Evidence map›Paper›PMID 17932104›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2008

A repressive role for prohibitin in estrogen signaling.

Bin He, Qin Feng, Atish Mukherjee, David M Lonard, Francesco J DeMayo, Benita S Katzenellenbogen, John P Lydon, Bert W O'Malley

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

78 citing papers in PubMed, 132 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Prohibitin Links Cell Cycle, Motility and Invasion in Prostate Cancer Cells.International journal of molecular sciences · 2023
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. A Putative Prohibitin-Calcium Nexus inJournal of diabetes research · 2020
    Review
  18. Comparative Transcriptome Analyses ofFrontiers in microbiology · 2020
    Article
  19. Article
  20. The Journal of biological chemistry · 2019
    Article

18 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

8 authors at 2 institutions in 1 country.

Bin HeDepartment of Molecular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
Qin Feng
Atish Mukherjee
David M Lonard
Francesco J DeMayo
Benita S Katzenellenbogen
John P Lydon
Bert W O'Malley
Baylor College of Medicine · USUniversity of Illinois Urbana-Champaign · US

Funding

SEX HORMONE RECEPTOR COMPONENTS AND THE CELL GENOMER01HD007857 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI DAVID M LONARD, JOHN P LYDON · 1985 to 2026
$14.6M
Molecular Analysis of Uterine ReceptivityR01HD042311 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI LYDON, JOHN P · 2009 to 2023
$4.8M
ANTIESTROGENS: MECHANISM OF ANTAGONIST ACTIONR01CA018119 · NCI · UNIVERSITY OF ILLINOIS URBANA-CHAMPAIGN · PI KATZENELLENBOGEN, BENITA S · 1985 to 2008
$2.8M
Molecular Analysis of Uterine ReceptivityU01HD042311 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI DEMAYO, FRANCESCO JOHN · 2002 to 2006
$1.5M
ANTIESTROGENS: MECHANISM OF ANTAGONIST ACTIONR37CA018119 · NCI · UNIVERSITY OF ILLINOIS URBANA-CHAMPAIGN · PI KATZENELLENBOGEN, BENITA S · 1991 to 1998
–
SEX HORMONE RECEPTOR COMPONENTS &THE CELL GENOMER37HD007857 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI MC KEOWN, MICHAEL B · 1987 to 1996
–
NCI NIH HHS CA 07730NCI NIH HHS CA 18119NCI NIH HHS R01 CA018119NICHD NIH HHS HD 07857NICHD NIH HHS HD 42311NICHD NIH HHS R01 HD007857NICHD NIH HHS R01 HD042311NICHD NIH HHS U01 HD042311
6 · The paper itself

Abstract

Nuclear receptor-mediated gene expression is regulated by corepressors and coactivators. In this study we demonstrate that prohibitin (PHB), a potential tumor suppressor, functions as a potent transcriptional corepressor for estrogen receptor alpha (ERalpha). Overexpression of PHB inhibits ERalpha transcriptional activity, whereas depletion of endogenous PHB increases the expression of ERalpha target genes in MCF-7 breast cancer cells. Chromatin immunoprecipitation experiments demonstrate that PHB is associated with the estrogen-regulated pS2 promoter in the absence of hormone and dissociates after estradiol treatment. We demonstrate that PHB interacts with the repressor of estrogen receptor activity (REA), a protein related to PHB, to form heteromers and enhance the protein stability of both corepressors. Interestingly, the corepressor activity of PHB is cross-squelched by the coexpression of REA (and vice versa), suggesting that PHB and REA repress transcription only when they are not paired. We further demonstrate that coiled-coil domains located in the middle of PHB and REA are responsible for their heteromerization, stabilization, and cross-squelching actions. Finally, ablation of PHB function in the mouse results in early embryonic lethality, whereas mice heterozygous for the PHB null allele exhibit a hyperproliferative mammary gland phenotype. Our results indicate that PHB functions as a transcriptional corepressor for ERalpha in vitro and in vivo, and that its heteromerization with REA acts as a novel mechanism to limit its corepressor activity.

Indexed as

AnimalsBlotting, WesternCell LineCell Line, TumorChromatin ImmunoprecipitationDimerizationEstrogen Receptor alphaEstrogensFemaleHumansImmunoprecipitationMiceMice, KnockoutModels, GeneticProhibitinsPromoter Regions, GeneticEstrogen Receptor alphaEstrogensPHB2 protein, humanPHB protein, humanProhibitinsRepressor ProteinsTFF1 protein, humanTrefoil Factor-1Tumor Suppressor Proteins

Identifiers

PMID17932104
PMCPMC2234581
OpenAlexW2037239368

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.