Evidence map›Paper›PMID 18287247›Full record

ArticleMolecular pharmacology2008

Regulation of Smad-mediated gene transcription by RGS3.

Douglas M Yau, Nan Sethakorn, Sebastien Taurin, Steven Kregel, Nathan Sandbo, Blanca Camoretti-Mercado, Anne I Sperling, Nickolai O Dulin

Open access · greenAbstract read
In one paragraph

Article in Molecular pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

11 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. RGS3 controls T lymphocyte migration in a model of Th2-mediated airway inflammation.American journal of physiology. Lung cellular and molecular physiology · 2013
    Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Non-canonical functions of RGS proteins.Cellular signalling · 2010
    Review
  11. Article
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 1 institution in 1 country.

Douglas M YauSection of Pulmonary and Critical Care Medicine, the University of Chicago Department of Medicine, 5841 S. Maryland Ave, MC 6076, Chicago, IL 60637, USA.
Nan Sethakorn
Sebastien Taurin
Steven Kregel
Nathan Sandbo
Blanca Camoretti-Mercado
Anne I Sperling
Nickolai O Dulin
University of Chicago · US

Funding

RESEARCH TRAINING IN RESPIRATORY BIOLOGYT32HL007605 · NHLBI · UNIVERSITY OF CHICAGO · PI Yun Fang, Gokhan M. Mutlu · 1985 to 2026
$18.1M
Ruth L. Kirschstein National Research Service Award (NRSA) Institutional Research Training Grant (Parent T32)T32HD007009 · NICHD · UNIVERSITY OF CHICAGO · PI NANCY B SCHWARTZ · 1985 to 2026
$13.0M
Activation of protein kinase A by endothelin-1R01HL071755 · NHLBI · UNIVERSITY OF CHICAGO · PI DULIN, NICKOLAI O · 2005 to 2009
$1.5M
Novel functions of RGS3R01GM085058 · NIGMS · UNIVERSITY OF CHICAGO · PI DULIN, NICKOLAI O · 2009 to 2012
$1.2M
NHLBI NIH HHS HL071755NHLBI NIH HHS HL07605NHLBI NIH HHS R01 HL071755NHLBI NIH HHS T32 HL007605NICHD NIH HHS T32 HD007009NIGMS NIH HHS R01 GM085058
6 · The paper itself

Abstract

Regulator of G protein signaling (RGS) proteins are united into a family by the presence of the homologous RGS domain that binds the alpha subunits of heterotrimeric G proteins and accelerates their GTPase activity. A member of this family, RGS3 regulates the signaling mediated by G(q) and G(i) proteins by binding the corresponding Galpha subunits. Here we show that RGS3 interacts with the novel partners Smad2, Smad3, and Smad4-the transcription factors that are activated through a transforming growth factor-beta (TGF-beta) receptor signaling. This interaction is mediated by the region of RGS3 outside of the RGS domain and by Smad's Mad homology 2 domain. Overexpression of RGS3 results in inhibition of Smad-mediated gene transcription. RGS3 does not affect TGF-beta-induced Smad phosphorylation, but it prevents heteromerization of Smad3 with Smad4, which is required for transcriptional activity of Smads. This translates to functional inhibition of TGF-beta-induced myofibroblast differentiation by RGS3. In conclusion, this study identifies a novel, noncanonical role of RGS3 in regulation of TGF-beta signaling through its interaction with Smads and interfering with Smad heteromerization.

Indexed as

Transcription, GeneticActinsAnimalsBinding SitesCHO CellsCricetinaeCricetulusDNA, ComplementaryGTPase-Activating ProteinsGTP-Binding ProteinsHumansImmunoprecipitationProtein BindingProtein Structure, TertiaryRGS ProteinsSignal TransductionActinsDNA, ComplementaryGTPase-Activating ProteinsGTP-Binding ProteinsRGS3 protein, humanRGS ProteinsSmad2 ProteinSmad3 ProteinSmad4 ProteinSmad ProteinsTransforming Growth Factor beta

Identifiers

PMID18287247
PMCPMC3329871
OpenAlexW2153283074

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.