Evidence map›Paper›PMID 25931565›Full record

ArticleScience (New York, N.Y.)2015

DNA repair. Proteomics reveals dynamic assembly of repair complexes during bypass of DNA cross-links.

Markus Räschle, Godelieve Smeenk, Rebecca K Hansen, Tikira Temu, Yasuyoshi Oka, Marco Y Hein, Nagarjuna Nagaraj, David T Long, Johannes C Walter, Kay Hofmann and 5 more

Open access · greenAbstract read
In one paragraph

Article in Science (New York, N.Y.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 170 papers.

0numbers the graph read from it
0cells of the map it votes in
170citing papers in PubMed
10.4field-weighted citation impact, top 1% 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

170 citing papers in PubMed, 236 citations in OpenAlex.

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  12. C1orf112 promotes breast cancer growth by modulating the cell cycle.Frontiers in bioengineering and biotechnology · 2026
    Article
  13. Review
  14. RecessiveDiagnostics (Basel, Switzerland) · 2025
    Article
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110 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

15 authors at 3 institutions in 2 countries.

Markus RäschleDepartment of Proteomics and Signal Transduction, Max Planck Institute of Biochemistry, 82152 Martinsried, Germany.
Godelieve SmeenkUbiquitin Signaling Group, Department of Disease Biology, Novo Nordisk Foundation Center for Protein Research, University of Copenhagen, DK-2200 Copenhagen, Denmark.
Rebecca K HansenUbiquitin Signaling Group, Department of Disease Biology, Novo Nordisk Foundation Center for Protein Research, University of Copenhagen, DK-2200 Copenhagen, Denmark.
Tikira TemuDepartment of Proteomics and Signal Transduction, Max Planck Institute of Biochemistry, 82152 Martinsried, Germany.
Yasuyoshi OkaUbiquitin Signaling Group, Department of Disease Biology, Novo Nordisk Foundation Center for Protein Research, University of Copenhagen, DK-2200 Copenhagen, Denmark.
Marco Y HeinDepartment of Proteomics and Signal Transduction, Max Planck Institute of Biochemistry, 82152 Martinsried, Germany.
Nagarjuna NagarajDepartment of Proteomics and Signal Transduction, Max Planck Institute of Biochemistry, 82152 Martinsried, Germany.
David T LongHoward Hughes Medical Institute and Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA.
Johannes C WalterHoward Hughes Medical Institute and Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA.
Kay HofmannInstitute of Genetics, University of Cologne, 50674 Cologne, Germany.
Zuzana StorchovaMaintenance of Genome Stability Group, Max Planck Institute of Biochemistry, 82152 Martinsried, Germany.
Jürgen CoxDepartment of Proteomics and Signal Transduction, Max Planck Institute of Biochemistry, 82152 Martinsried, Germany.
Simon Bekker-JensenUbiquitin Signaling Group, Department of Disease Biology, Novo Nordisk Foundation Center for Protein Research, University of Copenhagen, DK-2200 Copenhagen, Denmark. simon.bekker-jensen@cpr.ku.dk niels.mailand@cpr.ku.dk mmann@biochem.mpg.de.
Niels MailandUbiquitin Signaling Group, Department of Disease Biology, Novo Nordisk Foundation Center for Protein Research, University of Copenhagen, DK-2200 Copenhagen, Denmark. simon.bekker-jensen@cpr.ku.dk niels.mailand@cpr.ku.dk mmann@biochem.mpg.de.
Matthias MannDepartment of Proteomics and Signal Transduction, Max Planck Institute of Biochemistry, 82152 Martinsried, Germany. Novo Nordisk Foundation Center for Protein Research, Proteomics Program, University of Copenhagen, DK-2200 Copenhagen, Denmark. simon.bekker-jensen@cpr.ku.dk niels.mailand@cpr.ku.dk mmann@biochem.mpg.de.
Max Planck Institute of Biochemistry · DEHoward Hughes Medical Institute · USUniversity of Cologne · DE

Funding

The Fanconi anemia pathway: role in DNA interstrand cross-link repairR01HL098316 · NHLBI · HARVARD MEDICAL SCHOOL · PI Johannes Walter · 2010 to 2026
$6.3M
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 K99 GM102325
6 · The paper itself

Abstract

DNA interstrand cross-links (ICLs) block replication fork progression by inhibiting DNA strand separation. Repair of ICLs requires sequential incisions, translesion DNA synthesis, and homologous recombination, but the full set of factors involved in these transactions remains unknown. We devised a technique called chromatin mass spectrometry (CHROMASS) to study protein recruitment dynamics during perturbed DNA replication in Xenopus egg extracts. Using CHROMASS, we systematically monitored protein assembly and disassembly on ICL-containing chromatin. Among numerous prospective DNA repair factors, we identified SLF1 and SLF2, which form a complex with RAD18 and together define a pathway that suppresses genome instability by recruiting the SMC5/6 cohesion complex to DNA lesions. Our study provides a global analysis of an entire DNA repair pathway and reveals the mechanism of SMC5/6 relocalization to damaged DNA in vertebrate cells.

Indexed as

DNA DamageDNA RepairDNA ReplicationAnimalsChromatinDNA-Binding ProteinsDNA Repair EnzymesMass SpectrometryProteomicsRNA-Binding ProteinsXenopusChromatinDNA-Binding ProteinsDNA Repair EnzymesRNA-Binding Proteins

Identifiers

PMID25931565
PMCPMC5331883
OpenAlexW1994045445

What OpenQuestion holds

Textmetadata
LicenceTDM
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.