Evidence map›Paper›PMID 11980720›Full record

ArticleThe EMBO journal2002

WSTF-ISWI chromatin remodeling complex targets heterochromatic replication foci.

Ludmila Bozhenok, Paul A Wade, Patrick Varga-Weisz

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 110 papers.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed
11.1field-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

110 citing papers in PubMed, 238 citations in OpenAlex.

  1. Review
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  6. Professor Emma Whitelaw, a pioneer of epigenetic inheritance.Frontiers in epigenetics and epigenomics · 2025
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50 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Ludmila BozhenokMarie Curie Research Institute, Oxted, Surrey RH8 0TL, UK.
Paul A Wade
Patrick Varga-Weisz
Marie Curie · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Williams Syndrome Transcription Factor (WSTF), the product of the WBSCR9 gene, is invariably deleted in the haploinsufficiency Williams-Beuren Syndrome. Along with the nucleosome-dependent ATPase ISWI, WSTF forms a novel chromatin remodeling complex, WICH (WSTF-ISWI chromatin remodeling complex), which is conserved in vertebrates. The WICH complex was purified to homogeneity from Xenopus egg extract and was found to contain only WSTF and ISWI. In mouse cells, WSTF interacts with the SNF2H isoform of ISWI. WSTF accumulates in pericentric heterochromatin coincident with the replication of these structures, suggesting a role for WSTF in the replication of heterochromatin. Such a role is supported by the in vitro activity of both the mouse and frog WICH complexes: they are involved in the assembly of regular spaced nucleosomal arrays. In contrast to the related ISWI-interacting protein ACF1/WCRF180, WSTF binds stably to mitotic chromosomes. As dysfunction of other chromatin remodeling factors often has severe effects on development, haploinsufficiency of WSTF may explain some of the phenotypes associated with this disease.

Indexed as

Adenosine TriphosphatasesAnimalsBromodomain Containing ProteinsFemaleGene DeletionHeLa CellsHeterochromatinHumansMacromolecular SubstancesMiceNucleosomesOocytesReplication OriginStem CellsTranscription FactorsWilliams SyndromeAdenosine TriphosphatasesBAZ1B protein, humanBaz1b protein, mouseBromodomain Containing ProteinsHeterochromatinISWI proteinMacromolecular SubstancesNucleosomesTranscription Factors

Identifiers

PMID11980720
PMCPMC125993
OpenAlexW2153612581

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.