Evidence map›Paper›PMID 35197580›Full record

ArticleCommunications biology2022

H3K27ac nucleosomes facilitate HMGN localization at regulatory sites to modulate chromatin binding of transcription factors.

Shaofei Zhang, Yuri Postnikov, Alexei Lobanov, Takashi Furusawa, Tao Deng, Michael Bustin

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

23 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Epigenetic remodeling during early embryonic development.Frontiers in cell and developmental biology · 2026
    Review
  7. Article
  8. Article
  9. Article
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  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Regulation of Chromatin Architecture by Transcription Factor Binding.bioRxiv : the preprint server for biology · 2023
    Article
  20. Article
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

6 authors at 2 institutions in 1 country.

Shaofei ZhangProtein Section, Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, Maryland, USA.
Yuri PostnikovProtein Section, Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, Maryland, USA.
Alexei LobanovCCR Collaborative Bioinformatics Resource, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Takashi FurusawaProtein Section, Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, Maryland, USA.
Tao DengProtein Section, Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, Maryland, USA.
Michael BustinProtein Section, Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, Maryland, USA. bustinm@mail.nih.gov.ORCID http://orcid.org/0000-0002-5147-7242
National Cancer Institute · USNational Institutes of Health · US

Funding

Chromosomal Proteins and Chromosomal FunctionsZIABC004496 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI BUSTIN, MICHAEL · 2009 to 2023
$12.9M
Biological Functions of Chromosomal ProteinsZIABC011154 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI BUSTIN, MICHAEL · 2009 to 2023
$11.0M
CCR NIH HHS HHSN261200800001CNCI NIH HHS HHSN261200800001E
6 · The paper itself

Abstract

Nucleosomes containing acetylated H3K27 are a major epigenetic mark of active chromatin and identify cell-type specific chromatin regulatory regions which serve as binding sites for transcription factors. Here we show that the ubiquitous nucleosome binding proteins HMGN1 and HMGN2 bind preferentially to H3K27ac nucleosomes at cell-type specific chromatin regulatory regions. HMGNs bind directly to the acetylated nucleosome; the H3K27ac residue and linker DNA facilitate the preferential binding of HMGNs to the modified nucleosomes. Loss of HMGNs increases the levels of H3K27me3 and the histone H1 occupancy at enhancers and promoters and alters the interaction of transcription factors with chromatin. These experiments indicate that the H3K27ac epigenetic mark enhances the interaction of architectural protein with chromatin regulatory sites and identify determinants that facilitate the localization of HMGN proteins at regulatory sites to modulate cell-type specific gene expression.

Indexed as

HMGN ProteinsNucleosomesChromatinProtein BindingTranscription FactorsChromatinHMGN ProteinsNucleosomesTranscription Factors

Identifiers

PMID35197580
PMCPMC8866397
OpenAlexW4213133991

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.