Evidence map›Paper›PMID 34887904›Full record

ReviewFrontiers in genetics2021

RAD52: Paradigm of Synthetic Lethality and New Developments.

Matthew J Rossi, Sarah F DiDomenico, Mikir Patel, Alexander V Mazin

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.3field-weighted citation impact, top 6% 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

36 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Targeting RAD52 overcomes PARP inhibitor resistance in preclinicalbioRxiv : the preprint server for biology · 2025
    Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. A new wave of innovations within the DNA damage response.Signal transduction and targeted therapy · 2023
    Review
  20. 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

4 authors at 1 institution in 1 country.

Matthew J RossiDepartment of Biochemistry and Structural Biology, University of Texas Health Science Center, San Antonio, TX, United States.
Sarah F DiDomenicoDepartment of Biochemistry and Structural Biology, University of Texas Health Science Center, San Antonio, TX, United States.
Mikir PatelDepartment of Biochemistry and Structural Biology, University of Texas Health Science Center, San Antonio, TX, United States.
Alexander V MazinDepartment of Biochemistry and Structural Biology, University of Texas Health Science Center, San Antonio, TX, United States.
The University of Texas Health Science Center at San Antonio · US

Funding

AML mutation-guided drugging of DNA repairR01CA237286 · NCI · TEMPLE UNIV OF THE COMMONWEALTH · PI MAZIN, ALEXANDER V, SKORSKI, TOMASZ · 2020 to 2024
$2.8M
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 R01 CA188347NCI NIH HHS R01 CA237286NIGMS NIH HHS R01 GM136717
6 · The paper itself

Abstract

DNA double-strand breaks and inter-strand cross-links are the most harmful types of DNA damage that cause genomic instability that lead to cancer development. The highest fidelity pathway for repairing damaged double-stranded DNA is termed Homologous recombination (HR). Rad52 is one of the key HR proteins in eukaryotes. Although it is critical for most DNA repair and recombination events in yeast, knockouts of mammalian RAD52 lack any discernable phenotypes. As a consequence, mammalian RAD52 has been long overlooked. That is changing now, as recent work has shown RAD52 to be critical for backup DNA repair pathways in HR-deficient cancer cells. Novel findings have shed light on RAD52's biochemical activities. RAD52 promotes DNA pairing (D-loop formation), single-strand DNA and DNA:RNA annealing, and inverse strand exchange. These activities contribute to its multiple roles in DNA damage repair including HR, single-strand annealing, break-induced replication, and RNA-mediated repair of DNA. The contributions of RAD52 that are essential to the viability of HR-deficient cancer cells are currently under investigation. These new findings make RAD52 an attractive target for the development of anti-cancer therapies against BRCA-deficient cancers.

Indexed as

break induced replicationhomologous recombinationRad52single strand annealingsynthetic lethality

Identifiers

PMID34887904
PMCPMC8650160
OpenAlexW3215731027

What OpenQuestion holds

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LicenceCC BY
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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.