Evidence map›Paper›PMID 18258596›Full record

ArticleThe Journal of biological chemistry2008

Isolation and characterization of a novel H1.2 complex that acts as a repressor of p53-mediated transcription.

Kyunghwan Kim, Jongkyu Choi, Kyu Heo, Hyunjung Kim, David Levens, Kimitoshi Kohno, Edward M Johnson, Hugh W Brock, Woojin An

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

69 citing papers in PubMed, 113 citations in OpenAlex.

  1. Article
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  9. Review
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  12. Review
  13. Molecular and Cellular Functions of the Linker Histone H1.2.Frontiers in cell and developmental biology · 2021
    Review
  14. The missing linkGenes & development · 2021
    Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article

9 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

9 authors at 4 institutions in 3 countries.

Kyunghwan KimDepartment of Biochemistry and Molecular Biology, University of Southern California Keck School of Medicine, Los Angeles, CA 90089, USA.
Jongkyu Choi
Kyu Heo
Hyunjung Kim
David Levens
Kimitoshi Kohno
Edward M Johnson
Hugh W Brock
Woojin An
University of Southern California · USEastern Virginia Medical School · USUniversity of British Columbia · CAUniversity of Occupational and Environmental Health Japan · JP

Funding

Mechanisms of transcription factor integration at the c-myc promoterZIASC009144 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI LEVENS, DAVID L. · 2009 to 2025
$9.5M
Mechanisms of transcription factor integration at the c-myc promoterZ01SC009144 · SC · DIVISION OF CLINICAL SCIENCES - NCI · PI LEVENS, DAVID L. · 1996 to 2008
$3.1M
6 · The paper itself

Abstract

Linker histone H1 has been generally viewed as a global repressor of transcription by preventing the access of transcription factors to sites in chromatin. However, recent studies suggest that H1 can interact with other regulatory factors for its action as a negative modulator of specific genes. To investigate these aspects, we established a human cell line expressing H1.2, one of the H1 subtypes, for the purification of H1-interacting proteins. Our results showed that H1.2 can stably associate with sets of cofactors and ribosomal proteins that can significantly repress p53-dependent, p300-mediated chromatin transcription. This repressive action of H1.2 complex involves direct interaction of H1.2 with p53, which in turn blocks p300-mediated acetylation of chromatin. YB1 and PURalpha, two factors present in the H1.2 complex, together with H1.2 can closely recapitulate the repressive action of the entire H1.2 complex in transcription. Chromatin immunoprecipitation and RNA interference analyses further confirmed that the recruitment of YB1, PURalpha, and H1.2 to the p53 target gene Bax is required for repression of p53-induced transcription. Therefore, these results reveal a previously unrecognized function of H1 as a transcriptional repressor as well as the underlying mechanism involving specific sets of factors in this repression process.

Indexed as

Acetylationbcl-2-Associated X ProteinChromatinDNA-Binding ProteinsE1A-Associated p300 ProteinGene Expression RegulationHeLa CellsHistonesHumansNuclear ProteinsRepressor ProteinsRNA InterferenceTranscription FactorsTranscription, GeneticTumor Suppressor Protein p53Y-Box-Binding Protein 1BAX protein, humanbcl-2-Associated X ProteinChromatinDNA-Binding ProteinsE1A-Associated p300 ProteinEP300 protein, humanHistonesNuclear ProteinsPURA protein, humanRepressor ProteinsTP53 protein, humanTranscription FactorsTumor Suppressor Protein p53Y-Box-Binding Protein 1YBX1 protein, human

Identifiers

PMID18258596
PMCPMC2431041
OpenAlexW2144160911

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.