Evidence map›Paper›PMID 18583028›Full record

ArticleMolecular and cellular endocrinology2008

Modulation of transcription parameters in glucocorticoid receptor-mediated repression.

Yunguang Sun, Yong-Guang Tao, Benjamin L Kagan, Yuangzheng He, S Stoney Simons

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular endocrinology, 2008. 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
1.7field-weighted citation impact, top 15% 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, 26 citations in OpenAlex.

  1. Review
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  14. N-acetylcysteine protects pancreatic islet against glucocorticoid toxicity.Redox report : communications in free radical research · 2011
    Article
  15. A theoretical framework for gene induction and experimental comparisons.Proceedings of the National Academy of Sciences of the United States of America · 2010
    Article
  16. Article
  17. Review
  18. What goes on behind closed doors: physiological versus pharmacological steroid hormone actions.BioEssays : news and reviews in molecular, cellular and developmental biology · 2008
    Review
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

5 authors at 2 institutions in 1 country.

Yunguang SunSteroid Hormones Section, NIDDK/CEB, National Institutes of Health, Bethesda, MD, United States.
Yong-Guang Tao
Benjamin L Kagan
Yuangzheng He
S Stoney Simons
National Institute of Diabetes and Digestive and Kidney Diseases · USNational Institutes of Health · US

Funding

Modulation of parameters of glucocorticoid receptor-mediated gene repressionZ01DK047040 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI SIMONS, S STONEY · 2007 to 2008
$472k
Intramural NIH HHS Z01 DK047040
6 · The paper itself

Abstract

Glucocorticoid receptors (GRs) affect both gene induction and gene repression. The disparities of receptor binding to DNA and increased vs. decreased gene expression have suggested significant mechanistic differences between GR-mediated induction and repression. Numerous transcription factors are known to modulate three parameters of gene induction: the total activity (Vmax) and position of the dose-response curve with glucocorticoids (EC50) and the percent partial agonist activity with antiglucocorticoids. We have examined the effects on GR-mediated repression of five modulators (coactivators TIF2 [GRIP1, SRC-2] and SRC-1, corepressor SMRT, and comodulators STAMP and Ubc9), a glucocorticoid steroid (deacylcortivazol [DAC]) of very different structure, and an inhibitor of histone deacetylation (trichostatin A [TSA]). These factors interact with different domains of GR and thus are sensitive topological probes of GR action. These agents altered the Vmax, EC50, and percent partial agonist activity of endogenous and exogenous repressed genes similarly to that previously observed for GR-regulated gene induction. Collectively, these results suggest that GR-mediated induction and repression share many of the same molecular interactions and that the causes for different levels of gene transcription arise from more distal downstream steps.

Indexed as

AnimalsCarrier ProteinsCell Line, TumorDexamethasoneDNA-Binding ProteinsDose-Response Relationship, DrugDown-RegulationEnzyme InhibitorsGlucocorticoidsHistone AcetyltransferasesHistone Deacetylase InhibitorsHistone DeacetylasesHumansHydroxamic AcidsMatrix Metalloproteinase 13Molecular StructureCarrier ProteinsdeacylcortivazolDexamethasoneDNA-Binding ProteinsEnzyme InhibitorsGlucocorticoidsHistone AcetyltransferasesHistone Deacetylase InhibitorsHistone DeacetylasesHydroxamic AcidsMatrix Metalloproteinase 13NCOA1 protein, humanNCOA2 protein, humanNCOR2 protein, humanNcor2 protein, ratNuclear Receptor Coactivator 1Nuclear Receptor Coactivator 2Nuclear Receptor Co-Repressor 2PregnatrienesReceptors, GlucocorticoidRepressor ProteinsTranscription Factor AP-1Transcription Factorstrichostatin ATTLL5 protein, humanUbiquitin-Conjugating EnzymesUbiquitin-Conjugating Enzyme UBC9

Identifiers

PMID18583028
PMCPMC2662735
OpenAlexW1969500227

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.