Evidence map›Paper›PMID 28334891›Full record

ArticleNucleic acids research2017

RAD51 interconnects between DNA replication, DNA repair and immunity.

Souparno Bhattacharya, Kalayarasan Srinivasan, Salim Abdisalaam, Fengtao Su, Prithvi Raj, Igor Dozmorov, Ritu Mishra, Edward K Wakeland, Subroto Ghose, Shibani Mukherjee and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
112citing papers in PubMed, 1 pooled it
6.7field-weighted citation impact, top 2% 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

112 citing papers in PubMed, 1 synthesis or guideline pooled it, 164 citations in OpenAlex.

  1. Pooled it
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  16. Role of BRCA1 in glioblastoma etiology.Cellular oncology (Dordrecht, Netherlands) · 2024
    Review
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52 more citing papers are in PubMed but not listed here.

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

11 authors at 1 institution in 1 country.

Souparno BhattacharyaDepartment of Radiation Oncology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Kalayarasan SrinivasanDepartment of Radiation Oncology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Salim AbdisalaamDepartment of Radiation Oncology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Fengtao SuDepartment of Radiation Oncology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Prithvi RajDepartment of Immunology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Igor DozmorovDepartment of Immunology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Ritu MishraDepartment of Radiation Oncology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Edward K WakelandDepartment of Immunology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Subroto GhoseDepartment of Molecular Psychiatry, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Shibani MukherjeeDepartment of Molecular Psychiatry, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Aroumougame AsaithambyDepartment of Radiation Oncology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
The University of Texas Southwestern Medical Center · US

Funding

Molecular Roles for Werner Syndrome Protein in Replication Fork MaintenanceR01AG053341 · NIA · UT SOUTHWESTERN MEDICAL CENTER · PI AROUMOUGAME, ASAITHAMBY · 2016 to 2020
$1.7M
NIA NIH HHS R01 AG053341
6 · The paper itself

Abstract

RAD51, a multifunctional protein, plays a central role in DNA replication and homologous recombination repair, and is known to be involved in cancer development. We identified a novel role for RAD51 in innate immune response signaling. Defects in RAD51 lead to the accumulation of self-DNA in the cytoplasm, triggering a STING-mediated innate immune response after replication stress and DNA damage. In the absence of RAD51, the unprotected newly replicated genome is degraded by the exonuclease activity of MRE11, and the fragmented nascent DNA accumulates in the cytosol, initiating an innate immune response. Our data suggest that in addition to playing roles in homologous recombination-mediated DNA double-strand break repair and replication fork processing, RAD51 is also implicated in the suppression of innate immunity. Thus, our study reveals a previously uncharacterized role of RAD51 in initiating immune signaling, placing it at the hub of new interconnections between DNA replication, DNA repair, and immunity.

Indexed as

DNA ReplicationCell Line, TumorDNADNA-Binding ProteinsDNA Breaks, Double-StrandedEpithelial CellsFibroblastsGenes, ReporterHumansHydroxamic AcidsImmunity, InnateLuminescent ProteinsMembrane ProteinsMRE11 Homologue ProteinPyrimidinonesRad51 Recombinase6-(4-hydroxyphenyl)-2-thioxo-2,3-dihydro-4(1H)-pyrimidinoneDNADNA-Binding ProteinsHydroxamic AcidsLuminescent ProteinsMembrane ProteinsMRE11 Homologue ProteinMRE11 protein, humanPyrimidinonesRAD51 protein, humanRad51 RecombinaseRed Fluorescent ProteinSTING1 protein, humanSTING ProteinThionesVorinostat

Identifiers

PMID28334891
PMCPMC5416901
OpenAlexW2590759939

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.