Evidence map›Paper›PMID 24990377›Full record

ArticleNucleic acids research2014

Human ISWI complexes are targeted by SMARCA5 ATPase and SLIDE domains to help resolve lesion-stalled transcription.

Özge Z Aydin, Jurgen A Marteijn, Cristina Ribeiro-Silva, Aida Rodríguez López, Nils Wijgers, Godelieve Smeenk, Haico van Attikum, Raymond A Poot, Wim Vermeulen, Hannes Lans

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% 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

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.

  1. Pooled it
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  12. Professor Emma Whitelaw, a pioneer of epigenetic inheritance.Frontiers in epigenetics and epigenomics · 2025
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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

10 authors at 2 institutions in 1 country.

Özge Z AydinDepartment of Genetics, Medical Genetics Cluster, Cancer Genomics Netherlands, Erasmus MC, Rotterdam, 3015 GE, The Netherlands.
Jurgen A MarteijnDepartment of Genetics, Medical Genetics Cluster, Cancer Genomics Netherlands, Erasmus MC, Rotterdam, 3015 GE, The Netherlands.
Cristina Ribeiro-SilvaDepartment of Genetics, Medical Genetics Cluster, Cancer Genomics Netherlands, Erasmus MC, Rotterdam, 3015 GE, The Netherlands.
Aida Rodríguez LópezDepartment of Genetics, Medical Genetics Cluster, Cancer Genomics Netherlands, Erasmus MC, Rotterdam, 3015 GE, The Netherlands.
Nils WijgersDepartment of Genetics, Medical Genetics Cluster, Cancer Genomics Netherlands, Erasmus MC, Rotterdam, 3015 GE, The Netherlands.
Godelieve SmeenkDepartment of Toxicogenetics, Leiden University Medical Center, Leiden, 2333 ZC, The Netherlands.
Haico van AttikumDepartment of Toxicogenetics, Leiden University Medical Center, Leiden, 2333 ZC, The Netherlands.
Raymond A PootDepartment of Cell Biology, Medical Genetics Cluster, Erasmus MC, Rotterdam, 3015 GE, The Netherlands.
Wim VermeulenDepartment of Genetics, Medical Genetics Cluster, Cancer Genomics Netherlands, Erasmus MC, Rotterdam, 3015 GE, The Netherlands.
Hannes LansDepartment of Genetics, Medical Genetics Cluster, Cancer Genomics Netherlands, Erasmus MC, Rotterdam, 3015 GE, The Netherlands w.lans@erasmusmc.nl.ORCID http://orcid.org/0000-0003-4417-5358
Erasmus MC · NLLeiden University Medical Center · NL

Funding

European Research Council 340988
6 · The paper itself

Abstract

Chromatin compaction of deoxyribonucleic acid (DNA) presents a major challenge to the detection and removal of DNA damage. Helix-distorting DNA lesions that block transcription are specifically repaired by transcription-coupled nucleotide excision repair, which is initiated by binding of the CSB protein to lesion-stalled RNA polymerase II. Using live cell imaging, we identify a novel function for two distinct mammalian ISWI adenosine triphosphate (ATP)-dependent chromatin remodeling complexes in resolving lesion-stalled transcription. Human ISWI isoform SMARCA5/SNF2H and its binding partners ACF1 and WSTF are rapidly recruited to UV-C induced DNA damage to specifically facilitate CSB binding and to promote transcription recovery. SMARCA5 targeting to UV-C damage depends on transcription and histone modifications and requires functional SWI2/SNF2-ATPase and SLIDE domains. After initial recruitment to UV damage, SMARCA5 re-localizes away from the center of DNA damage, requiring its HAND domain. Our studies support a model in which SMARCA5 targeting to DNA damage-stalled transcription sites is controlled by an ATP-hydrolysis-dependent scanning and proofreading mechanism, highlighting how SWI2/SNF2 chromatin remodelers identify and bind nucleosomes containing damaged DNA.

Indexed as

DNA RepairTranscription, GeneticAdenosine TriphosphatasesBromodomain Containing ProteinsCell LineChromatin Assembly and DisassemblyChromosomal Proteins, Non-HistoneDNA DamageDNA HelicasesDNA Repair EnzymesHistonesHumansPoly-ADP-Ribose Binding ProteinsProtein Structure, TertiaryTranscription FactorsUltraviolet RaysAdenosine TriphosphatasesBAZ1A protein, humanBAZ1B protein, humanBromodomain Containing ProteinsChromosomal Proteins, Non-HistoneDNA HelicasesDNA Repair EnzymesERCC6 protein, humanHistonesPoly-ADP-Ribose Binding ProteinsSMARCA5 protein, humanTranscription Factors

Identifiers

PMID24990377
PMCPMC4117783
OpenAlexW2100871132

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.