Evidence map›Paper›PMID 19744931›Full record

ArticleThe Journal of biological chemistry2009

Function of histone deacetylase 6 as a cofactor of nuclear receptor coregulator LCoR.

Ana Palijan, Isabelle Fernandes, Yolande Bastien, Liqun Tang, Mark Verway, Maria Kourelis, Luz E Tavera-Mendoza, Zhi Li, Veronique Bourdeau, Sylvie Mader and 2 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

37 citing papers in PubMed, 62 citations in OpenAlex.

  1. Review
  2. Article
  3. HDAC6: A unique HDAC family member as a cancer target.Cellular oncology (Dordrecht, Netherlands) · 2022
    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

12 authors at 3 institutions in 2 countries.

Ana PalijanDepartment of Physiology, McGill University, Montreal, Quebec H3G 1Y6, Canada.
Isabelle Fernandes
Yolande Bastien
Liqun Tang
Mark Verway
Maria Kourelis
Luz E Tavera-Mendoza
Zhi Li
Veronique Bourdeau
Sylvie Mader
Xiang Jiao Yang
John H White
McGill University · CAUniversité de Montréal · CADana-Farber Cancer Institute · US

Funding

Canadian Institutes of Health Research MT-11704
6 · The paper itself

Abstract

Ligand-dependent corepressor LCoR was identified as a protein that interacts with the estrogen receptor alpha (ERalpha) ligand binding domain in a hormone-dependent manner. LCoR also interacts directly with histone deacetylase 3 (HDAC3) and HDAC6. Notably, HDAC6 has emerged as a marker of breast cancer prognosis. However, although HDAC3 is nuclear, HDAC6 is cytoplasmic in many cells. We found that HDAC6 is partially nuclear in estrogen-responsive MCF7 cells, colocalizes with LCoR, represses transactivation of estrogen-inducible reporter genes, and augments corepression by LCoR. In contrast, no repression was observed upon HDAC6 expression in COS7 cells, where it is exclusively cytoplasmic. LCoR binds to HDAC6 in vitro via a central domain, and repression by LCoR mutants lacking this domain was attenuated. Kinetic chromatin immunoprecipitation assays revealed hormone-dependent recruitment of LCoR to promoters of ERalpha-induced target genes in synchrony with ERalpha. HDAC6 was also recruited to these promoters, and repeat chromatin immunoprecipitation experiments confirmed the corecruitment of LCoR with ERalpha and with HDAC6. Remarkably, however, although we find evidence for corecruitment of LCoR and ERalpha on genes repressed by the receptor, LCoR and HDAC6 failed to coimmunoprecipitate, suggesting that they are part of distinct complexes on these genes. Although small interfering RNA-mediated knockdown of LCoR or HDAC6 augmented expression of an estrogen-sensitive reporter gene in MCF7 cells, unexpectedly their ablation led to reduced expression of some endogenous estrogen target genes. Taken together, these data establish that HDAC6 can function as a cofactor of LCoR but suggest that they may act in enhance expressing some target genes.

Indexed as

Breast NeoplasmsCell Line, TumorEstrogen Receptor alphaEstrogensFemaleHistone Deacetylase 6Histone DeacetylasesHumansNuclear ProteinsPromoter Regions, GeneticRepressor ProteinsEstrogen Receptor alphaEstrogensHDAC6 protein, humanHistone Deacetylase 6Histone DeacetylasesLCOR protein, humanNuclear ProteinsRepressor Proteins

Identifiers

PMID19744931
PMCPMC2781582
OpenAlexW2084262863

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.