Evidence map›Paper›PMID 18722177›Full record

ArticleMolecular cell2008

CCAR1, a key regulator of mediator complex recruitment to nuclear receptor transcription complexes.

Jeong Hoon Kim, Catherine K Yang, Kyu Heo, Robert G Roeder, Woojin An, Michael R Stallcup

Open access · greenAbstract read
In one paragraph

Article in Molecular cell, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

99 citing papers in PubMed, 162 citations in OpenAlex.

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  10. Landscape of NcRNAs involved in drug resistance of breast cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Review
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39 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

6 authors at 2 institutions in 1 country.

Jeong Hoon KimDepartment of Biochemistry and Molecular Biology and the Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA 90089, USA.
Catherine K YangDepartment of Biochemistry and Molecular Biology and the Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA 90089, USA.
Kyu HeoDepartment of Biochemistry and Molecular Biology and the Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA 90089, USA.
Robert G RoederLaboratory of Biochemistry and Molecular Biology, The Rockefeller University, New York, NY 10021, USA.
Woojin AnDepartment of Biochemistry and Molecular Biology and the Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA 90089, USA.
Michael R StallcupDepartment of Biochemistry and Molecular Biology and the Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA 90089, USA. Electronic address: stallcup@usc.edu.
University of Southern California · USRockefeller University · US

Funding

Transcription activation by nuclear coactivatorsR01DK043093 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI STALLCUP, MICHAEL R · 1990 to 2019
$6.5M
VIRAL AND CHEMICAL CARCINOGENESIST32CA009320 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI JONES, PETER A · 1985 to 2012
$2.5M
GRADUATE TRAINING IN GASTROENTEROLOGY AND LIVER DISEASEST32DK007100 · NIDDK · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI COMBES, BURTON · 1986 to 1994
–
NCI NIH HHS T32 CA009320NIDDK NIH HHS DK07100NIDDK NIH HHS DK43093NIDDK NIH HHS R01 DK043093
6 · The paper itself

Abstract

DNA-bound transcription factors recruit many coactivator proteins to remodel chromatin and activate transcription. The Mediator complex is believed to recruit RNA polymerase II to most protein-encoding genes. It is generally assumed that interaction of Mediator subunits with DNA-binding transcription factors is responsible for Mediator recruitment to promoters. However, we report here that Mediator recruitment by nuclear receptors (NR) requires a coactivator protein, CCAR1 (cell-cycle and apoptosis regulator 1). CCAR1 associates with components of the Mediator and p160 coactivator complexes and is recruited to endogenous NR target genes in response to the appropriate hormone. Reduction of endogenous CCAR1 levels inhibited hormone-induced expression of endogenous NR target genes, hormone-induced recruitment of Mediator components and RNA polymerase II to target gene promoters, and estrogen-dependent growth of breast cancer cells. Thus, CCAR1 regulates expression of key proliferation-inducing genes. CCAR1 also functions as a p53 coactivator, suggesting a broader role in transcriptional regulation.

Indexed as

Transcription, GeneticAnimalsApoptosis Regulatory ProteinsCell Cycle ProteinsCell Line, TumorCell ProliferationChlorocebus aethiopsCOS CellsEstrogensGene Expression Regulation, NeoplasticHumansPromoter Regions, GeneticProtein BindingProtein Structure, TertiaryReceptors, Cytoplasmic and NuclearReceptors, EstrogenApoptosis Regulatory ProteinsCCAR1 protein, humanCell Cycle ProteinsEstrogensReceptors, Cytoplasmic and NuclearReceptors, EstrogenReceptors, GlucocorticoidTrans-ActivatorsTumor Suppressor Protein p53

Identifiers

PMID18722177
PMCPMC2562329
OpenAlexW2053665091

What OpenQuestion holds

Textmetadata
LicenceTDM
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.