Evidence map›Paper›PMID 23212907›Full record

ArticleThe Journal of biological chemistry2013

Regulation of the G-protein regulatory-Gαi signaling complex by nonreceptor guanine nucleotide exchange factors.

Sukru Sadik Oner, Ellen M Maher, Meital Gabay, Gregory G Tall, Joe B Blumer, Stephen M Lanier

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing 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

27 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. AGS3 and GαMolecules (Basel, Switzerland) · 2020
    Article
  7. Article
  8. Ric-8A, a GEF, and a Chaperone for G Protein α-Subunits: Evidence for the Two-Faced Interface.BioEssays : news and reviews in molecular, cellular and developmental biology · 2020
    Article
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  11. Review
  12. Article
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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

6 authors at 2 institutions in 1 country.

Sukru Sadik OnerDepartment of Cell and Molecular Pharmacology and Experimental Therapeutics, Medical University of South Carolina, Charleston, South Carolina 29425, USA.
Ellen M Maher
Meital Gabay
Gregory G Tall
Joe B Blumer
Stephen M Lanier
Medical University of South Carolina · USUniversity of Rochester Medical Center · US

Funding

Regulation of Heterotrimeric G proteins by non-receptor activatorsR01GM088242 · NIGMS · UNIVERSITY OF ROCHESTER · PI TALL, GREGORY GORDON · 2009 to 2022
$4.2M
ACCESSORY PROTEINS AND G-PROTEIN SIGNALING MECHANISMSR01DA025896 · NIDA · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI LANIER, STEPHEN M. · 2008 to 2012
$1.6M
AGS4 in G-protein Signal ProcessingR01GM086510 · NIGMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BLUMER, JOE B · 2009 to 2013
$1.5M
NIDA NIH HHS DA025896NIDA NIH HHS R01 DA025896NIGMS NIH HHS GM086510NIGMS NIH HHS GM088242NIGMS NIH HHS R01 GM086510NIGMS NIH HHS R01 GM088242
6 · The paper itself

Abstract

Group II activators of G-protein signaling (AGS) serve as binding partners for Gα(i/o/t) via one or more G-protein regulatory (GPR) motifs. GPR-Gα signaling modules may be differentially regulated by cell surface receptors or by different nonreceptor guanine nucleotide exchange factors. We determined the effect of the nonreceptor guanine nucleotide exchange factors AGS1, GIV/Girdin, and Ric-8A on the interaction of two distinct GPR proteins, AGS3 and AGS4, with Gα(il) in the intact cell by bioluminescence resonance energy transfer (BRET) in human embryonic kidney 293 cells. AGS3-Rluc-Gα(i1)-YFP and AGS4-Rluc-Gα(i1)-YFP BRET were regulated by Ric-8A but not by Gα-interacting vesicle-associated protein (GIV) or AGS1. The Ric-8A regulation was biphasic and dependent upon the amount of Ric-8A and Gα(i1)-YFP. The inhibitory regulation of GPR-Gα(i1) BRET by Ric-8A was blocked by pertussis toxin. The enhancement of GPR-Gα(i1) BRET observed with Ric-8A was further augmented by pertussis toxin treatment. The regulation of GPR-Gα(i) interaction by Ric-8A was not altered by RGS4. AGS3-Rluc-Gα(i1)-YFP and AGS4-Rluc-G-Gα(i1)-YFP BRET were observed in both pellet and supernatant subcellular fractions and were regulated by Ric-8A in both fractions. The regulation of the GPR-Gα(i1) complex by Ric-8A, as well as the ability of Ric-8A to restore Gα expression in Ric8A(-/-) mouse embryonic stem cells, involved two helical domains at the carboxyl terminus of Ric-8A. These data indicate a dynamic interaction between GPR proteins, Gα(i1) and Ric-8A, in the cell that influences subcellular localization of the three proteins and regulates complex formation.

Indexed as

Signal TransductionAnimalsBioluminescence Resonance Energy Transfer TechniquesCell FractionationGTP-Binding Protein alpha Subunits, Gi-GoGuanine Nucleotide Exchange FactorsHEK293 CellsHumansMiceMutant ProteinsNeuronsPertussis Toxinras ProteinsRecombinant Fusion ProteinsRGS ProteinsSubcellular FractionsGTP-Binding Protein alpha Subunits, Gi-GoGuanine Nucleotide Exchange FactorsMutant ProteinsPertussis Toxinras ProteinsRecombinant Fusion ProteinsRGS4 proteinRGS ProteinsRic8a protein, mouseVesicular Transport Proteins

Identifiers

PMID23212907
PMCPMC3561525
OpenAlexW2169366070

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.