Evidence map›Paper›PMID 32542389›Full record

ArticleNucleic acids research2020

Genome-wide CRISPR synthetic lethality screen identifies a role for the ADP-ribosyltransferase PARP14 in DNA replication dynamics controlled by ATR.

Ashna Dhoonmoon, Emily M Schleicher, Kristen E Clements, Claudia M Nicolae, George-Lucian Moldovan

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 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.8field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 30 citations in OpenAlex.

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  12. A small-molecule inhibitor of TopBP1 exerts anti-MYC activity and synergy with PARP inhibitors.Proceedings of the National Academy of Sciences of the United States of America · 2023
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  19. Research Progress on Mono-ADP-Ribosyltransferases in Human Cell Biology.Frontiers in cell and developmental biology · 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

5 authors at 1 institution in 1 country.

Ashna DhoonmoonDepartment of Biochemistry and Molecular Biology, The Pennsylvania State University College of Medicine, Hershey, PA 17033, USA.
Emily M SchleicherDepartment of Biochemistry and Molecular Biology, The Pennsylvania State University College of Medicine, Hershey, PA 17033, USA.
Kristen E ClementsDepartment of Biochemistry and Molecular Biology, The Pennsylvania State University College of Medicine, Hershey, PA 17033, USA.
Claudia M NicolaeDepartment of Biochemistry and Molecular Biology, The Pennsylvania State University College of Medicine, Hershey, PA 17033, USA.
George-Lucian MoldovanDepartment of Biochemistry and Molecular Biology, The Pennsylvania State University College of Medicine, Hershey, PA 17033, USA.
Pennsylvania State University · US

Funding

The Role of Mono-ADP-Ribosylation by PARP14 in RadioresistanceR01ES026184 · NIEHS · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI George Lucian Moldovan · 2016 to 2026
$3.6M
The role of DNA damage tolerance pathways in human cellsR01GM134681 · NIGMS · UNIVERSITY OF VIRGINIA · PI George Lucian Moldovan, Claudia M Nicolae · 2019 to 2026
$3.0M
Novel roles of PARP10-mediated Genomic Stability and Cellular TransformationF31CA243301 · NCI · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI SCHLEICHER, EMILY · 2019 to 2021
$90k
NCI NIH HHS F31 CA243301NIEHS NIH HHS R01 ES026184NIGMS NIH HHS R01 GM134681
6 · The paper itself

Abstract

The DNA damage response is essential to maintain genomic stability, suppress replication stress, and protect against carcinogenesis. The ATR-CHK1 pathway is an essential component of this response, which regulates cell cycle progression in the face of replication stress. PARP14 is an ADP-ribosyltransferase with multiple roles in transcription, signaling, and DNA repair. To understand the biological functions of PARP14, we catalogued the genetic components that impact cellular viability upon loss of PARP14 by performing an unbiased, comprehensive, genome-wide CRISPR knockout genetic screen in PARP14-deficient cells. We uncovered the ATR-CHK1 pathway as essential for viability of PARP14-deficient cells, and identified regulation of DNA replication dynamics as an important mechanistic contributor to the synthetic lethality observed. Our work shows that PARP14 is an important modulator of the response to ATR-CHK1 pathway inhibitors.

Indexed as

DNA ReplicationSynthetic Lethal MutationsAtaxia Telangiectasia Mutated ProteinsCell Line, TumorCheckpoint Kinase 1CRISPR-Cas SystemsHumansPoly(ADP-ribose) PolymerasesAtaxia Telangiectasia Mutated ProteinsATR protein, humanCheckpoint Kinase 1CHEK1 protein, humanPARP14 protein, humanPoly(ADP-ribose) Polymerases

Identifiers

PMID32542389
PMCPMC7367200
OpenAlexW3034378985

What Socratic 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 Socratic graph.