Evidence map›Paper›PMID 15642950›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2005

Altered pharmacology and distinct coactivator usage for estrogen receptor-dependent transcription through activating protein-1.

Edwin Cheung, Mari Luz Acevedo, Philip A Cole, W Lee Kraus

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

34 citing papers in PubMed, 68 citations in OpenAlex.

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  18. Molecular mechanism of estrogen-estrogen receptor signaling.Reproductive medicine and biology · 2017
    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

4 authors at 4 institutions in 3 countries.

Edwin CheungDepartment of Molecular Biology and Genetics, Cornell University, Ithaca, NY 14853, USA.
Mari Luz Acevedo
Philip A Cole
W Lee Kraus
Agency for Science, Technology and Research · SGCornell University · USJohns Hopkins University · USUniversity of Puerto Rico System · PR

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
Protein Acylation and Methylation Mechanisms_Administrative SupplementR37GM062437 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI COLE, PHILIP A · 2013 to 2022
$4.1M
Mechanisms &Inhibition of Histone AcetyltransferasesR01GM062437 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI COLE, PHILIP A · 2001 to 2012
$3.8M
NIDDK NIH HHS DK58110NIDDK NIH HHS R01 DK058110NIGMS NIH HHS GM62437NIGMS NIH HHS R01 GM062437NIGMS NIH HHS R37 GM062437
6 · The paper itself

Abstract

Estrogen signaling occurs through at least two distinct molecular pathways: (i) direct binding of liganded estrogen receptors (ERs) to estrogen-responsive DNA elements (EREs) (the "ER/ERE pathway") and (ii) indirect recruitment of liganded ERs to activating protein-1 (AP-1)-responsive DNA elements via heterodimers of Fos and Jun (the "ER/AP-1 pathway"). We have developed a biochemical assay for examining ligand-regulated transcription by ERs in the ER/AP-1 pathway. This assay recapitulates the altered (i.e., agonistic) pharmacology of selective estrogen receptor modulator drugs in this pathway reported previously by using various cell-based assays. We used our biochemical assay to examine the detailed mechanisms of ER/AP-1-dependent transcription. Our studies indicate that (i) ERalpha/AP-1 complexes play a critical role in promoting the formation of stable RNA polymerase II preinitiation complexes leading to transcription initiation, (ii) chromatin is a key determinant of estrogen and selective estrogen receptor modulator signaling in the ERalpha/AP-1 pathway, (iii) distinct domains of ERalpha are required for recruitment to DNA-bound Fos/Jun heterodimers and transcriptional activation at AP-1 sites, and (iv) different enhancer/activator combinations in the ERalpha and AP-1 pathways use coactivators in distinct ways. These studies have increased our understanding of the molecular mechanisms underlying ligand-dependent signaling in the ER/AP-1 pathway and demonstrate the usefulness of this biochemical approach.

Indexed as

Transcription, GeneticChromatinDimerizationEnhancer Elements, GeneticEstrogen Receptor alphaHumansLigandsOncogene Proteins v-fosProto-Oncogene Proteins c-junSignal TransductionTranscriptional ActivationTranscription Factor AP-1ChromatinEstrogen Receptor alphaLigandsOncogene Proteins v-fosProto-Oncogene Proteins c-junTranscription Factor AP-1

Identifiers

PMID15642950
PMCPMC545529
OpenAlexW2040449012

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.