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Federico Gatto Department of Internal Medicine, Rotterdam, The Netherlands
Endocrinology Unit, IRCCS Ospedale Policlinico San Martino, Genoa, Italy

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Richard A Feelders Department of Internal Medicine, Rotterdam, The Netherlands
Pituitary Center Rotterdam, Erasmus MC, Rotterdam, The Netherlands

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Rob van der Pas Department of Internal Medicine, Rotterdam, The Netherlands

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Peter van Koetsveld Department of Internal Medicine, Rotterdam, The Netherlands

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Eleonora Bruzzone Department of Internal Medicine and & Medical Specialties (DIMI) and Center of Excellence for Biomedical Research (CEBR), University of Genoa, Genoa, Italy

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Marica Arvigo Department of Internal Medicine and & Medical Specialties (DIMI) and Center of Excellence for Biomedical Research (CEBR), University of Genoa, Genoa, Italy

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Fadime Dogan Department of Internal Medicine, Rotterdam, The Netherlands

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Steven Lamberts Department of Internal Medicine, Rotterdam, The Netherlands

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Diego Ferone Endocrinology Unit, IRCCS Ospedale Policlinico San Martino, Genoa, Italy
Department of Internal Medicine and & Medical Specialties (DIMI) and Center of Excellence for Biomedical Research (CEBR), University of Genoa, Genoa, Italy

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Leo Hofland Department of Internal Medicine, Rotterdam, The Netherlands
Pituitary Center Rotterdam, Erasmus MC, Rotterdam, The Netherlands

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treatment ( Pivonello et al . 2004 , de Bruin et al . 2009 b , Chinezu et al . 2014 ). Noteworthy, both SSTs and DRs belong to the superfamily of G-protein-coupled receptors (GPCRs), which is known to be tightly regulated by β-arrestins in its

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-19-0311
Volume/Issue:
Volume 245: Issue 1
Restricted access
Sébastien Marion UMR 6175, INRA/CNRS/Université de Tours, Station de Physiologie de la Reproduction et des Comportements, 37380 Nouzilly, France

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Elodie Kara UMR 6175, INRA/CNRS/Université de Tours, Station de Physiologie de la Reproduction et des Comportements, 37380 Nouzilly, France

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Pascale Crepieux UMR 6175, INRA/CNRS/Université de Tours, Station de Physiologie de la Reproduction et des Comportements, 37380 Nouzilly, France

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Vincent Piketty UMR 6175, INRA/CNRS/Université de Tours, Station de Physiologie de la Reproduction et des Comportements, 37380 Nouzilly, France

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Nadine Martinat UMR 6175, INRA/CNRS/Université de Tours, Station de Physiologie de la Reproduction et des Comportements, 37380 Nouzilly, France

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Florian Guillou UMR 6175, INRA/CNRS/Université de Tours, Station de Physiologie de la Reproduction et des Comportements, 37380 Nouzilly, France

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Eric Reiter UMR 6175, INRA/CNRS/Université de Tours, Station de Physiologie de la Reproduction et des Comportements, 37380 Nouzilly, France

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signaling is their phosphorylation by the G protein-coupled receptor kinases (GRKs). These serine–threonine kinases are able to phosphorylate agonist-occupied receptors and promote their desensitization. The association of β-arrestins with GRK

Article Type:
Research Article
DOI:
https://doi.org/10.1677/joe.1.06857
Volume/Issue:
Volume 190: Issue 2
Free access
Jonathan D Douros Novo Nordisk Research Center Indianapolis, Indianapolis, Indiana, USA

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Jacek Mokrosinski Novo Nordisk Research Center Indianapolis, Indianapolis, Indiana, USA

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Brian Finan Novo Nordisk Research Center Indianapolis, Indianapolis, Indiana, USA

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account for a mere ~50% of GLP-1-mediated insulin secretion in mouse islets and ~30% in human islets. Finally, it has recently been demonstrated that β-arrestin, an intracellular scaffolding protein canonically thought to facilitate ligand

Article Type:
Review Article
Collections:
Incretins
DOI:
https://doi.org/10.1530/JOE-23-0226
Volume/Issue:
Volume 261: Issue 2
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Claudia Campana Department of Internal Medicine, Division of Endocrinology, Erasmus Medical Center, Rotterdam, The Netherlands
Endocrinology Unit, Department of Internal Medicine and Medical Specialties, School of Medical and Pharmaceutical Sciences, University of Genova, Genova, Italy

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Anand M Iyer Department of Internal Medicine, Division of Endocrinology, Erasmus Medical Center, Rotterdam, The Netherlands

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Diego Ferone Endocrinology Unit, Department of Internal Medicine and Medical Specialties, School of Medical and Pharmaceutical Sciences, University of Genova, Genova, Italy
Endocrinology Unit, IRCCS Ospedale Policlinico San Martino, Genova, Italy

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Federico Gatto Endocrinology Unit, IRCCS Ospedale Policlinico San Martino, Genova, Italy

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Leo J Hofland Department of Internal Medicine, Division of Endocrinology, Erasmus Medical Center, Rotterdam, The Netherlands

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either to lysosomes for further degradation or recycled back to the cell membrane ( Gatto & Hofland 2011 ). Receptor phosphorylation by GPCR kinases (GRKs) and β-arrestin (ARRB) recruitment to the cell membrane play a crucial role in the desensitization

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-23-0298
Volume/Issue:
Volume 260: Issue 3
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Nabanita S Datta Division of Endocrinology, Department of Internal Medicine, Wayne State University School of Medicine, 1107 Elliman Building, 421 East Canfield Avenue, Detroit, Michigan 48201, USA

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Tareq A Samra Division of Endocrinology, Department of Internal Medicine, Wayne State University School of Medicine, 1107 Elliman Building, 421 East Canfield Avenue, Detroit, Michigan 48201, USA

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Chandrika D Mahalingam Division of Endocrinology, Department of Internal Medicine, Wayne State University School of Medicine, 1107 Elliman Building, 421 East Canfield Avenue, Detroit, Michigan 48201, USA

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Tanuka Datta Division of Endocrinology, Department of Internal Medicine, Wayne State University School of Medicine, 1107 Elliman Building, 421 East Canfield Avenue, Detroit, Michigan 48201, USA

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Abdul B Abou-Samra Division of Endocrinology, Department of Internal Medicine, Wayne State University School of Medicine, 1107 Elliman Building, 421 East Canfield Avenue, Detroit, Michigan 48201, USA

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of the hormonal responses. Desensitization of GPCRs involves GPCR kinases (GRKs) that phosphorylate C-terminal serine and threonine residues of agonist-stimulated GPCRs and binding of the members of the β-arrestins ( Pitcher et al . 1998 , Oakley

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-10-0227
Volume/Issue:
Volume 207: Issue 3
Free access
Maria L Price Institute of Metabolism and Systems Research and Centre for Endocrinology, Diabetes and Metabolism, University of Birmingham, Birmingham, UK
Centre of Membrane Proteins and Receptors (COMPARE), Universities of Birmingham and Nottingham, Birmingham, UK

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Cameron D Ley Institute of Metabolism and Systems Research and Centre for Endocrinology, Diabetes and Metabolism, University of Birmingham, Birmingham, UK
Centre of Membrane Proteins and Receptors (COMPARE), Universities of Birmingham and Nottingham, Birmingham, UK

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Caroline M Gorvin Institute of Metabolism and Systems Research and Centre for Endocrinology, Diabetes and Metabolism, University of Birmingham, Birmingham, UK
Centre of Membrane Proteins and Receptors (COMPARE), Universities of Birmingham and Nottingham, Birmingham, UK

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is evidence that heterotetramers may occur. GHSR1a is understood to primarily signal via G q/11 pathways to activate Ca 2+ i pathways. This involves both constitutive and agonist-mediated signalling, and association between GHSR1a and β-arrestins

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-21-0206
Volume/Issue:
Volume 252: Issue 1
Open access
Alessandro Pocai Diabetes and Endocrinology, Merck Research Laboratories, Merck Sharp and Dohme Corp., 126 East Lincoln Avenue, Rahway, New Jersey 07065, USA

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, Baggio et al . 2004 , Jorgensen et al . 2007 , Pocai et al . 2009 , Kosinski et al . 2012 ). Despite being a full agonist at the human GLP1R, OXM was found to be a full agonist in recruiting β-arrestin 2 to the GCGR, but partial agonists in

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-12-0368
Volume/Issue:
Volume 215: Issue 3
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Yuta Kasahara Department of Obstetrics and Gynecology, The Jikei University School of Medicine, Tokyo, Japan

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Hiroshi Kishi Department of Obstetrics and Gynecology, The Jikei University School of Medicine, Tokyo, Japan

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Ryo Yokomizo Department of Obstetrics and Gynecology, The Jikei University School of Medicine, Tokyo, Japan

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Aikou Okamoto Department of Obstetrics and Gynecology, The Jikei University School of Medicine, Tokyo, Japan

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increases the degradation and ubiquitination of β-arrestin protein, followed by the decreased internalization of serotonin receptor, a kind of GPCR ( Luessen et al. 2019 ). β-Arrestin is a key player in the regulation of GPCR internalization; it controls

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-22-0254
Volume/Issue:
Volume 257: Issue 1
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Thierry Métayé Biophysics Laboratory, Pathology, Endocrine Surgery, Nuclear Medicine and Biophysics, Departments of

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Pierre Levillain Biophysics Laboratory, Pathology, Endocrine Surgery, Nuclear Medicine and Biophysics, Departments of

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Jean-Louis Kraimps Biophysics Laboratory, Pathology, Endocrine Surgery, Nuclear Medicine and Biophysics, Departments of

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Rémy Perdrisot Biophysics Laboratory, Pathology, Endocrine Surgery, Nuclear Medicine and Biophysics, Departments of

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G protein-coupled receptor kinase expression by β-adrenergic receptor stimulation and blockade . Circulation 98 1783 – 1789 . Iacovelli L Franchetti R Masini M De Blasi A 1996 GRK2 and β-arrestin1 as negative regulators of thyrotropin

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-07-0562
Volume/Issue:
Volume 198: Issue 1
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A Hassan School of Biological Sciences, University of Canterbury, Christchurch, New Zealand

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D Mason School of Biological Sciences, University of Canterbury, Christchurch, New Zealand

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and β-arrestins are expressed in rat anterior pituitary cells, demonstrating that, at least in this species, pituitary cells have the intracellular machinery necessary for regulation of the V1b receptor by GRKs. Furthermore, recent evidence has shown

Article Type:
Research Article
DOI:
https://doi.org/10.1677/joe.1.05654
Volume/Issue:
Volume 184: Issue 1
Free access