Evidence map›Paper›PMID 28145434›Full record

ArticleNature communications2017

β-arrestin-2 is an essential regulator of pancreatic β-cell function under physiological and pathophysiological conditions.

Lu Zhu, Joana Almaça, Prasanna K Dadi, Hao Hong, Wataru Sakamoto, Mario Rossi, Regina J Lee, Nicholas C Vierra, Huiyan Lu, Yinghong Cui and 13 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
7.9field-weighted citation impact, top 2% 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

48 citing papers in PubMed, 77 citations in OpenAlex.

  1. Review
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  11. Pharmacological reviews · 2023
    Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Intracellular ATP Signaling Contributes to FAM3A-Induced PDX1 Upregulation in Pancreatic Beta Cells.Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association · 2022
    Article
  18. Article
  19. Article
  20. The therapeutic potential of GLP-1 receptor biased agonism.British journal of pharmacology · 2022 · on this map
    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

23 authors at 8 institutions in 2 countries.

Lu ZhuMolecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892, USA.
Joana AlmaçaDivision of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Miami Miller School of Medicine, Miami, Florida 33136, USA.
Prasanna K DadiDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, Tennessee 37232, USA.
Hao HongMolecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892, USA.
Wataru SakamotoMolecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892, USA.
Mario RossiMolecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892, USA.
Regina J LeeMolecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892, USA.
Nicholas C VierraDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, Tennessee 37232, USA.
Huiyan LuMouse Transgenic Core Facility, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892, USA.
Yinghong CuiMolecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892, USA.
Sara M McMillinMolecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892, USA.
Nicole A PerryDepartment of Pharmacology, Vanderbilt University, Nashville, Tennessee 37232, USA.
Vsevolod V GurevichDepartment of Pharmacology, Vanderbilt University, Nashville, Tennessee 37232, USA.ORCID 0000-0002-3950-5351
Amy LeeDepartment of Molecular Physiology and Biophysics, University of Iowa, Iowa City, Iowa 52242, USA.
Bryan KuoLaboratory of Bioengineering and Physical Science, National Institute of Biomedical Imaging and Bioengineering, Bethesda, Maryland 20892, USA.
Richard D LeapmanLaboratory of Bioengineering and Physical Science, National Institute of Biomedical Imaging and Bioengineering, Bethesda, Maryland 20892, USA.
Franz M MatschinskyDepartment of Biochemistry and Biophysics, University of Pennsylvania School of Medicine, Philadelphia, Pennslvania 19104, USA.
Nicolai M DolibaDepartment of Biochemistry and Biophysics, University of Pennsylvania School of Medicine, Philadelphia, Pennslvania 19104, USA.
Nikhil M UrsDepartment of Cell Biology, Duke University Medical Center, Durham, North Carolina 27710, USA.
Marc G CaronDepartment of Cell Biology, Duke University Medical Center, Durham, North Carolina 27710, USA.
David A JacobsonDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, Tennessee 37232, USA.
Alejandro CaicedoDivision of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Miami Miller School of Medicine, Miami, Florida 33136, USA.
Jürgen WessMolecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892, USA.
National Institute of Diabetes and Digestive and Kidney Diseases · USVanderbilt University · USDuke University · USNational Institute of Biomedical Imaging and Bioengineering · USUniversity of Miami · USUniversity of Pennsylvania · USNanjing University of Chinese Medicine · CNUniversity of Iowa · US

Funding

VIRAL VECTOR COREP30DK019525 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI MITCHELL A. LAZAR · 1986 to 2026
$48.3M
Role of G protein-coupled receptors in regulating glucose and energy homeostasisZIADK075021 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI WESS, JURGEN · 2009 to 2025
$37.0M
Three-Dimensional Cell and Tissue Reconstruction by Serial Block Face SEMZIAEB000086 · NIBIB · NATIONAL INSTITUTE OF BIOMEDICAL IMAGING AND BIOENGINEERING · PI LEAPMAN, RICHARD · 2013 to 2025
$23.6M
STRUCTURE/FUNCTION STUDIES OF VISUAL ARRESTINR01EY011500 · NEI · VANDERBILT UNIVERSITY · PI T M Iverson · 1997 to 2026
$12.3M
Akt/GSK-3 Signaling Cascade and the Actions of DopamineR37MH073853 · NIMH · DUKE UNIVERSITY · PI CARON, MARC G. · 2011 to 2020
$6.4M
Regulation of auditory calcium channelsR01DC009433 · NIDCD · UNIVERSITY OF IOWA · PI LEE, AMY · 2009 to 2018
$3.6M
Two-Pore-Domain Potassium Channels as Novel Targets for Modulating Islet Hormone SecretionR01DK097392 · NIDDK · VANDERBILT UNIVERSITY · PI JACOBSON, DAVID AARON · 2013 to 2022
$3.3M
Targeted Engineering of Designer Arrestins to Regulate Cell SignalingR35GM122491 · NIGMS · VANDERBILT UNIVERSITY · PI GUREVICH, VSEVOLOD V. · 2017 to 2021
$2.6M
Arrestin interactions with non-receptor binding partnersR01GM077561 · NIGMS · VANDERBILT UNIVERSITY · PI GUREVICH, VSEVOLOD V. · 2007 to 2015
$2.3M
Regulation of Neuronal Calcium ChannelsR01NS084190 · NINDS · UNIVERSITY OF IOWA · PI LEE, AMY · 2014 to 2018
$2.2M
The Role of Innervation for Hormone Secretion in Human IsletsR01DK084321 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI CAICEDO, ALEJANDRO · 2011 to 2015
$1.8M
Cholinergic signaling in the human pancreatic isletR01DK111538 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI CAICEDO, ALEJANDRO · 2016 to 2018
$1.2M
NEI NIH HHS R01 EY011500NIDCD NIH HHS R01 DC009433NIDDK NIH HHS K01 DK081666NIDDK NIH HHS K01 DK111757NIDDK NIH HHS P30 DK019525NIDDK NIH HHS R01 DK084321NIDDK NIH HHS R01 DK097392NIDDK NIH HHS R01 DK111538NIDDK NIH HHS R56 DK084321NIEHS NIH HHS R21 ES025673NIGMS NIH HHS R01 GM077561NIGMS NIH HHS R01 GM109955NIGMS NIH HHS R35 GM122491NIMH NIH HHS R37 MH073853NINDS NIH HHS R01 NS084190
6 · The paper itself

Abstract

β-arrestins are critical signalling molecules that regulate many fundamental physiological functions including the maintenance of euglycemia and peripheral insulin sensitivity. Here we show that inactivation of the β-arrestin-2 gene, barr2, in β-cells of adult mice greatly impairs insulin release and glucose tolerance in mice fed with a calorie-rich diet. Both glucose and KCl-induced insulin secretion and calcium responses were profoundly reduced in β-arrestin-2 (barr2) deficient β-cells. In human β-cells, barr2 knockdown abolished glucose-induced insulin secretion. We also show that the presence of barr2 is essential for proper CAMKII function in β-cells. Importantly, overexpression of barr2 in β-cells greatly ameliorates the metabolic deficits displayed by mice consuming a high-fat diet. Thus, our data identify barr2 as an important regulator of β-cell function, which may serve as a new target to improve β-cell function.

Indexed as

Animalsbeta-Arrestin 2Calcium-Calmodulin-Dependent Protein Kinase Type 2Cell LineCell Line, TumorDiet, High-FatGene ExpressionHumansInsulinInsulin-Secreting CellsInsulin SecretionIslets of LangerhansMice, Inbred C57BLMice, KnockoutMice, TransgenicSignal Transductionbeta-Arrestin 2Calcium-Calmodulin-Dependent Protein Kinase Type 2Insulin

Identifiers

PMID28145434
PMCPMC5296650
OpenAlexW2583996845

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Registered trials

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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.