inhibitor p21DaunorubicinDNA ReplicationHCT116 CellsHumansHydroxyureaNucleic Acid Synthesis InhibitorsPromoter Regions, GeneticProtein KinasesProtein Serine-Threonine KinasesAtaxia Telangiectasia Mutated ProteinsATR protein, humanCaffeineCDKN1A protein, humanCell Cycle ProteinsCheckpoint Kinase 1Checkpoint Kinase 2CHEK1 protein, humanCHEK2 protein, humanCyclin-Dependent Kinase Inhibitor p21DaunorubicinHydroxyureaNucleic Acid Synthesis InhibitorsProtein KinasesProtein Serine-Threonine KinasesRNA, MessengerTranscription FactorsTumor Suppressor Protein p53

Identifiers

PMID19487575
PMCPMC2701578
OpenAlexW2157462690

What OpenQuestion holds

Textmetadata
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.