Evidence map›Paper›PMID 21966451›Full record

ArticlePloS one2011

Repression of androgen receptor transcription through the E2F1/DNMT1 axis.

Conrad David Valdez, Joanne N Davis, Hana M Odeh, Tristan L Layfield, Craig S Cousineau, Thomas R Berton, David G Johnson, Kirk J Wojno, Mark L Day

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.7field-weighted citation impact, top 23% 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

18 citing papers in PubMed, 33 citations in OpenAlex.

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  17. Retinoblastoma tumor suppressor protein in pancreatic progenitors controls α- and β-cell fate.Proceedings of the National Academy of Sciences of the United States of America · 2013
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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

9 authors at 3 institutions in 1 country.

Conrad David ValdezDepartment of Urology, University of Michigan Comprehensive Cancer Center, University of Michigan, Ann Arbor, Michigan, United States of America.
Joanne N Davis
Hana M Odeh
Tristan L Layfield
Craig S Cousineau
Thomas R Berton
David G Johnson
Kirk J Wojno
Mark L Day
University of Michigan–Ann Arbor · USMichigan United · USThe University of Texas MD Anderson Cancer Center · US

Funding

HORMONE REGULATED INVOLUTION SIGNALED THROUGH E CADHERINR01DK056137 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI DAY, MARK L · 2000 to 2003
$953k
Rb/E2F in Hormone Signaling of Prostate EpitheliumR01DK066610 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI DAY, MARK L · 2004 to 2006
$673k
NIDDK NIH HHS R01 DK-056137NIDDK NIH HHS R01 DK056137NIDDK NIH HHS R01 DK-066610NIDDK NIH HHS R01 DK066610
6 · The paper itself

Abstract

Although androgen receptor (AR) function has been extensively studied, regulation of the AR gene itself has been much less characterized. In this study, we observed a dramatic reduction in the expression of androgen receptor mRNA and protein in hyperproliferative prostate epithelium of keratin 5 promoter driven E2F1 transgenic mice. To confirm an inhibitory function for E2F1 on AR transcription, we showed that E2F1 inhibited the transcription of endogenous AR mRNA, subsequent AR protein, and AR promoter activity in both human and mouse epithelial cells. E2F1 also inhibited androgen-stimulated activation of two AR target gene promoters. To elucidate the molecular mechanism of E2F-mediated inhibition of AR, we evaluated the effects of two functional E2F1 mutants on AR promoter activity and found that the transactivation domain appears to mediate E2F1 repression of the AR promoter. Because DNMT1 is a functional intermediate of E2F1 we examined DNMT1 function in AR repression. Repression of endogenous AR in normal human prostate epithelial cells was relieved by DNMT1 shRNA knock down. DNMT1 was shown to be physically associated within the AR minimal promoter located 22 bps from the transcription start site; however, methylation remained unchanged at the promoter regardless of DNMT1 expression. Taken together, our results suggest that DNMT1 operates either as a functional intermediary or in cooperation with E2F1 inhibiting AR gene expression in a methylation independent manner.

Indexed as

Blotting, NorthernBlotting, WesternCell Line, TumorChromatin ImmunoprecipitationDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesDNA MethylationE2F1 Transcription FactorHumansMetribolonePolymerase Chain ReactionPromoter Regions, GeneticReceptors, AndrogenDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesDNMT1 protein, humanDnmt1 protein, mouseE2F1 protein, humanE2F1 Transcription FactorMetriboloneReceptors, Androgen

Identifiers

PMID21966451
PMCPMC3180375
OpenAlexW2130949711

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.