Evidence map›Paper›PMID 25567982›Full record

ArticleNucleic acids research2015

Bcl2 inhibits recruitment of Mre11 complex to DNA double-strand breaks in response to high-linear energy transfer radiation.

Maohua Xie, Dongkyoo Park, Shuo You, Rui Li, Taofeek K Owonikoko, Ya Wang, Paul W Doetsch, Xingming Deng

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

15 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. MRN complex is an essential effector of DNA damage repair.Journal of Zhejiang University. Science. B · 2021
    Review
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  6. 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

8 authors at 2 institutions in 1 country.

Maohua XieDepartments of Radiation Oncology, Division of Cancer Biology, Emory University School of Medicine and Winship Cancer Institute of Emory University, Atlanta, Georgia 30322, USA.
Dongkyoo ParkDepartments of Radiation Oncology, Division of Cancer Biology, Emory University School of Medicine and Winship Cancer Institute of Emory University, Atlanta, Georgia 30322, USA.
Shuo YouDepartments of Radiation Oncology, Division of Cancer Biology, Emory University School of Medicine and Winship Cancer Institute of Emory University, Atlanta, Georgia 30322, USA.
Rui LiDepartments of Radiation Oncology, Division of Cancer Biology, Emory University School of Medicine and Winship Cancer Institute of Emory University, Atlanta, Georgia 30322, USA.
Taofeek K OwonikokoHematology and Medical Oncology, Emory University School of Medicine and Winship Cancer Institute of Emory University, Atlanta, Georgia 30322, USA.
Ya WangDepartments of Radiation Oncology, Division of Cancer Biology, Emory University School of Medicine and Winship Cancer Institute of Emory University, Atlanta, Georgia 30322, USA.
Paul W DoetschDepartments of Radiation Oncology, Division of Cancer Biology, Emory University School of Medicine and Winship Cancer Institute of Emory University, Atlanta, Georgia 30322, USA Biochemistry, Emory University School of Medicine and Winship Cancer Institute of Emory University, Atlanta, Georgia 30322, USA.
Xingming DengDepartments of Radiation Oncology, Division of Cancer Biology, Emory University School of Medicine and Winship Cancer Institute of Emory University, Atlanta, Georgia 30322, USA xdeng4@emory.edu.
Emory University · USWinship Cancer Institute

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High-linear energy transfer ionizing radiation, derived from high charge (Z) and energy (E) (HZE) particles, induces clustered/complex DNA double-strand breaks (DSBs) that include small DNA fragments, which are not repaired by the non-homologous end-joining (NHEJ) pathway. The homologous recombination (HR) DNA repair pathway plays a major role in repairing DSBs induced by HZE particles. The Mre11 complex (Mre11/Rad50/NBS1)-mediated resection of DSB ends is a required step in preparing for DSB repair via the HR DNA repair pathway. Here we found that expression of Bcl2 results in decreased HR activity and retards the repair of DSBs induced by HZE particles (i.e. (56)iron and (28)silicon) by inhibiting Mre11 complex activity. Exposure of cells to (56)iron or (28)silicon promotes Bcl2 to interact with Mre11 via the BH1 and BH4 domains. Purified Bcl2 protein directly suppresses Mre11 complex-mediated DNA resection in vitro. Expression of Bcl2 reduces the ability of Mre11 to bind DNA following exposure of cells to HZE particles. Our findings suggest that, after cellular exposure to HZE particles, Bcl2 may inhibit Mre11 complex-mediated DNA resection leading to suppression of the HR-mediated DSB repair in surviving cells, which may potentially contribute to tumor development.

Indexed as

DNA Breaks, Double-StrandedDNA RepairCell LineCell NucleusDNADNA-Binding ProteinsHistonesHomologous RecombinationHumansIntracellular Signaling Peptides and ProteinsLinear Energy TransferMRE11 Homologue ProteinProtein Interaction Domains and MotifsProto-Oncogene Proteins c-bcl-2Radiation, IonizingTumor Suppressor p53-Binding Protein 1DNADNA-Binding ProteinsH2AX protein, humanHistonesIntracellular Signaling Peptides and ProteinsMRE11 Homologue ProteinMRE11 protein, humanProto-Oncogene Proteins c-bcl-2TP53BP1 protein, humanTumor Suppressor p53-Binding Protein 1

Identifiers

PMID25567982
PMCPMC4333404
OpenAlexW2129030243

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.