Evidence map›Paper›PMID 33275133›Full record

ArticleNucleic acids research2020

The function of RAD52 N-terminal domain is essential for viability of BRCA-deficient cells.

Kritika Hanamshet, Alexander V Mazin

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 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Targeting RAD52 overcomes PARP inhibitor resistance in preclinicalbioRxiv : the preprint server for biology · 2025
    Article
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  11. Review
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  15. Review
  16. Single-Strand Annealing in Cancer.International journal of molecular sciences · 2021
    Review
  17. Review
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

2 authors at 1 institution in 1 country.

Kritika HanamshetDepartment of Biochemistry and Molecular Biology, Drexel University College of Medicine, Philadelphia, PA 19102, USA.
Alexander V MazinDepartment of Biochemistry and Molecular Biology, Drexel University College of Medicine, Philadelphia, PA 19102, USA.
Drexel University · US

Funding

X-Ray Crystallography and Macromolecular CharacterizationP30CA056036 · NCI · THOMAS JEFFERSON UNIVERSITY · PI Andrew Chapman · 1995 to 2026
$94.8M
Small Molecule inhibitors as a new approach to study human RAD51 recombinaseR01CA188347 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI MAZIN, ALEXANDER V · 2015 to 2019
$2.5M
Mechanisms of RNA-dependent DNA repair in humansR01GM136717 · NIGMS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI MAZIN, ALEXANDER V · 2020 to 2023
$1.8M
NCI NIH HHS P30 CA056036NCI NIH HHS R01 CA188347NIGMS NIH HHS R01 GM136717
6 · The paper itself

Abstract

RAD52 is a member of the homologous recombination pathway that is important for survival of BRCA-deficient cells. Inhibition of RAD52 leads to lethality in BRCA-deficient cells. However, the exact mechanism of how RAD52 contributes to viability of BRCA-deficient cells remains unknown. Two major activities of RAD52 were previously identified: DNA or RNA pairing, which includes DNA/RNA annealing and strand exchange, and mediator, which is to assist RAD51 loading on RPA-covered ssDNA. Here, we report that the N-terminal domain (NTD) of RAD52 devoid of the potential mediator function is essential for maintaining viability of BRCA-deficient cells owing to its ability to promote DNA/RNA pairing. We show that RAD52 NTD forms nuclear foci upon DNA damage in BRCA-deficient human cells and promotes DNA double-strand break repair through two pathways: homology-directed repair (HDR) and single-strand annealing (SSA). Furthermore, we show that mutations in the RAD52 NTD that disrupt these activities fail to maintain viability of BRCA-deficient cells.

Indexed as

BRCA1 ProteinBreast NeoplasmsRad51 RecombinaseRad52 DNA Repair and Recombination ProteinRecombinational DNA RepairBRCA2 ProteinCell Line, TumorDNA DamageDNA, Single-StrandedFemaleGene Expression Regulation, NeoplasticGene Knockout TechniquesHumansMutationProtein BindingBRCA1 ProteinBRCA1 protein, humanBRCA2 ProteinBRCA2 protein, humanDNA, Single-StrandedRad51 RecombinaseRad52 DNA Repair and Recombination ProteinRAD52 protein, human

Identifiers

PMID33275133
PMCPMC7736796
OpenAlexW3110369638

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.