Evidence map›Paper›PMID 32209474›Full record

ArticleCell reports2020

Chromatin Remodeling and Immediate Early Gene Activation by SLFN11 in Response to Replication Stress.

Junko Murai, Hongliang Zhang, Lorinc Pongor, Sai-Wen Tang, Ukhyun Jo, Fumiya Moribe, Yixiao Ma, Masaru Tomita, Yves Pommier

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

54 citing papers in PubMed, 83 citations in OpenAlex.

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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

9 authors at 4 institutions in 2 countries.

Junko MuraiDevelopmental Therapeutics Branch and Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892, USA; Institute for Advanced Biosciences, Keio University, Tsuruoka, Yamagata 997-0052, Japan; Graduate School of Media and Governance, Keio University, Fujisawa, Kanagawa 252-0882, Japan. Electronic address: muraij@ttck.keio.ac.jp.
Hongliang ZhangDevelopmental Therapeutics Branch and Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892, USA.
Lorinc PongorDevelopmental Therapeutics Branch and Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892, USA.
Sai-Wen TangDevelopmental Therapeutics Branch and Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892, USA.
Ukhyun JoDevelopmental Therapeutics Branch and Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892, USA.
Fumiya MoribeDevelopmental Therapeutics Branch and Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892, USA.
Yixiao MaInstitute for Advanced Biosciences, Keio University, Tsuruoka, Yamagata 997-0052, Japan; Graduate School of Media and Governance, Keio University, Fujisawa, Kanagawa 252-0882, Japan.
Masaru TomitaInstitute for Advanced Biosciences, Keio University, Tsuruoka, Yamagata 997-0052, Japan; Graduate School of Media and Governance, Keio University, Fujisawa, Kanagawa 252-0882, Japan.
Yves PommierDevelopmental Therapeutics Branch and Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892, USA. Electronic address: pommier@nih.gov.
Center for Cancer Research · USNational Cancer Institute · USKeio University · JPKeio University Shonan Fujisawa · JP

Funding

DNA Repair, Cell Cycle Checkpoints and Apoptosis as Targets for Anticancer DrugsZIABC006150 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI POMMIER, YVES · 2009 to 2025
$23.0M
PROTEIN-ASSOCIATED DNA BREAKS AS INDICATOR OF TOPOISOMERASE INHIBITIONZ01BC006150 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI POMMIER, YVES · 1996 to 2008
$1.5M
DNA TOPOISOMERASES AS TARGET OF ACTION OF ANTICANCER DRUGSZ01BC006161 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI POMMIER, YVES · 1996 to 2008
$1.5M
Intramural NIH HHS Z01 BC006150Intramural NIH HHS Z01 BC006161
6 · The paper itself

Abstract

Schlafen 11 (SLFN11) was recently discovered as a cellular restriction factor against replication stress. Here, we show that SLFN11 increases chromatin accessibility genome wide, prominently at active promoters in response to replication stress induced by the checkpoint kinase 1 (CHK1) inhibitor prexasertib or the topoisomerase I (TOP1) inhibitor camptothecin. Concomitantly, SLFN11 selectively activates cellular stress response pathways by inducing the transcription of the immediate early genes (IEGs), including JUN, FOS, EGR1, NFKB2, and ATF3, together with the cell cycle arrest genes CDKN1A (p21

Indexed as

Genes, Immediate-EarlyAdenosine TriphosphatasesCell LineChromatin Assembly and DisassemblyDNA HelicasesDNA ReplicationHumansModels, BiologicalNuclear ProteinsPromoter Regions, GeneticRNA, MessengerStress, PhysiologicalTranscriptional ActivationTranscription, GeneticTumor Suppressor Protein p53Adenosine TriphosphatasesDNA HelicasesNuclear ProteinsRNA, MessengerSLFN11 protein, humanTumor Suppressor Protein p53ATRcell cycle checkpointCHK1chromatinDNA damageFOSJUNnative immune responsereplication stresstopoisomerase inhibitor

Identifiers

PMID32209474
PMCPMC7240837
OpenAlexW3013462684

What OpenQuestion holds

Textmetadata
LicenceTDM
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.