Evidence map›Paper›PMID 34481157›Full record

ArticleDNA repair2021

The RNF8 and RNF168 Ubiquitin Ligases Regulate Pro- and Anti-Resection Activities at Broken DNA Ends During Non-Homologous End Joining.

Bo-Ruei Chen, Yinan Wang, Zih-Jie Shen, Amelia Bennett, Issa Hindi, Jessica K Tyler, Barry P Sleckman

Open access · hybridAbstract read
In one paragraph

Article in DNA repair, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

8 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Ubiquitin Proteasome Gene Signatures in Ependymoma Molecular Subtypes.International journal of molecular sciences · 2022
    Review
  6. Review
  7. Review
  8. Article
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.

Bo-Ruei ChenDivision of Hematology and Oncology, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, 35233, United States; O'Neal Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL, 35233, United States.
Yinan WangDepartment of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, NY, 10065, United States.
Zih-Jie ShenDepartment of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, NY, 10065, United States.
Amelia BennettDepartment of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, NY, 10065, United States.
Issa HindiDepartment of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, NY, 10065, United States.
Jessica K TylerDepartment of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, NY, 10065, United States.
Barry P SleckmanDivision of Hematology and Oncology, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, 35233, United States; O'Neal Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL, 35233, United States. Electronic address: bps@uab.edu.
Cornell University · USUniversity of Alabama at Birmingham · US

Funding

THE V(D)J RECOMBINATION REACTION AND ITS IMPACT ON LYMPHOCYTE DEVELOPMENTR01AI047829 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI SLECKMAN, BARRY P · 2000 to 2021
$7.0M
ATM FUNCTION DURING V(D)J RECOMBINATIONR01AI074953 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI SLECKMAN, BARRY P · 2009 to 2023
$5.9M
Chromatin's Role in Repair of Radiation-induced Damage.R01CA095641 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI TYLER, JESSICA K · 2002 to 2023
$5.2M
Chromatin Assembly, Structure and FunctionR01GM064475 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI TYLER, JESSICA K · 2002 to 2019
$4.4M
Novel pathways that regulate DNA double-strand break repair events in mammalian cellsR35GM139816 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI TYLER, JESSICA K · 2021 to 2025
$2.1M
NCI NIH HHS R01 CA095641NIAID NIH HHS R01 AI047829NIAID NIH HHS R01 AI074953NIGMS NIH HHS R01 GM064475NIGMS NIH HHS R35 GM139816
6 · The paper itself

Abstract

The RING-type E3 ubiquitin ligases RNF8 and RNF168 recruit DNA damage response (DDR) factors to chromatin flanking DNA double strand breaks (DSBs) including 53BP1, which protects DNA ends from resection during DNA DSB repair by non-homologous end joining (NHEJ). Deficiency of RNF8 or RNF168 does not lead to demonstrable NHEJ defects, but like deficiency of 53BP1, the combined deficiency of XLF and RNF8 or RNF168 leads to diminished NHEJ in lymphocytes arrested in G

Indexed as

DNA-Binding ProteinsUbiquitinDNADNA End-Joining RepairDNA RepairTumor Suppressor p53-Binding Protein 1UbiquitinationUbiquitin-Protein LigasesDNADNA-Binding ProteinsTumor Suppressor p53-Binding Protein 1UbiquitinUbiquitin-Protein LigasesDNA end resectionNHEJRNF168RNF8V(D)J recombinationXLF

Identifiers

PMID34481157
PMCPMC9586520
OpenAlexW3198737610

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.