Loss of α-cell GRK2 modulates glucagon response and supports cardiac function.

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Title: Loss of α-cell GRK2 modulates glucagon response and supports cardiac function.
Authors: Snyder J; Department of Pharmacology and Physiology, Drexel University College of Medicine, Philadelphia, Pennsylvania., Underwood L; Department of Medicine, Division of Cardiovascular Diseases, University of Alabama at Birmingham, Birmingham, Alabama., Jiang CS; Department of Medicine, Division of Cardiovascular Diseases, University of Alabama at Birmingham, Birmingham, Alabama., Kaml V; Department of Medicine, Division of Cardiovascular Diseases, University of Alabama at Birmingham, Birmingham, Alabama., Rajasekaran S; Department of Medicine, Division of Cardiovascular Diseases, University of Alabama at Birmingham, Birmingham, Alabama., Xie L; Department of Medicine, Division of Cardiovascular Diseases, University of Alabama at Birmingham, Birmingham, Alabama., Dotson CR; Department of Medicine, Division of Cardiovascular Diseases, University of Alabama at Birmingham, Birmingham, Alabama., Sato PY; Department of Medicine, Division of Cardiovascular Diseases, University of Alabama at Birmingham, Birmingham, Alabama. Electronic address: psato@uab.edu.
Source: Molecular pharmacology [Mol Pharmacol] 2026 Apr; Vol. 108 (4), pp. 100115. Date of Electronic Publication: 2026 Mar 04.
Publication Type: Journal Article
Journal Info: Publisher: American Society for Pharmacology and Experimental Therapeutics Country of Publication: Netherlands NLM ID: 0035623 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1521-0111 (Electronic) Linking ISSN: 0026895X NLM ISO Abbreviation: Mol Pharmacol Subsets: MEDLINE
Database: MEDLINE Ultimate
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  Data: <searchLink fieldCode="AU" term="%22Snyder+J%22">Snyder J</searchLink>; Department of Pharmacology and Physiology, Drexel University College of Medicine, Philadelphia, Pennsylvania.<br /><searchLink fieldCode="AU" term="%22Underwood+L%22">Underwood L</searchLink>; Department of Medicine, Division of Cardiovascular Diseases, University of Alabama at Birmingham, Birmingham, Alabama.<br /><searchLink fieldCode="AU" term="%22Jiang+CS%22">Jiang CS</searchLink>; Department of Medicine, Division of Cardiovascular Diseases, University of Alabama at Birmingham, Birmingham, Alabama.<br /><searchLink fieldCode="AU" term="%22Kaml+V%22">Kaml V</searchLink>; Department of Medicine, Division of Cardiovascular Diseases, University of Alabama at Birmingham, Birmingham, Alabama.<br /><searchLink fieldCode="AU" term="%22Rajasekaran+S%22">Rajasekaran S</searchLink>; Department of Medicine, Division of Cardiovascular Diseases, University of Alabama at Birmingham, Birmingham, Alabama.<br /><searchLink fieldCode="AU" term="%22Xie+L%22">Xie L</searchLink>; Department of Medicine, Division of Cardiovascular Diseases, University of Alabama at Birmingham, Birmingham, Alabama.<br /><searchLink fieldCode="AU" term="%22Dotson+CR%22">Dotson CR</searchLink>; Department of Medicine, Division of Cardiovascular Diseases, University of Alabama at Birmingham, Birmingham, Alabama.<br /><searchLink fieldCode="AU" term="%22Sato+PY%22">Sato PY</searchLink>; Department of Medicine, Division of Cardiovascular Diseases, University of Alabama at Birmingham, Birmingham, Alabama. Electronic address: psato@uab.edu.
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  Data: <searchLink fieldCode="JN" term="%220035623%22">Molecular pharmacology</searchLink> [Mol Pharmacol] 2026 Apr; Vol. 108 (4), pp. 100115. <i>Date of Electronic Publication: </i>2026 Mar 04.
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        Value: 10.1016/j.molpha.2026.100115
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              Text: 2026 Apr
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              Y: 2026
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