Evidence map›Paper›PMID 21804131›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2011

Targeted deletion of one or two copies of the G protein β subunit Gβ5 gene has distinct effects on body weight and behavior in mice.

Qiang Wang, Konstantin Levay, Tatyana Chanturiya, Galina Dvoriantchikova, Karen L Anderson, Suzy D C Bianco, Cintia B Ueta, R Damaris Molano, Antonello Pileggi, Eugenia V Gurevich and 2 more

Open access · greenAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

19 citing papers in PubMed, 31 citations in OpenAlex.

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  8. Regulator of G-protein signaling Gβ5-R7 is a crucial activator of muscarinic M3 receptor-stimulated insulin secretion.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017
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  13. Regulator of G protein signaling 6 is a critical mediator of both reward-related behavioral and pathological responses to alcohol.Proceedings of the National Academy of Sciences of the United States of America · 2015
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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

12 authors at 4 institutions in 1 country.

Qiang WangDepartment of Molecular and Cellular Pharmacology, University of Miami Miller School of Medicine, Miami, Florida, 33136, USA.
Konstantin Levay
Tatyana Chanturiya
Galina Dvoriantchikova
Karen L Anderson
Suzy D C Bianco
Cintia B Ueta
R Damaris Molano
Antonello Pileggi
Eugenia V Gurevich
Oksana Gavrilova
Vladlen Z Slepak
University of Miami · USMiami Transplant Institute · USNational Institute of Diabetes and Digestive and Kidney Diseases · USVanderbilt University · US

Funding

Metabolic Studies of Mouse Models of Obesity and DiabetesZICDK070002 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI GAVRILOVA, OKSANA · 2009 to 2025
$15.0M
Strategies to Improve Long Term Islet Graft SurvivalU01DK070460 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI RICORDI, CAMILLO · 2004 to 2012
$11.6M
ISLET CELL RESOURCE FOR DIABETES RESEARCH AND TREATMENTU42RR016603 · NCRR · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI RICORDI, CAMILLO · 2001 to 2009
$7.8M
Interaction of RGS Protein with G beta subunit G beta 5.R01GM060019 · NIGMS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI SLEPAK, VLADLEN Z · 1999 to 2013
$3.8M
Insulin Producing Cells from Amniotic Stem Cells for Diabetes TherapyR01EB008009 · NIBIB · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI ATALA, ANTHONY · 2007 to 2009
$3.3M
Signaling regulation in the striatum in Parkinson's diseaseR01NS065868 · NINDS · VANDERBILT UNIVERSITY · PI GUREVICH, EUGENIA V · 2009 to 2013
$1.7M
NCRR NIH HHS NIHU42 RR016603NCRR NIH HHS U42 RR016603NIBIB NIH HHS 1R01 EB008009NIBIB NIH HHS R01 EB008009NIDDK NIH HHS DK70460NIDDK NIH HHS U01 DK070460NIGMS NIH HHS GM 060019NIGMS NIH HHS R01 GM060019NINDS NIH HHS NS065868NINDS NIH HHS R01 NS065868
6 · The paper itself

Abstract

We investigated the physiological role of Gβ5, a unique G protein β subunit that dimerizes with regulators of G protein signaling (RGS) proteins of the R7 family instead of Gγ. Gβ5 is essential for stability of these complexes, so that its knockout (KO)causes degradation of the entire Gβ5-R7 family. We report that the Gβ5-KO mice remain leaner than the wild type (WT) throughout their lifetime and are resistant to a high-fat diet. They have a 5-fold increase in locomotor activity, increased thermogenesis, and lower serum insulin, all of which correlate with a higher level of secreted epinephrine. Heterozygous (HET) mice are 2-fold more active than WT mice. Surprisingly, with respect to body weight, the HET mice display a phenotype opposite to that of the KO mice: by the age of 6 mo, they are ≥ 15% heavier than the WT and have increased adiposity, insulin resistance, and liver steatosis. These changes occur in HET mice fed a normal diet and without apparent hyperphagia, mimicking basic characteristics of human metabolic syndrome. We conclude that even a partial reduction in Gβ5-R7 level can perturb normal animal metabolism and behavior. Our data on Gβ5 haploinsufficient mice may explain earlier observations of genetic linkage between R7 family mutations and obesity in humans.

Indexed as

Behavior, AnimalMotor ActivityAnimalsBlood GlucoseBody WeightCatecholaminesDiet, High-FatEatingEnergy MetabolismEpinephrineGTP-Binding Protein beta SubunitsHeterozygoteInsulinMiceMice, KnockoutBlood GlucoseCatecholaminesEpinephrineGnb5 protein, mouseGTP-Binding Protein beta SubunitsInsulin

Identifiers

PMID21804131
PMCPMC3205839
OpenAlexW2150309719

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.