Evidence map›Paper›PMID 33440161›Full record

ArticleCell reports2021

RAD52 Adjusts Repair of Single-Strand Breaks via Reducing DNA-Damage-Promoted XRCC1/LIG3α Co-localization.

Jian Wang, You-Take Oh, Zhentian Li, Juan Dou, Siyuan Tang, Xiang Wang, Hongyan Wang, Shunichi Takeda, Ya Wang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

  1. Article
  2. The Influence of Circadian Rhythms on DNA Damage Repair in Skin Photoaging.International journal of molecular sciences · 2024
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
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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.

Jian WangDepartment of Radiation Oncology, Emory University School of Medicine and the Winship Cancer Institute of Emory University, Atlanta, GA 30322, USA.
You-Take OhDepartment of Radiation Oncology, Emory University School of Medicine and the Winship Cancer Institute of Emory University, Atlanta, GA 30322, USA.
Zhentian LiDepartment of Radiation Oncology, Emory University School of Medicine and the Winship Cancer Institute of Emory University, Atlanta, GA 30322, USA.
Juan DouDepartment of Radiation Oncology, Emory University School of Medicine and the Winship Cancer Institute of Emory University, Atlanta, GA 30322, USA.
Siyuan TangDepartment of Radiation Oncology, Emory University School of Medicine and the Winship Cancer Institute of Emory University, Atlanta, GA 30322, USA.
Xiang WangDepartment of Radiation Oncology, Emory University School of Medicine and the Winship Cancer Institute of Emory University, Atlanta, GA 30322, USA.
Hongyan WangDepartment of Radiation Oncology, Emory University School of Medicine and the Winship Cancer Institute of Emory University, Atlanta, GA 30322, USA.
Shunichi TakedaCREST Research Project, Radiation Genetics, Faculty of Medicine, Kyoto University, Yoshida-konoe, Sakyo-ku, Kyoto 606-8501, Japan. Electronic address: stakeda@rg.med.kyoto-u.ac.jp.
Ya WangDepartment of Radiation Oncology, Emory University School of Medicine and the Winship Cancer Institute of Emory University, Atlanta, GA 30322, USA. Electronic address: ywang94@emory.edu.

Funding

Winship Cancer Institute Cancer Center Support GrantP30CA138292 · NCI · EMORY UNIVERSITY · PI Suresh S Ramalingam · 2009 to 2026
$47.5M
miR-21 signaling in tumor response to radiation treatmentR01CA186129 · NCI · EMORY UNIVERSITY · PI WANG, YA · 2014 to 2018
$1.6M
Mechanism for miR-21-modulated radioresistanceR21CA185882 · NCI · EMORY UNIVERSITY · PI WANG, YA · 2015 to 2016
$373k
NCI NIH HHS P30 CA138292NCI NIH HHS R01 CA186129NCI NIH HHS R21 CA185882
6 · The paper itself

Abstract

Radiation sensitive 52 (RAD52) is an important factor for double-strand break repair (DSBR). However, deficiency in vertebrate/mammalian Rad52 has no apparent phenotype. The underlying mechanism remains elusive. Here, we report that RAD52 deficiency increased cell survival after camptothecin (CPT) treatment. CPT generates single-strand breaks (SSBs) that further convert to double-strand breaks (DSBs) if they are not repaired. RAD52 inhibits SSB repair (SSBR) through strong single-strand DNA (ssDNA) and/or poly(ADP-ribose) (PAR) binding affinity to reduce DNA-damage-promoted X-Ray Repair Cross Complementing 1 (XRCC1)/ligase IIIα (LIG3α) co-localization. The inhibitory effects of RAD52 on SSBR neutralize the role of RAD52 in DSBR, suggesting that RAD52 may maintain a balance between cell survival and genomic integrity. Furthermore, we demonstrate that blocking RAD52 oligomerization that disrupts RAD52's DSBR, while retaining its ssDNA binding capacity that is required for RAD52's inhibitory effects on SSBR, sensitizes cells to different DNA-damaging agents. This discovery provides guidance for developing efficient RAD52 inhibitors in cancer therapy.

Indexed as

DNA DamageAnimalsDNA Ligase ATPDNA, Single-StrandedHumansMicePoly-ADP-Ribose Binding ProteinsRad52 DNA Repair and Recombination ProteinX-ray Repair Cross Complementing Protein 1DNA Ligase ATPDNA, Single-StrandedPoly-ADP-Ribose Binding ProteinsRad52 DNA Repair and Recombination ProteinRAD52 protein, humanRad52 protein, mouseX-ray Repair Cross Complementing Protein 1XRCC1 protein, humanXrcc1 protein, mouseDNA damageDNA repairRAD52single-strand breaksXRCC1

Identifiers

PMID33440161
PMCPMC7872142

What OpenQuestion holds

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Registered trials

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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.