Evidence map›Paper›PMID 24347639›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

Tumor suppressor and deubiquitinase BAP1 promotes DNA double-strand break repair.

Helen Yu, Helen Pak, Ian Hammond-Martel, Mehdi Ghram, Amélie Rodrigue, Salima Daou, Haithem Barbour, Luc Corbeil, Josée Hébert, Elliot Drobetsky and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 219 papers.

0numbers the graph read from it
0cells of the map it votes in
219citing papers in PubMed
8.4field-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

219 citing papers in PubMed, 383 citations in OpenAlex.

  1. Trial
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  7. Regulation of ferroptosis by BAP1.Cell death and differentiation · 2026
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  9. Phenotype-Specific Recalibration of MAVE Data Enables Repurposing ofmedRxiv : the preprint server for health sciences · 2026
    Article
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159 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

13 authors at 3 institutions in 1 country.

Helen YuMaisonneuve-Rosemont Hospital Research Center, Department of Medicine, Université de Montréal, Montréal, QC, Canada H1T 2M4.
Helen Pak
Ian Hammond-Martel
Mehdi Ghram
Amélie Rodrigue
Salima Daou
Haithem Barbour
Luc Corbeil
Josée Hébert
Elliot Drobetsky
Jean Yves Masson
Javier M Di Noia
El Bachir Affar
Hôpital Maisonneuve-Rosemont · CAUniversité de Montréal · CAUniversité Laval · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

The cellular response to highly genotoxic DNA double-strand breaks (DSBs) involves the exquisite coordination of multiple signaling and repair factors. Here, we conducted a functional RNAi screen and identified BAP1 as a deubiquitinase required for efficient assembly of the homologous recombination (HR) factors BRCA1 and RAD51 at ionizing radiation (IR) -induced foci. BAP1 is a chromatin-associated protein frequently inactivated in cancers of various tissues. To further investigate the role of BAP1 in DSB repair, we used a gene targeting approach to knockout (KO) this deubiquitinase in chicken DT40 cells. We show that BAP1-deficient cells are (i) sensitive to IR and other agents that induce DSBs, (ii) defective in HR-mediated immunoglobulin gene conversion, and (iii) exhibit an increased frequency of chromosomal breaks after IR treatment. We also show that BAP1 is recruited to chromatin in the proximity of a single site-specific I-SceI-induced DSB. Finally, we identified six IR-induced phosphorylation sites in BAP1 and showed that mutation of these residues inhibits BAP1 recruitment to DSB sites. We also found that both BAP1 catalytic activity and its phosphorylation are critical for promoting DNA repair and cellular recovery from DNA damage. Our data reveal an important role for BAP1 in DSB repair by HR, thereby providing a possible molecular basis for its tumor suppressor function.

Indexed as

DNA Breaks, Double-StrandedDNA RepairGene Expression Regulation, NeoplasticHomologous RecombinationAnimalsBRCA1 ProteinCell LineCell Line, TumorChickensDNA DamageHEK293 CellsHeLa CellsHumansImmunoglobulinsMCF-7 CellsMicroscopy, FluorescenceBAP1 protein, humanBRCA1 ProteinBRCA1 protein, humanImmunoglobulinsRAD51 protein, humanRad51 RecombinaseTumor Suppressor ProteinsUbiquitin Thiolesterase

Identifiers

PMID24347639
PMCPMC3890818
OpenAlexW2072355125

What OpenQuestion holds

Textmetadata
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.