Evidence map›Paper›PMID 18775326›Full record

ArticleMolecular cell2008

RGS13 acts as a nuclear repressor of CREB.

Zhihui Xie, Timothy R Geiger, Eric N Johnson, Jennifer K Nyborg, Kirk M Druey

Open access · bronzeAbstract 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 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

32 citing papers in PubMed, 55 citations in OpenAlex.

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  19. A finer tuning of G-protein signaling through regulated control of RGS proteins.American journal of physiology. Heart and circulatory physiology · 2012
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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

5 authors at 3 institutions in 1 country.

Zhihui XieMolecular Signal Transduction Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Timothy R Geiger
Eric N Johnson
Jennifer K Nyborg
Kirk M Druey
Colorado State University · USNational Institutes of Health · USNational Institute of Allergy and Infectious Diseases · US

Funding

Heterotrimeric G Protein Signaling In Allergic InflammationZIAAI000746 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI DRUEY, KIRK M · 2009 to 2025
$4.6M
TRANSCRIPTIONAL REGULATION BY THE HTLV-I TAX PROTEINR01CA055035 · NCI · COLORADO STATE UNIVERSITY-FORT COLLINS · PI NYBORG, JENNIFER K. · 1994 to 2013
$3.9M
HETEROTRIMERIC G PROTEIN SIGNALING IN ALLERGIC INFLAMMATIONZ01AI000746 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI DRUEY, KIRK M · 1998 to 2008
$1.1M
TAX1 REGULATION OF HTLV-I TRANSCRIPTION AND REPLICATIONR55CA055035 · NCI · COLORADO STATE UNIVERSITY-FORT COLLINS · PI NYBORG, JENNIFER K. · 1991 to 1991
–
Intramural NIH HHS Z01 AI000746Intramural NIH HHS Z99 AI999999NCI NIH HHS CA55035NCI NIH HHS R01 CA055035
6 · The paper itself

Abstract

Cyclic AMP-induced phosphorylation of the transcription factor CREB elicits expression of genes mediating diverse biological functions. In lymphoid organs, the neurotransmitter norepinephrine stimulates beta(2)-adrenergic receptors on B lymphocytes to promote CREB-dependent expression of genes like the B cell Oct 2 coactivator (OCA-B). Although CREB phosphorylation recruits cofactors such as CBP/p300 to stimulate transcription, bona fide endogenous inhibitors of CREB-coactivator or CREB-DNA interactions have not emerged. Here, we identified RGS13, a member of the Regulator of G protein Signaling (RGS) protein family, as a nuclear factor that suppresses CREB-mediated gene expression. cAMP or Ca(2+) signaling promoted RGS13 accumulation in the nucleus, where it formed a complex with phosphorylated CREB and CBP/p300. RGS13 reduced the apparent affinity of pCREB for both the CRE and CBP. B lymphocytes from Rgs13(-/-) mice had more beta(2)-agonist-induced OCA-B expression. Thus, RGS13 inhibits CREB-dependent transcription of target genes through disruption of complexes formed at the promoter.

Indexed as

Gene Expression RegulationAnimalsB-LymphocytesCell LineCell NucleusCREB-Binding ProteinCyclic AMP-Dependent Protein KinasesCyclic AMP Response Element-Binding ProteinGTP-Binding Protein alpha Subunits, GsHumansMiceMice, KnockoutNuclear ProteinsPromoter Regions, GeneticRecombinant Fusion ProteinsRepressor ProteinsCREB-Binding ProteinCyclic AMP-Dependent Protein KinasesCyclic AMP Response Element-Binding ProteinGTP-Binding Protein alpha Subunits, GsNuclear ProteinsRecombinant Fusion ProteinsRepressor ProteinsRGS13 protein, humanRGS Proteins

Identifiers

PMID18775326
PMCPMC2600481
OpenAlexW2033812812

What OpenQuestion holds

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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.