Evidence map›Paper›PMID 33536335›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2021

SLFN11 promotes CDT1 degradation by CUL4 in response to replicative DNA damage, while its absence leads to synthetic lethality with ATR/CHK1 inhibitors.

Ukhyun Jo, Yasuhisa Murai, Sirisha Chakka, Lu Chen, Ken Cheng, Junko Murai, Liton Kumar Saha, Lisa M Miller Jenkins, Yves Pommier

Open access · hybridAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
4.7field-weighted citation impact, top 3% 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

52 citing papers in PubMed, 73 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 3 institutions in 2 countries.

Ukhyun JoDevelopmental Therapeutics Branch, Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20814; ukhyun.jo@nih.gov yves.pommier@nih.gov.
Yasuhisa MuraiDevelopmental Therapeutics Branch, Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20814.ORCID 0000-0002-3305-1248
Sirisha ChakkaNational Center for Advancing Translational Sciences, Functional Genomics Laboratory, NIH, Rockville, MD 20850.
Lu ChenNational Center for Advancing Translational Sciences, Functional Genomics Laboratory, NIH, Rockville, MD 20850.
Ken ChengNational Center for Advancing Translational Sciences, Functional Genomics Laboratory, NIH, Rockville, MD 20850.
Junko MuraiInstitute for Advanced Biosciences, Keio University, 997-0052 Yamagata, Japan.
Liton Kumar SahaDevelopmental Therapeutics Branch, Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20814.
Lisa M Miller JenkinsLaboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892.ORCID 0000-0003-1245-1338
Yves PommierDevelopmental Therapeutics Branch, Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20814; ukhyun.jo@nih.gov yves.pommier@nih.gov.
National Cancer Institute · USNational Center for Advancing Translational Sciences · USKeio University · 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
Trans-NIH RNAi Facility (TNRF)ZICTR000041 · NCATS · NATIONAL CENTER FOR ADVANCING TRANSLATIONAL SCIENCES · PI CHENG, KEN · 2015 to 2025
$9.4M
CPTR - Mass Spectrometry UnitZICBC011430 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI JENKINS, LISA · 2012 to 2025
$9.4M
6 · The paper itself

Abstract

Schlafen-11 (SLFN11) inactivation in ∼50% of cancer cells confers broad chemoresistance. To identify therapeutic targets and underlying molecular mechanisms for overcoming chemoresistance, we performed an unbiased genome-wide RNAi screen in

Indexed as

DNA ReplicationProteolysisAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsCell Line, TumorCheckpoint Kinase 1Chromosomes, HumanCullin ProteinsDNA-Binding ProteinsDNA DamageDrug Resistance, NeoplasmEnzyme StabilityGenome, HumanHumansMitosisModels, BiologicalAtaxia Telangiectasia Mutated ProteinsCDT1 protein, humanCell Cycle ProteinsCheckpoint Kinase 1CHEK1 protein, humanCUL4A protein, humanCullin ProteinsDDB1 protein, humanDNA-Binding ProteinsNuclear ProteinsProtein Kinase InhibitorsSLFN11 protein, humanATR/CHK1 inhibitorCDT1CUL4SLFN11

Identifiers

PMID33536335
PMCPMC8017720
OpenAlexW3126675804

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.