Evidence map›Paper›PMID 11909941›Full record

ArticleMolecular and cellular biology2002

Histone H1 represses estrogen receptor alpha transcriptional activity by selectively inhibiting receptor-mediated transcription initiation.

Edwin Cheung, Alla S Zarifyan, W Lee Kraus

Abstract read
In one paragraph

Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

  1. Article
  2. Review
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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

3 authors.

Edwin CheungDepartment of Molecular Biology and Genetics, Cornell University, Ithaca, New York 14853, USA.
Alla S Zarifyan
W Lee Kraus

Funding

Dose-Dependent Effects of Hormone on the Activity of Estrogen Receptor Enhancers and Target GenesR01DK058110 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI WILLIAM Lee KRAUS · 2000 to 2026
$10.4M
NIDDK NIH HHS DK58110NIDDK NIH HHS R01 DK058110
6 · The paper itself

Abstract

Chromatin is the physiological template for many nuclear processes in eukaryotes, including transcription by RNA polymerase II. In vivo, chromatin is assembled from genomic DNA, core histones, linker histones such as histone H1, and nonhistone chromatin-associated proteins. Histone H1 is thought to act as a general repressor of transcription by promoting the compaction of chromatin into higher-order structures. We have used a biochemical approach, including an in vitro chromatin assembly and transcription system, to examine the effects of histone H1 on estrogen receptor alpha (ER alpha)-mediated transcription with chromatin templates. We show that histone H1 acts as a potent repressor of ligand- and coactivator-regulated transcription by ER alpha. Histone H1 exerts its repressive effect without inhibiting the sequence-specific binding of ER alpha to chromatin or the overall extent of targeted acetylation of nucleosomal histones by the coactivator p300. Instead, histone H1 acts by blocking a specific step in the ER alpha-dependent transcription process, namely, transcription initiation, without affecting transcription reinitiation. Together, our data indicate that histone H1 acts selectively to reduce the overall level of productive transcription initiation by restricting promoter accessibility and preventing the ER alpha-dependent formation of a stable transcription pre-initiation complex.

Indexed as

AcetylationAnimalsCattleChromatinDNA Polymerase IIDrosophilaEstrogen Receptor alphaHistonesHumansIn Vitro TechniquesNuclear ProteinsNucleosomesPromoter Regions, GeneticReceptors, EstrogenRepressor ProteinsTrans-ActivatorsChromatinDNA Polymerase IIEstrogen Receptor alphaHistonesNuclear ProteinsNucleosomesReceptors, EstrogenRepressor ProteinsTrans-ActivatorsTranscription Factors

Identifiers

PMID11909941
PMCPMC133703

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.