Evidence map›Paper›PMID 30154076›Full record

ArticleThe EMBO journal2018

SHLD2/FAM35A co-operates with REV7 to coordinate DNA double-strand break repair pathway choice.

Steven Findlay, John Heath, Vincent M Luo, Abba Malina, Théo Morin, Yan Coulombe, Billel Djerir, Zhigang Li, Arash Samiei, Estelle Simo-Cheyou and 17 more

Open access · hybridAbstract read
In one paragraph

Article in The EMBO journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed, 1 pooled it
6.9field-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

95 citing papers in PubMed, 1 synthesis or guideline pooled it, 155 citations in OpenAlex.

  1. Pooled it
  2. Mechanisms and disease relevance of DNA break repair pathway choice.Nature reviews. Molecular cell biology · 2026
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  12. eLife · 2024
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35 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

27 authors at 7 institutions in 2 countries.

Steven FindlayLady Davis Institute for Medical Research, Segal Cancer Centre, Jewish General Hospital, Montreal, QC, Canada.
John HeathLady Davis Institute for Medical Research, Segal Cancer Centre, Jewish General Hospital, Montreal, QC, Canada.
Vincent M LuoLady Davis Institute for Medical Research, Segal Cancer Centre, Jewish General Hospital, Montreal, QC, Canada.
Abba MalinaLady Davis Institute for Medical Research, Segal Cancer Centre, Jewish General Hospital, Montreal, QC, Canada.ORCID 0000-0002-8511-9005
Théo MorinDepartment of Biology, Université de Sherbrooke, Sherbrooke, QC, Canada.
Yan CoulombeGenome Stability Laboratory, CHU de Québec Research Center, Quebec City, QC, Canada.
Billel DjerirDepartment of Biology, Université de Sherbrooke, Sherbrooke, QC, Canada.
Zhigang LiLady Davis Institute for Medical Research, Segal Cancer Centre, Jewish General Hospital, Montreal, QC, Canada.
Arash SamieiLady Davis Institute for Medical Research, Segal Cancer Centre, Jewish General Hospital, Montreal, QC, Canada.
Estelle Simo-CheyouLady Davis Institute for Medical Research, Segal Cancer Centre, Jewish General Hospital, Montreal, QC, Canada.
Martin KaramDivision of Experimental Medicine, McGill University, Montreal, QC, Canada.
Halil BagciInstitut de Recherches Cliniques de Montréal (IRCM), Montreal, QC, Canada.
Dolev RahatDepartment of Developmental Biology and Cancer Research, The Institute for Medical Research Israel-Canada, The Hebrew University of Jerusalem, Jerusalem, Israel.
Damien GraptonLady Davis Institute for Medical Research, Segal Cancer Centre, Jewish General Hospital, Montreal, QC, Canada.
Elise G LavoieLady Davis Institute for Medical Research, Segal Cancer Centre, Jewish General Hospital, Montreal, QC, Canada.
Christian DoveLady Davis Institute for Medical Research, Segal Cancer Centre, Jewish General Hospital, Montreal, QC, Canada.
Husam KhaledLady Davis Institute for Medical Research, Segal Cancer Centre, Jewish General Hospital, Montreal, QC, Canada.
Hellen KuasneRosalind and Morris Goodman Cancer Research Centre, McGill University, Montreal, QC, Canada.
Koren K MannLady Davis Institute for Medical Research, Segal Cancer Centre, Jewish General Hospital, Montreal, QC, Canada.
Kathleen Oros KleinLady Davis Institute for Medical Research, Segal Cancer Centre, Jewish General Hospital, Montreal, QC, Canada.
Celia M GreenwoodLady Davis Institute for Medical Research, Segal Cancer Centre, Jewish General Hospital, Montreal, QC, Canada.
Yuval TabachDepartment of Developmental Biology and Cancer Research, The Institute for Medical Research Israel-Canada, The Hebrew University of Jerusalem, Jerusalem, Israel.
Morag ParkRosalind and Morris Goodman Cancer Research Centre, McGill University, Montreal, QC, Canada.
Jean-Francois CôtéInstitut de Recherches Cliniques de Montréal (IRCM), Montreal, QC, Canada.ORCID 0000-0001-7055-2642
Jean-Yves MassonGenome Stability Laboratory, CHU de Québec Research Center, Quebec City, QC, Canada.
Alexandre MaréchalDepartment of Biology, Université de Sherbrooke, Sherbrooke, QC, Canada.
Alexandre OrthweinLady Davis Institute for Medical Research, Segal Cancer Centre, Jewish General Hospital, Montreal, QC, Canada alexandre.orthwein@mcgill.ca.ORCID 0000-0002-7350-3413
Jewish General Hospital · CAUniversité de Sherbrooke · CAGenome Canada · CAHebrew University of Jerusalem · ILMcGill University Health Centre · CAMontreal Clinical Research Institute · CAMcGill University · CA

Funding

CIHR 376245CIHR 376288
6 · The paper itself

Abstract

DNA double-strand breaks (DSBs) can be repaired by two major pathways: non-homologous end-joining (NHEJ) and homologous recombination (HR). DNA repair pathway choice is governed by the opposing activities of 53BP1, in complex with its effectors RIF1 and REV7, and BRCA1. However, it remains unknown how the 53BP1/RIF1/REV7 complex stimulates NHEJ and restricts HR to the S/G2 phases of the cell cycle. Using a mass spectrometry (MS)-based approach, we identify 11 high-confidence REV7 interactors and elucidate the role of SHLD2 (previously annotated as FAM35A and RINN2) as an effector of REV7 in the NHEJ pathway. FAM35A depletion impairs NHEJ-mediated DNA repair and compromises antibody diversification by class switch recombination (CSR) in B cells. FAM35A accumulates at DSBs in a 53BP1-, RIF1-, and REV7-dependent manner and antagonizes HR by limiting DNA end resection. In fact, FAM35A is part of a larger complex composed of REV7 and SHLD1 (previously annotated as C20orf196 and RINN3), which promotes NHEJ and limits HR Together, these results establish SHLD2 as a novel effector of REV7 in controlling the decision-making process during DSB repair.

Indexed as

DNA Breaks, Double-StrandedDNA End-Joining RepairCell Cycle ProteinsDNA-Binding ProteinsG2 PhaseHEK293 CellsHumansMad2 ProteinsS PhaseTelomere-Binding ProteinsTumor Suppressor p53-Binding Protein 1Cell Cycle ProteinsDNA-Binding ProteinsMAD2L2 protein, humanMad2 ProteinsRif1 protein, humanSHLD2 protein, humanTelomere-Binding ProteinsTP53BP1 protein, humanTumor Suppressor p53-Binding Protein 1DNA double‐strand breakDNA repair pathway choicenon‐homologous end‐joiningREV7

Identifiers

PMID30154076
PMCPMC6138439
OpenAlexW2952607431

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.