Evidence map›Paper›PMID 12192044›Full record

ArticleMolecular and cellular biology2002

Targeted recruitment of Rpd3 histone deacetylase represses transcription by inhibiting recruitment of Swi/Snf, SAGA, and TATA binding protein.

Jutta Deckert, Kevin Struhl

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 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
–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

27 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Histone deacetylase-mediated regulation of endolysosomal pH.The Journal of biological chemistry · 2018
    Pooled it
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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

2 authors.

Jutta DeckertDepartment of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02115, USA.
Kevin Struhl

Funding

MOLECULAR MECHANISMS OF GLOBAL REPRESSION IN YEASTR01GM053720 · NIGMS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI STRUHL, KEVIN · 1995 to 2008
$2.9M
NIGMS NIH HHS GM 53720NIGMS NIH HHS R01 GM053720
6 · The paper itself

Abstract

Certain DNA-binding repressors inhibit transcription by recruiting Rpd3 histone deacetylase complexes to promoters and generating domains of histone deacetylation that extend over a limited number of nucleosomes. Here, we show that the degree of Rpd3-dependent repression depends on the activator and the level of activation, not the extent of histone deacetylation. In all cases tested, activator binding is unaffected by histone deacetylation. In contrast, Rpd3-dependent repression is associated with decreased occupancy by TATA binding protein (TBP), the Swi/Snf nucleosome-remodeling complex, and the SAGA histone acetylase complex. Transcriptional repression is bypassed by direct recruitment of TBP and several TBP-associated factors, but not by natural activation domains or direct recruitment of polymerase II holoenzyme components. These results suggest that the domain of localized histone deacetylation generated by recruitment of Rpd3 mediates repression by inhibiting recruitment of chromatin-modifying activities and TBP.

Indexed as

Nuclear ProteinsRepressor ProteinsAcetyltransferasesAllelesChromatinDNA-Binding ProteinsHistone AcetyltransferasesHistone DeacetylasesHistonesModels, GeneticPrecipitin TestsPromoter Regions, GeneticProtein BindingProtein KinasesSaccharomyces cerevisiae ProteinsTATA-Box Binding ProteinAcetyltransferasesChromatinDNA-Binding ProteinsHistone AcetyltransferasesHistone DeacetylasesHistonesNuclear ProteinsProtein KinasesRepressor ProteinsSaccharomyces cerevisiae ProteinsTATA-Box Binding ProteinTranscription Factors

Identifiers

PMID12192044
PMCPMC135627

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.