Evidence map›Paper›PMID 25219499›Full record

ArticleMolecular cell2014

BRCA1 promotes unloading of the CMG helicase from a stalled DNA replication fork.

David T Long, Vladimir Joukov, Magda Budzowska, Johannes C Walter

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed, 1 pooled it
7.4field-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

81 citing papers in PubMed, 1 synthesis or guideline pooled it, 122 citations in OpenAlex.

  1. Pooled it
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  17. BRCA1 and Breast Cancer: Molecular Mechanisms and Therapeutic Strategies.Frontiers in cell and developmental biology · 2022
    Review
  18. Article
  19. Coordinating DNA Replication and Mitosis through Ubiquitin/SUMO and CDK1.International journal of molecular sciences · 2021
    Review
  20. Article

21 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

4 authors at 2 institutions in 1 country.

David T LongDepartment of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA.
Vladimir JoukovDepartment of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA.
Magda BudzowskaDepartment of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA.
Johannes C WalterDepartment of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA; Howard Hughes Medical Institute, Harvard Medical School, Boston, MA 02115, USA. Electronic address: johannes_walter@hms.harvard.edu.
Harvard University · USHoward Hughes Medical Institute · US

Funding

The Fanconi anemia pathway: role in DNA interstrand cross-link repairR01HL098316 · NHLBI · HARVARD MEDICAL SCHOOL · PI Johannes Walter · 2010 to 2026
$6.3M
The mechanism of vertebrate DNA replication terminationR01GM080676 · NIGMS · HARVARD MEDICAL SCHOOL · PI WALTER, JOHANNES · 2007 to 2019
$3.7M
Dynamics of BRCA1-Mediated Double-Strand Break RepairK99GM102325 · NIGMS · HARVARD MEDICAL SCHOOL · PI LONG, DAVID THOMAS · 2013 to 2014
$112k
Howard Hughes Medical InstituteNHLBI NIH HHS HL098316NHLBI NIH HHS R01 HL098316NIGMS NIH HHS GM80676NIGMS NIH HHS K99 GM102325NIGMS NIH HHS K99GM102325NIGMS NIH HHS R01 GM080676
6 · The paper itself

Abstract

The tumor suppressor protein BRCA1 promotes homologous recombination (HR), a high-fidelity mechanism to repair DNA double-strand breaks (DSBs) that arise during normal replication and in response to DNA-damaging agents. Recent genetic experiments indicate that BRCA1 also performs an HR-independent function during the repair of DNA interstrand crosslinks (ICLs). Here we show that BRCA1 is required to unload the CMG helicase complex from chromatin after replication forks collide with an ICL. Eviction of the stalled helicase allows leading strands to be extended toward the ICL, followed by endonucleolytic processing of the crosslink, lesion bypass, and DSB repair. Our results identify BRCA1-dependent helicase unloading as a critical, early event in ICL repair.

Indexed as

Models, GeneticAnimalsBRCA1 ProteinChromatinDNA-Binding ProteinsDNA Breaks, Double-StrandedDNA HelicasesDNA RepairDNA ReplicationSignal TransductionUbiquitinXenopus laevisXenopus ProteinsBRCA1 ProteinChromatinDNA-Binding ProteinsDNA HelicasesUbiquitinXenopus Proteins

Identifiers

PMID25219499
PMCPMC4185004
OpenAlexW2084915123

What OpenQuestion holds

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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.