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Sunita M C De Sousa Endocrine & Metabolic Unit, Royal Adelaide Hospital, Adelaide, Australia
South Australian Adult Genetics Unit, Royal Adelaide Hospital, Adelaide, Australia
Adelaide Medical School, University of Adelaide, Adelaide, Australia

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Nèle F Lenders Department of Endocrinology, St Vincent’s Hospital, Sydney, NSW, Australia
Garvan Institute of Medical Research, Sydney, NSW, Australia
St Vincent’s Clinical School, University of New South Wales, Sydney, NSW, Australia

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Lydia S Lamb Garvan Institute of Medical Research, Sydney, NSW, Australia
St Vincent’s Clinical School, University of New South Wales, Sydney, NSW, Australia

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Warrick J Inder Department of Diabetes and Endocrinology, Princess Alexandra Hospital, Brisbane, Australia
Academy for Medical Education, Faculty of Medicine, the University of Queensland, Brisbane, Australia

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Ann McCormack Department of Endocrinology, St Vincent’s Hospital, Sydney, NSW, Australia
Garvan Institute of Medical Research, Sydney, NSW, Australia
St Vincent’s Clinical School, University of New South Wales, Sydney, NSW, Australia

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). GNAS was the first gene found to harbour driver mutations in PAs. In 1989, Landis et al. categorised eight PA operative specimens from acromegalic patients as having low or high adenylyl cyclase activity. The authors hypothesised that constitutive

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Marie M Devillers Sorbonne Paris Cité, Université Paris-Diderot, CNRS, INSERM, Biologie Fonctionnelle et Adaptative UMR 8251, Physiologie de l’Axe Gonadotrope U1133, Paris, France

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Florence Petit Sorbonne Paris Cité, Université Paris-Diderot, CNRS, INSERM, Biologie Fonctionnelle et Adaptative UMR 8251, Physiologie de l’Axe Gonadotrope U1133, Paris, France

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Victoria Cluzet Sorbonne Paris Cité, Université Paris-Diderot, CNRS, INSERM, Biologie Fonctionnelle et Adaptative UMR 8251, Physiologie de l’Axe Gonadotrope U1133, Paris, France

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Charlotte M François Sorbonne Paris Cité, Université Paris-Diderot, CNRS, INSERM, Biologie Fonctionnelle et Adaptative UMR 8251, Physiologie de l’Axe Gonadotrope U1133, Paris, France

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Frank Giton APHP CIB GHU Sud Henri Mondor, INSERM IMRB U955, Eq.07, Faculté de Médecine, Créteil, France

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Ghislaine Garrel Sorbonne Paris Cité, Université Paris-Diderot, CNRS, INSERM, Biologie Fonctionnelle et Adaptative UMR 8251, Physiologie de l’Axe Gonadotrope U1133, Paris, France

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Joëlle Cohen-Tannoudji Sorbonne Paris Cité, Université Paris-Diderot, CNRS, INSERM, Biologie Fonctionnelle et Adaptative UMR 8251, Physiologie de l’Axe Gonadotrope U1133, Paris, France

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Céline J Guigon Sorbonne Paris Cité, Université Paris-Diderot, CNRS, INSERM, Biologie Fonctionnelle et Adaptative UMR 8251, Physiologie de l’Axe Gonadotrope U1133, Paris, France

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granulosa cells ( Pellatt et al. 2011 ), since AMH did not alter Fshr transcript abundance, albeit we cannot exclude that it could have affected FSHR protein levels. However, one can hypothesize that AMH could inhibit FSH-stimulated adenylyl cyclase

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Cecilia Brännmark Department of Physiology/Metabolic Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden

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Emma I Kay Department of Physiology/Metabolic Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden
Bioscience Metabolism, Research and Early Development, Cardiovascular, Renal and Metabolism, Biopharmaceuticals R&D, AstraZeneca, Gothenburg, Sweden

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Unn Örtegren Kugelberg Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden

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Belén Chanclón Department of Physiology/Metabolic Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden

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Man Mohan Shrestha Department of Physiology/Metabolic Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden

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Ingrid Wernstedt Asterholm Department of Physiology/Metabolic Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden

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Peter Strålfors Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden

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Charlotta S Olofsson Department of Physiology/Metabolic Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden

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selectivity and allows cells to modify their responses by the restricted organization of downstream target mediators, such as adenylyl cyclases (ACs), phosphodiesterases (PDEs), PKA and Epac ( Ostrom & Insel 2004 , Insel et al. 2005 ). Thus, depletion of

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Sihan Lv Department of Endocrinology, Shanghai Tenth People’s Hospital, School of Medicine, Tongji University, Shanghai, China

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Xinchen Qiu Department of Endocrinology, Shanghai Tenth People’s Hospital, School of Medicine, Tongji University, Shanghai, China
Translational Medical Center for Stem Cell Therapy & Institute for Regenerative Medicine, Shanghai East Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, China

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Jian Li Department of Endocrinology, Shanghai Tenth People’s Hospital, School of Medicine, Tongji University, Shanghai, China
Translational Medical Center for Stem Cell Therapy & Institute for Regenerative Medicine, Shanghai East Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, China

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Jinye Liang Translational Medical Center for Stem Cell Therapy & Institute for Regenerative Medicine, Shanghai East Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, China

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Weida Li Translational Medical Center for Stem Cell Therapy & Institute for Regenerative Medicine, Shanghai East Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, China

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Chao Zhang Translational Medical Center for Stem Cell Therapy & Institute for Regenerative Medicine, Shanghai East Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, China

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Zhen-Ning Zhang Translational Medical Center for Stem Cell Therapy & Institute for Regenerative Medicine, Shanghai East Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, China

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Bing Luan Department of Endocrinology, Shanghai Tenth People’s Hospital, School of Medicine, Tongji University, Shanghai, China

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of stimulatory G protein (Gs) and elevation of intracellular cAMP levels resulting from activation of adenylyl cyclase. In the meantime, cAMP could also be secreted out of the cells and function as a paracrine or endocrine molecule ( Northrop & Parks

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Xin-gang Yao
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Xin Xu
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Gai-hong Wang
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Min Lei
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Ling-ling Quan Key Laboratory of Receptor Research, College of Life and Environmental Sciences, Department of Pharmacology, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, 555 Zuchongzhi Road, Shanghai 201203, China

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Yan-hua Cheng Key Laboratory of Receptor Research, College of Life and Environmental Sciences, Department of Pharmacology, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, 555 Zuchongzhi Road, Shanghai 201203, China

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Ping Wan Key Laboratory of Receptor Research, College of Life and Environmental Sciences, Department of Pharmacology, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, 555 Zuchongzhi Road, Shanghai 201203, China

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Jin-pei Zhou Key Laboratory of Receptor Research, College of Life and Environmental Sciences, Department of Pharmacology, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, 555 Zuchongzhi Road, Shanghai 201203, China

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Jing Chen
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Li-hong Hu
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Xu Shen
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-potentiated GSIS in INS-832/13 cells. As demonstrated in Fig. 3 A, BBT (20 μM) increased intracellular cAMP with 16.8 mM glucose. Accordingly, we determined whether cAMP was essential for the BBT-potentiated GSIS. In the assay, MDL-12,330A (an adenylyl cyclase (AC

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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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). Most of the TSH effects are mediated by cAMP via an adenylyl cyclase-activating Gα protein, although at higher concentrations the TSH stimulates inositol 1,3,4-trisphosphate generation in human thyroid cells ( Van Sande et al . 2006 ). A key role for

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Joyce Emons
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Bas E Dutilh Department of Paediatrics, Centre for Molecular and Biomolecular Informatics, Department of Human Molecular Genetics, Medical Research Center, Molecular Oncology Laboratory, Department of Cell Biology, Department of Tissue Regeneration, Leiden University Medical Center, 2300 ZA Leiden, The Netherlands

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Eva Decker Department of Paediatrics, Centre for Molecular and Biomolecular Informatics, Department of Human Molecular Genetics, Medical Research Center, Molecular Oncology Laboratory, Department of Cell Biology, Department of Tissue Regeneration, Leiden University Medical Center, 2300 ZA Leiden, The Netherlands

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Heide Pirzer Department of Paediatrics, Centre for Molecular and Biomolecular Informatics, Department of Human Molecular Genetics, Medical Research Center, Molecular Oncology Laboratory, Department of Cell Biology, Department of Tissue Regeneration, Leiden University Medical Center, 2300 ZA Leiden, The Netherlands

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Carsten Sticht Department of Paediatrics, Centre for Molecular and Biomolecular Informatics, Department of Human Molecular Genetics, Medical Research Center, Molecular Oncology Laboratory, Department of Cell Biology, Department of Tissue Regeneration, Leiden University Medical Center, 2300 ZA Leiden, The Netherlands

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Norbert Gretz Department of Paediatrics, Centre for Molecular and Biomolecular Informatics, Department of Human Molecular Genetics, Medical Research Center, Molecular Oncology Laboratory, Department of Cell Biology, Department of Tissue Regeneration, Leiden University Medical Center, 2300 ZA Leiden, The Netherlands

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Gudrun Rappold Department of Paediatrics, Centre for Molecular and Biomolecular Informatics, Department of Human Molecular Genetics, Medical Research Center, Molecular Oncology Laboratory, Department of Cell Biology, Department of Tissue Regeneration, Leiden University Medical Center, 2300 ZA Leiden, The Netherlands

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Ewan R Cameron Department of Paediatrics, Centre for Molecular and Biomolecular Informatics, Department of Human Molecular Genetics, Medical Research Center, Molecular Oncology Laboratory, Department of Cell Biology, Department of Tissue Regeneration, Leiden University Medical Center, 2300 ZA Leiden, The Netherlands

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James C Neil Department of Paediatrics, Centre for Molecular and Biomolecular Informatics, Department of Human Molecular Genetics, Medical Research Center, Molecular Oncology Laboratory, Department of Cell Biology, Department of Tissue Regeneration, Leiden University Medical Center, 2300 ZA Leiden, The Netherlands

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Gary S Stein Department of Paediatrics, Centre for Molecular and Biomolecular Informatics, Department of Human Molecular Genetics, Medical Research Center, Molecular Oncology Laboratory, Department of Cell Biology, Department of Tissue Regeneration, Leiden University Medical Center, 2300 ZA Leiden, The Netherlands

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Andre J van Wijnen Department of Paediatrics, Centre for Molecular and Biomolecular Informatics, Department of Human Molecular Genetics, Medical Research Center, Molecular Oncology Laboratory, Department of Cell Biology, Department of Tissue Regeneration, Leiden University Medical Center, 2300 ZA Leiden, The Netherlands

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Jan Maarten Wit
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Janine N Post Department of Paediatrics, Centre for Molecular and Biomolecular Informatics, Department of Human Molecular Genetics, Medical Research Center, Molecular Oncology Laboratory, Department of Cell Biology, Department of Tissue Regeneration, Leiden University Medical Center, 2300 ZA Leiden, The Netherlands

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Marcel Karperien Department of Paediatrics, Centre for Molecular and Biomolecular Informatics, Department of Human Molecular Genetics, Medical Research Center, Molecular Oncology Laboratory, Department of Cell Biology, Department of Tissue Regeneration, Leiden University Medical Center, 2300 ZA Leiden, The Netherlands

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involving membrane-bound receptors like GPR30, resulting in the activation of adenylyl cyclases and MAPKs ( Filardo et al . 2002 ). In addition, Teplyuk et al . (2008) describe a direct role for Runx2 in G-protein-coupled signaling for controlling growth

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Olena A Fedorenko School of Life Sciences, University of Nottingham, Nottingham, UK

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Pawitra Pulbutr Faculty of Pharmacy, Mahasarakham University, Mahasarakham, Thailand

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Elin Banke Department of Physiology/Metabolic Physiology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, Göteborg, Sweden

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Nneoma E Akaniro-Ejim School of Life Sciences, University of Nottingham, Nottingham, UK

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Donna C Bentley School of Sport, Exercise and Health Sciences, Loughborough University, Loughborough, UK

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Charlotta S Olofsson Department of Physiology/Metabolic Physiology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, Göteborg, Sweden

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Sue Chan School of Life Sciences, University of Nottingham, Nottingham, UK

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Paul A Smith School of Life Sciences, University of Nottingham, Nottingham, UK

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unlikely to involve the Ca 2+ -sensitive, isoform III, of adenylyl cyclase found in WFA ( Wang et al. 2009 ) since changes in Ca 2+ influx do not affect adipocyte cAMP levels under basal conditions ( Ziegler et al. 1980 ). However, adipocyte

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Christian Hölscher Division of Biomedical and Life Sciences, Faculty of Health and Medicine, Lancaster University, Lancaster LA1 4YQ, UK

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injected peripherally ( Holscher 2011 ). Figure 2 Overview of the main pathways induced by GLP-1 in neurons. The GLP-1 receptor is a member of a different classes of receptors compared with the IR. Activation of the GLP-1R activates an adenylyl cyclase and

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Aline Cordeiro Biophysics Institute Carlos Chagas Filho, Federal University of Rio de Janeiro, Centro de Ciências da Saúde, Avenida Carlos Chagas Filho, 373, Bloco G, Cidade Universitária - Ilha do Fundão, Rio de Janeiro - RJ 21941-902, Brazil

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Luana Lopes Souza Biophysics Institute Carlos Chagas Filho, Federal University of Rio de Janeiro, Centro de Ciências da Saúde, Avenida Carlos Chagas Filho, 373, Bloco G, Cidade Universitária - Ilha do Fundão, Rio de Janeiro - RJ 21941-902, Brazil

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Marcelo Einicker-Lamas Biophysics Institute Carlos Chagas Filho, Federal University of Rio de Janeiro, Centro de Ciências da Saúde, Avenida Carlos Chagas Filho, 373, Bloco G, Cidade Universitária - Ilha do Fundão, Rio de Janeiro - RJ 21941-902, Brazil

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Carmen Cabanelas Pazos-Moura Biophysics Institute Carlos Chagas Filho, Federal University of Rio de Janeiro, Centro de Ciências da Saúde, Avenida Carlos Chagas Filho, 373, Bloco G, Cidade Universitária - Ilha do Fundão, Rio de Janeiro - RJ 21941-902, Brazil

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on the adenylyl cyclase – cAMP – PKA pathway In the presence of a ligand, membrane surface Gs protein-coupled receptors (GPCR) replace GDP with GTP, leading to activation of adenylyl cyclase with consequent increased levels of cAMP. cAMP effects are

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