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Daniella B R Insuela Laboratório de Inflamação, Instituto de Nutrição, Laboratório de Imunofarmacologia, Instituto Oswaldo Cruz, Fundação Oswaldo Cruz, Avenida Brasil, n° 4365, Manguinhos, CEP 21040‐360 Rio de Janeiro, Brazil

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Julio B Daleprane Laboratório de Inflamação, Instituto de Nutrição, Laboratório de Imunofarmacologia, Instituto Oswaldo Cruz, Fundação Oswaldo Cruz, Avenida Brasil, n° 4365, Manguinhos, CEP 21040‐360 Rio de Janeiro, Brazil

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Luciana P Coelho Laboratório de Inflamação, Instituto de Nutrição, Laboratório de Imunofarmacologia, Instituto Oswaldo Cruz, Fundação Oswaldo Cruz, Avenida Brasil, n° 4365, Manguinhos, CEP 21040‐360 Rio de Janeiro, Brazil

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Adriana R Silva Laboratório de Inflamação, Instituto de Nutrição, Laboratório de Imunofarmacologia, Instituto Oswaldo Cruz, Fundação Oswaldo Cruz, Avenida Brasil, n° 4365, Manguinhos, CEP 21040‐360 Rio de Janeiro, Brazil

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Patrícia M R e Silva Laboratório de Inflamação, Instituto de Nutrição, Laboratório de Imunofarmacologia, Instituto Oswaldo Cruz, Fundação Oswaldo Cruz, Avenida Brasil, n° 4365, Manguinhos, CEP 21040‐360 Rio de Janeiro, Brazil

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Marco A Martins Laboratório de Inflamação, Instituto de Nutrição, Laboratório de Imunofarmacologia, Instituto Oswaldo Cruz, Fundação Oswaldo Cruz, Avenida Brasil, n° 4365, Manguinhos, CEP 21040‐360 Rio de Janeiro, Brazil

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Vinicius F Carvalho Laboratório de Inflamação, Instituto de Nutrição, Laboratório de Imunofarmacologia, Instituto Oswaldo Cruz, Fundação Oswaldo Cruz, Avenida Brasil, n° 4365, Manguinhos, CEP 21040‐360 Rio de Janeiro, Brazil

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seven-transmembrane receptors coupled to the G stimulatory (Gs) protein. When glucagon binds to its receptor, the α-subunit of Gs leads to the activation of adenylyl cyclase, with a subsequent increase in the intracellular levels of cAMP ( Qureshi et al

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-14-0648
Volume/Issue:
Volume 225: Issue 3
Free access
Tomoko Miyoshi
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Fumio Otsuka
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Hiroyuki Otani
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Kenichi Inagaki
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Junko Goto
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Misuzu Yamashita
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Toshio Ogura
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Yasumasa Iwasaki Department of Medicine and Clinical Science, Department of Endocrinology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-cho, Okayama City 700-8558, Japan

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Hirofumi Makino
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possibly by cAMP-independent mechanism. Importantly, exposure to a high concentration of OCT impairs the BRC effects suppressing FSK-induced cAMP production and BMP-4-Smad1,5,8 signaling in GH3 cells. AC, adenylyl cyclase; PKA, protein kinase-A. The

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-07-0549
Volume/Issue:
Volume 197: Issue 1
Free access
Audrey F Seasholtz Molecular and Behavioral Neuroscience Institute, University of Michigan, 109 Zina Pitcher Place, BSRB Room 5035, Ann Arbor, Michigan 48109, USA
Department of Biological Chemistry, University of Michigan, 109 Zina Pitcher Place, BSRB Room 5035, Ann Arbor, Michigan 48109, USA

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Miina Öhman Department of Psychiatry, University of Michigan, 109 Zina Pitcher Place, BSRB Room 5035, Ann Arbor, Michigan 48109, USA

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Amale Wardani Molecular and Behavioral Neuroscience Institute, University of Michigan, 109 Zina Pitcher Place, BSRB Room 5035, Ann Arbor, Michigan 48109, USA

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Robert C Thompson Molecular and Behavioral Neuroscience Institute, University of Michigan, 109 Zina Pitcher Place, BSRB Room 5035, Ann Arbor, Michigan 48109, USA
Department of Psychiatry, University of Michigan, 109 Zina Pitcher Place, BSRB Room 5035, Ann Arbor, Michigan 48109, USA

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types, the activation of CRHR1 or CRHR2 by CRH or urocortins results in the activation of the Gs-adenylyl cyclase pathway and increased cAMP levels; however, recent evidence has demonstrated that in some tissues and cell types both CRH receptors can

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-08-0139
Volume/Issue:
Volume 200: Issue 2
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Ramanaiah Mamillapalli Section of Endocrinology and Metabolism, Department of Internal Medicine, Yale University School of Medicine, TAC S131, PO Box 208020, New Haven, Connecticut 06520-8020, USA

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John Wysolmerski Section of Endocrinology and Metabolism, Department of Internal Medicine, Yale University School of Medicine, TAC S131, PO Box 208020, New Haven, Connecticut 06520-8020, USA

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adenylyl cyclase and reduce cAMP levels in several cell types, although this has not been thought to be a major contributor to the regulation of PTH secretion ( Hofer & Brown 2003 , Ward 2004 ). We have recently shown that inhibition of cAMP is important

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-09-0183
Volume/Issue:
Volume 204: Issue 3
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Joseph Aizen Marine Science Institute, The University of Texas at Austin, 750 Channel View Drive, Port Aransas, Texas 78373, USA

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Peter Thomas Marine Science Institute, The University of Texas at Austin, 750 Channel View Drive, Port Aransas, Texas 78373, USA

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-coupled estrogen receptor 1 (GPER1), formerly known as GPR30, is a novel, specific seven-transmembrane-domain estrogen receptor coupled to a stimulatory G protein (G s ) that mediates rapid, nongenomic estrogen actions through activation of adenylyl cyclase and

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-14-0576
Volume/Issue:
Volume 225: Issue 1
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Maureen J Charron Departments of Biochemistry, Obstetrics and Gynecology and Women's Health, Medicine, Department of Pediatrics, Albert Einstein College of Medicine, 1300 Morris Park Avenue, F312, Bronx, New York 10461, USA
Departments of Biochemistry, Obstetrics and Gynecology and Women's Health, Medicine, Department of Pediatrics, Albert Einstein College of Medicine, 1300 Morris Park Avenue, F312, Bronx, New York 10461, USA
Departments of Biochemistry, Obstetrics and Gynecology and Women's Health, Medicine, Department of Pediatrics, Albert Einstein College of Medicine, 1300 Morris Park Avenue, F312, Bronx, New York 10461, USA

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Patricia M Vuguin Departments of Biochemistry, Obstetrics and Gynecology and Women's Health, Medicine, Department of Pediatrics, Albert Einstein College of Medicine, 1300 Morris Park Avenue, F312, Bronx, New York 10461, USA

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-binding proteins to adenylyl cyclase resulting in an increase in cAMP production. cAMP activates signaling pathways that cause an increase in gluconeogenesis, glycogenolysis, and fatty acid oxidation. In addition, glucagon controls glucose, energy, and lipid

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-14-0614
Volume/Issue:
Volume 224: Issue 3
Free access
Ying Zhao Department of Molecular Medicine, Cornell University, Ithaca, New York, USA
School of Applied and Engineering Physics, Cornell University, Ithaca, New York, USA
Laboratory for Nanoscale Cell Biology, Max-Planck-Institute for Biophysical Chemistry, Goettingen, Germany

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Qinghua Fang School of Applied and Engineering Physics, Cornell University, Ithaca, New York, USA
Laboratory for Nanoscale Cell Biology, Max-Planck-Institute for Biophysical Chemistry, Goettingen, Germany

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Susanne G Straub Department of Molecular Medicine, Cornell University, Ithaca, New York, USA

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Manfred Lindau School of Applied and Engineering Physics, Cornell University, Ithaca, New York, USA
Laboratory for Nanoscale Cell Biology, Max-Planck-Institute for Biophysical Chemistry, Goettingen, Germany

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Geoffrey W G Sharp Department of Molecular Medicine, Cornell University, Ithaca, New York, USA

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, Schermerhorn & Sharp 2000 , Sieg et al. 2004 , Dezaki et al. 2007 ), thereby reversing or preventing the opening of voltage-dependent Ca 2+ channels; (ii) inhibition of adenylyl cyclase to prevent the augmentation of stimulated insulin release via

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-15-0435
Volume/Issue:
Volume 229: Issue 3
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Hyuck Joon Kwon Research Center for Cooperative Projects, Hokkaido University Graduate School of Medicine, Sapporo 060-8638, Japan

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signaling, mediates Ca 2+ -driven ATP oscillations in chondrogenesis. Consistent with this result, it was found that inhibition of cAMP synthesis with MDL12330A, an adenylyl cyclase inhibitor, eliminated the P ACTIN -PxRe oscillations ( Fig. 5 B

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-12-0131
Volume/Issue:
Volume 214: Issue 3
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Takahiko Kogai Physiology, Departments of

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Saima Sajid-Crockett Physiology, Departments of

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Lynell S Newmarch Physiology, Departments of

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Yan-Yun Liu Physiology, Departments of

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Gregory A Brent Physiology, Departments of
Physiology, Departments of

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et al . 2001 , Taki et al . 2002 ). TSH receptor activation stimulates adenylyl cyclase through the stimulatory Gα protein, followed by intracellular cAMP accumulation. The TSH/cAMP pathway stimulates the NIS proximal promoter ( Endo et al . 1997

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-08-0333
Volume/Issue:
Volume 199: Issue 2
Free access
E Louiset INSERM U413, INSERM U567, Department of Endocrinology, Laboratory of Cellular and Molecular Neuroendocrinology, European Institute for Peptide Research (IFRMP 23), University of Rouen, 76821 Mont-Saint-Aignan, France

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V Contesse INSERM U413, INSERM U567, Department of Endocrinology, Laboratory of Cellular and Molecular Neuroendocrinology, European Institute for Peptide Research (IFRMP 23), University of Rouen, 76821 Mont-Saint-Aignan, France

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L Groussin INSERM U413, INSERM U567, Department of Endocrinology, Laboratory of Cellular and Molecular Neuroendocrinology, European Institute for Peptide Research (IFRMP 23), University of Rouen, 76821 Mont-Saint-Aignan, France

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D Cartier INSERM U413, INSERM U567, Department of Endocrinology, Laboratory of Cellular and Molecular Neuroendocrinology, European Institute for Peptide Research (IFRMP 23), University of Rouen, 76821 Mont-Saint-Aignan, France

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C Duparc INSERM U413, INSERM U567, Department of Endocrinology, Laboratory of Cellular and Molecular Neuroendocrinology, European Institute for Peptide Research (IFRMP 23), University of Rouen, 76821 Mont-Saint-Aignan, France

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V Perraudin INSERM U413, INSERM U567, Department of Endocrinology, Laboratory of Cellular and Molecular Neuroendocrinology, European Institute for Peptide Research (IFRMP 23), University of Rouen, 76821 Mont-Saint-Aignan, France

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J Bertherat INSERM U413, INSERM U567, Department of Endocrinology, Laboratory of Cellular and Molecular Neuroendocrinology, European Institute for Peptide Research (IFRMP 23), University of Rouen, 76821 Mont-Saint-Aignan, France

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H Lefebvre INSERM U413, INSERM U567, Department of Endocrinology, Laboratory of Cellular and Molecular Neuroendocrinology, European Institute for Peptide Research (IFRMP 23), University of Rouen, 76821 Mont-Saint-Aignan, France
INSERM U413, INSERM U567, Department of Endocrinology, Laboratory of Cellular and Molecular Neuroendocrinology, European Institute for Peptide Research (IFRMP 23), University of Rouen, 76821 Mont-Saint-Aignan, France

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adenylyl cyclase-coupled GIP and LH receptors in bovine adrenocortical cells causes cortisol hypersecretion and adenomatous hyperproliferation in a mouse xenotransplantation model ( Mazzuco et al . 2006 a , b ). In conclusion, the present study provides

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-07-0413
Volume/Issue:
Volume 196: Issue 1
Free access