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Richard Hanna Department of Biology, East Carolina University, 1000 E. 5th Street, Greenville, North Carolina 27858-4553, USA
Marine Science Institute, University of Texas at Austin, 750 Channelview Drive, Port Aransas, Texas 78373, USA

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Yefei Pang Department of Biology, East Carolina University, 1000 E. 5th Street, Greenville, North Carolina 27858-4553, USA
Marine Science Institute, University of Texas at Austin, 750 Channelview Drive, Port Aransas, Texas 78373, USA

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Peter Thomas Department of Biology, East Carolina University, 1000 E. 5th Street, Greenville, North Carolina 27858-4553, USA
Marine Science Institute, University of Texas at Austin, 750 Channelview Drive, Port Aransas, Texas 78373, USA

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Yong Zhu Department of Biology, East Carolina University, 1000 E. 5th Street, Greenville, North Carolina 27858-4553, USA
Marine Science Institute, University of Texas at Austin, 750 Channelview Drive, Port Aransas, Texas 78373, USA

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-blots and 1:200 dilution for flow cytometry; Cell Signaling). Cells were split at least 48 h prior to testing to allow mPR protein expression to recover and then serum starved for 72 h to reduce basal MAPK activity. Activation was measured after 5-min

Article Type:
Research Article
DOI:
https://doi.org/10.1677/joe.1.06694
Volume/Issue:
Volume 190: Issue 2
Free access
Chandrika D Mahalingam Division of Endocrinology, Department of Orthopedic Surgery, Department of Urology and Pathology, Departments of Craniofacial Biology and Microbiology and Immunology, Barbara Ann Karmanos Cancer Institute, Cardiovascular Research Institute, Department of Internal Medicine, Wayne State University School of Medicine, Detroit, Michigan 48201, USA

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Tanuka Datta Division of Endocrinology, Department of Orthopedic Surgery, Department of Urology and Pathology, Departments of Craniofacial Biology and Microbiology and Immunology, Barbara Ann Karmanos Cancer Institute, Cardiovascular Research Institute, Department of Internal Medicine, Wayne State University School of Medicine, Detroit, Michigan 48201, USA

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Rashmi V Patil Division of Endocrinology, Department of Orthopedic Surgery, Department of Urology and Pathology, Departments of Craniofacial Biology and Microbiology and Immunology, Barbara Ann Karmanos Cancer Institute, Cardiovascular Research Institute, Department of Internal Medicine, Wayne State University School of Medicine, Detroit, Michigan 48201, USA

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Jaclynn Kreider Division of Endocrinology, Department of Orthopedic Surgery, Department of Urology and Pathology, Departments of Craniofacial Biology and Microbiology and Immunology, Barbara Ann Karmanos Cancer Institute, Cardiovascular Research Institute, Department of Internal Medicine, Wayne State University School of Medicine, Detroit, Michigan 48201, USA

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R Daniel Bonfil Division of Endocrinology, Department of Orthopedic Surgery, Department of Urology and Pathology, Departments of Craniofacial Biology and Microbiology and Immunology, Barbara Ann Karmanos Cancer Institute, Cardiovascular Research Institute, Department of Internal Medicine, Wayne State University School of Medicine, Detroit, Michigan 48201, USA
Division of Endocrinology, Department of Orthopedic Surgery, Department of Urology and Pathology, Departments of Craniofacial Biology and Microbiology and Immunology, Barbara Ann Karmanos Cancer Institute, Cardiovascular Research Institute, Department of Internal Medicine, Wayne State University School of Medicine, Detroit, Michigan 48201, USA

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Keith L Kirkwood Division of Endocrinology, Department of Orthopedic Surgery, Department of Urology and Pathology, Departments of Craniofacial Biology and Microbiology and Immunology, Barbara Ann Karmanos Cancer Institute, Cardiovascular Research Institute, Department of Internal Medicine, Wayne State University School of Medicine, Detroit, Michigan 48201, USA

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Steven A Goldstein Division of Endocrinology, Department of Orthopedic Surgery, Department of Urology and Pathology, Departments of Craniofacial Biology and Microbiology and Immunology, Barbara Ann Karmanos Cancer Institute, Cardiovascular Research Institute, Department of Internal Medicine, Wayne State University School of Medicine, Detroit, Michigan 48201, USA

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Abdul B Abou-Samra Division of Endocrinology, Department of Orthopedic Surgery, Department of Urology and Pathology, Departments of Craniofacial Biology and Microbiology and Immunology, Barbara Ann Karmanos Cancer Institute, Cardiovascular Research Institute, Department of Internal Medicine, Wayne State University School of Medicine, Detroit, Michigan 48201, USA

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Nabanita S Datta Division of Endocrinology, Department of Orthopedic Surgery, Department of Urology and Pathology, Departments of Craniofacial Biology and Microbiology and Immunology, Barbara Ann Karmanos Cancer Institute, Cardiovascular Research Institute, Department of Internal Medicine, Wayne State University School of Medicine, Detroit, Michigan 48201, USA
Division of Endocrinology, Department of Orthopedic Surgery, Department of Urology and Pathology, Departments of Craniofacial Biology and Microbiology and Immunology, Barbara Ann Karmanos Cancer Institute, Cardiovascular Research Institute, Department of Internal Medicine, Wayne State University School of Medicine, Detroit, Michigan 48201, USA
Division of Endocrinology, Department of Orthopedic Surgery, Department of Urology and Pathology, Departments of Craniofacial Biology and Microbiology and Immunology, Barbara Ann Karmanos Cancer Institute, Cardiovascular Research Institute, Department of Internal Medicine, Wayne State University School of Medicine, Detroit, Michigan 48201, USA

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-related peptide (PTHrP) bind to the PTH 1 receptor (PTH1R) and stimulate multiple signaling cascades including adenylate cyclase/protein kinase A, phospholipase C/protein kinase C, and mitogen-activated protein kinases (MAPKs); leading to pleiotropic anabolic and

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-11-0144
Volume/Issue:
Volume 211: Issue 2
Free access
Thangiah Geetha Center for Metabolic and Vascular Biology, Department of Pharmaceutical Sciences, Arizona State University, Tempe, Arizona 85287, USA

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Paul Langlais Center for Metabolic and Vascular Biology, Department of Pharmaceutical Sciences, Arizona State University, Tempe, Arizona 85287, USA

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Michael Caruso Center for Metabolic and Vascular Biology, Department of Pharmaceutical Sciences, Arizona State University, Tempe, Arizona 85287, USA

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Zhengping Yi Center for Metabolic and Vascular Biology, Department of Pharmaceutical Sciences, Arizona State University, Tempe, Arizona 85287, USA
Center for Metabolic and Vascular Biology, Department of Pharmaceutical Sciences, Arizona State University, Tempe, Arizona 85287, USA

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phosphatases), such as phosphorylation and dephosphorylation, through controlled protein–protein interactions. Two putative insulin-signaling pathways have emerged, the phosphatidylinositide 3 kinase (PI3K) and the MAPK-signaling pathways ( Siddle 2011

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-12-0145
Volume/Issue:
Volume 214: Issue 3
Free access
Eun-Jin Kang Department of Biomaterials Science, College of Natural Resources and Life Science/Life and Industry Convergence Research Institute, Pusan National University, Milyang, Republic of Korea

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So-Hye Hong Department of Biomaterials Science, College of Natural Resources and Life Science/Life and Industry Convergence Research Institute, Pusan National University, Milyang, Republic of Korea

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Jae-Eon Lee Department of Biomaterials Science, College of Natural Resources and Life Science/Life and Industry Convergence Research Institute, Pusan National University, Milyang, Republic of Korea

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Seung Chul Kim Department of Obstetrics and Gynecology, Biomedical Research Institute, Pusan National University School of Medicine, Milyang, Republic of Korea

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Hoe-Saeng Yang Department of Obstetrics and Gynecology, Medical College, Dongguk University, Seoul, Republic of Korea

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Pyong in Yi Department of Bioenvironmental Energy, College of Natural Resources and Life Science, Pusan National University, Milyang, Republic of Korea

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Sang-Myeong Lee College of Environmental and Bioresource Sciences, Chonbuk National University, Jeonju, Republic of Korea

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Beum-Soo An Department of Biomaterials Science, College of Natural Resources and Life Science/Life and Industry Convergence Research Institute, Pusan National University, Milyang, Republic of Korea

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.05% Tween 20 (TBS-T). The blocked membranes were incubated with antibodies specific for PRL, extracellular signal-regulated kinases 1/2 (ERK1/2), phosphorylated ERK1/2 (p-ERK1/2), p38-MAPK (p38), and phosphorylated p38 (p-p38) overnight at 4°C as well as

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-16-0088
Volume/Issue:
Volume 230: Issue 3
Free access
Feng-ying Gong Department of Endocrinology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, 1# Shuai Fu Yuan Hu Tong, Dong Dan, Beijing 100730, China

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Yi-fan Shi Department of Endocrinology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, 1# Shuai Fu Yuan Hu Tong, Dong Dan, Beijing 100730, China

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Jie-ying Deng Department of Endocrinology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, 1# Shuai Fu Yuan Hu Tong, Dong Dan, Beijing 100730, China

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/MEK), p38 mitogen-activated protein kinase ( MAPK ) and phosphoinositide 3-kinase (PI3-K)-dependent signaling pathways and the promoter sequence that spans the −196 to −132 bp of the gene, but is unrelated to Pit-1 protein ( Gong et al. 2005

Article Type:
Research Article
DOI:
https://doi.org/10.1677/joe.1.06736
Volume/Issue:
Volume 190: Issue 2
Free access
Kai Wang
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Jing Zheng Clinical and Translational Research Center, Perinatal Research Laboratories, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai 200040, China

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, Issbrucker et al . 2003 ), p38 MAPK plays a positive role in regulating FGF2-, but not VEGFA-stimulated angiogenic activities of OFPAE cells. It is noteworthy that distinct signaling pathways might differentially mediate endothelial cell responses to FGF2

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-11-0296
Volume/Issue:
Volume 212: Issue 3
Free access
Hiroki Saito
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Tomoya Nakamachi Department of Pharmacology, Department of Anatomy, Department of Clinical Pharmacy and Pharmacology, Department of Internal Medicine, Department of Molecular Pharmacology, Graduate School of Medical and Dental Science, Kagoshima University, 8-35-1 Sakuragaoka, Kagoshima 890-8544, Japan

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Kazuhiko Inoue
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Ryuji Ikeda Department of Pharmacology, Department of Anatomy, Department of Clinical Pharmacy and Pharmacology, Department of Internal Medicine, Department of Molecular Pharmacology, Graduate School of Medical and Dental Science, Kagoshima University, 8-35-1 Sakuragaoka, Kagoshima 890-8544, Japan

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Kazuo Kitamura Department of Pharmacology, Department of Anatomy, Department of Clinical Pharmacy and Pharmacology, Department of Internal Medicine, Department of Molecular Pharmacology, Graduate School of Medical and Dental Science, Kagoshima University, 8-35-1 Sakuragaoka, Kagoshima 890-8544, Japan

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Naoto Minamino Department of Pharmacology, Department of Anatomy, Department of Clinical Pharmacy and Pharmacology, Department of Internal Medicine, Department of Molecular Pharmacology, Graduate School of Medical and Dental Science, Kagoshima University, 8-35-1 Sakuragaoka, Kagoshima 890-8544, Japan

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Seiji Shioda Department of Pharmacology, Department of Anatomy, Department of Clinical Pharmacy and Pharmacology, Department of Internal Medicine, Department of Molecular Pharmacology, Graduate School of Medical and Dental Science, Kagoshima University, 8-35-1 Sakuragaoka, Kagoshima 890-8544, Japan

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Atsuro Miyata
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assays respectively. Data are presented as means± s.e.m . ( n =4). * P <0.05 vs vehicle-treated control group and # P <0.05 vs the group not treated with BIM23127. NMB-induced osteoblast proliferation via ERK1/2 activation ERK1/2 MAPK signaling is

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-12-0488
Volume/Issue:
Volume 217: Issue 2
Free access
Melyssa R Bratton Section of Hematology and Medical Oncology, Structural and Cellular Biology, Department of Medical Genetics, Center for Nuclear Receptors and Cell Signaling, Department of Medicine, Tulane University, 1430 Tulane Avenue, SL-78, New Orleans, Louisiana 70112, USA Departments of
Section of Hematology and Medical Oncology, Structural and Cellular Biology, Department of Medical Genetics, Center for Nuclear Receptors and Cell Signaling, Department of Medicine, Tulane University, 1430 Tulane Avenue, SL-78, New Orleans, Louisiana 70112, USA Departments of

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James W Antoon Section of Hematology and Medical Oncology, Structural and Cellular Biology, Department of Medical Genetics, Center for Nuclear Receptors and Cell Signaling, Department of Medicine, Tulane University, 1430 Tulane Avenue, SL-78, New Orleans, Louisiana 70112, USA Departments of

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Bich N Duong Section of Hematology and Medical Oncology, Structural and Cellular Biology, Department of Medical Genetics, Center for Nuclear Receptors and Cell Signaling, Department of Medicine, Tulane University, 1430 Tulane Avenue, SL-78, New Orleans, Louisiana 70112, USA Departments of

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Daniel E Frigo Section of Hematology and Medical Oncology, Structural and Cellular Biology, Department of Medical Genetics, Center for Nuclear Receptors and Cell Signaling, Department of Medicine, Tulane University, 1430 Tulane Avenue, SL-78, New Orleans, Louisiana 70112, USA Departments of

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Syreeta Tilghman Section of Hematology and Medical Oncology, Structural and Cellular Biology, Department of Medical Genetics, Center for Nuclear Receptors and Cell Signaling, Department of Medicine, Tulane University, 1430 Tulane Avenue, SL-78, New Orleans, Louisiana 70112, USA Departments of
Section of Hematology and Medical Oncology, Structural and Cellular Biology, Department of Medical Genetics, Center for Nuclear Receptors and Cell Signaling, Department of Medicine, Tulane University, 1430 Tulane Avenue, SL-78, New Orleans, Louisiana 70112, USA Departments of

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Bridgette M Collins-Burow Section of Hematology and Medical Oncology, Structural and Cellular Biology, Department of Medical Genetics, Center for Nuclear Receptors and Cell Signaling, Department of Medicine, Tulane University, 1430 Tulane Avenue, SL-78, New Orleans, Louisiana 70112, USA Departments of

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Steven Elliott Section of Hematology and Medical Oncology, Structural and Cellular Biology, Department of Medical Genetics, Center for Nuclear Receptors and Cell Signaling, Department of Medicine, Tulane University, 1430 Tulane Avenue, SL-78, New Orleans, Louisiana 70112, USA Departments of

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Yan Tang Section of Hematology and Medical Oncology, Structural and Cellular Biology, Department of Medical Genetics, Center for Nuclear Receptors and Cell Signaling, Department of Medicine, Tulane University, 1430 Tulane Avenue, SL-78, New Orleans, Louisiana 70112, USA Departments of

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Lilia I Melnik Section of Hematology and Medical Oncology, Structural and Cellular Biology, Department of Medical Genetics, Center for Nuclear Receptors and Cell Signaling, Department of Medicine, Tulane University, 1430 Tulane Avenue, SL-78, New Orleans, Louisiana 70112, USA Departments of

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Ling Lai Section of Hematology and Medical Oncology, Structural and Cellular Biology, Department of Medical Genetics, Center for Nuclear Receptors and Cell Signaling, Department of Medicine, Tulane University, 1430 Tulane Avenue, SL-78, New Orleans, Louisiana 70112, USA Departments of

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Jawed Alam Section of Hematology and Medical Oncology, Structural and Cellular Biology, Department of Medical Genetics, Center for Nuclear Receptors and Cell Signaling, Department of Medicine, Tulane University, 1430 Tulane Avenue, SL-78, New Orleans, Louisiana 70112, USA Departments of

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Barbara S Beckman Section of Hematology and Medical Oncology, Structural and Cellular Biology, Department of Medical Genetics, Center for Nuclear Receptors and Cell Signaling, Department of Medicine, Tulane University, 1430 Tulane Avenue, SL-78, New Orleans, Louisiana 70112, USA Departments of

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Steven M Hill Section of Hematology and Medical Oncology, Structural and Cellular Biology, Department of Medical Genetics, Center for Nuclear Receptors and Cell Signaling, Department of Medicine, Tulane University, 1430 Tulane Avenue, SL-78, New Orleans, Louisiana 70112, USA Departments of

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Brian G Rowan Section of Hematology and Medical Oncology, Structural and Cellular Biology, Department of Medical Genetics, Center for Nuclear Receptors and Cell Signaling, Department of Medicine, Tulane University, 1430 Tulane Avenue, SL-78, New Orleans, Louisiana 70112, USA Departments of

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John A McLachlan Section of Hematology and Medical Oncology, Structural and Cellular Biology, Department of Medical Genetics, Center for Nuclear Receptors and Cell Signaling, Department of Medicine, Tulane University, 1430 Tulane Avenue, SL-78, New Orleans, Louisiana 70112, USA Departments of

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Matthew E Burow Section of Hematology and Medical Oncology, Structural and Cellular Biology, Department of Medical Genetics, Center for Nuclear Receptors and Cell Signaling, Department of Medicine, Tulane University, 1430 Tulane Avenue, SL-78, New Orleans, Louisiana 70112, USA Departments of

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cascades such as the phosphatidylinositol 3-kinase (PI3K)–AKT and MAPK signaling cascades ( Dufourny et al . 1997 , Bartucci et al . 2001 , Dunn et al . 2001 , Kato 2001 , Brazil et al . 2002 , Cantley 2002 ) ultimately leads to activation of ERα

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DOI:
https://doi.org/10.1530/JOE-12-0097
Volume/Issue:
Volume 214: Issue 1
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Massimo Zerani
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Cristiano Boiti
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Danilo Zampini
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Gabriele Brecchia
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Cecilia Dall’Aglio
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Piero Ceccarelli
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Anna Gobbetti
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) leptin plus AC inhibitor (2-O-methyladenosine, 2 μM, Sigma); (VII) leptin plus JAK inhibitor (AG490, 2 μM, Calbiochem Corporation); (VIII) leptin plus MAPK/extracellular signal-regulated kinase kinase 1 and 2 (MEK1/2) inhibitor ( English et al. 2002

Article Type:
Research Article
DOI:
https://doi.org/10.1677/joe.1.05507
Volume/Issue:
Volume 183: Issue 2
Free access
Gregory S Y Ong Hudson Institute of Medical Research, Clayton, Victoria, Australia
Department of Molecular and Translational Sciences, Monash University, Clayton, Victoria, Australia
Department of Endocrinology and Diabetes, Fiona Stanley Hospital, Murdoch, Western Australia, Australia
Department of General Medicine, Sir Charles Gairdner Hospital, Nedlands, Western Australia, Australia

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Timothy J Cole Department of Biochemistry, Monash University, Clayton, Victoria, Australia

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Gregory H Tesch Department of Medicine, Monash University, Clayton, Victoria, Australia
Department of Nephrology, Monash Medical Centre, Clayton, Victoria, Australia

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James Morgan Hudson Institute of Medical Research, Clayton, Victoria, Australia
Department of Molecular and Translational Sciences, Monash University, Clayton, Victoria, Australia

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Jennifer K Dowling Hudson Institute of Medical Research, Clayton, Victoria, Australia
Royal College of Surgeons in Ireland, Dublin, Ireland

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Ashley Mansell Hudson Institute of Medical Research, Clayton, Victoria, Australia
Department of Molecular and Translational Sciences, Monash University, Clayton, Victoria, Australia

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Peter J Fuller Hudson Institute of Medical Research, Clayton, Victoria, Australia
Department of Molecular and Translational Sciences, Monash University, Clayton, Victoria, Australia

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Morag J Young Hudson Institute of Medical Research, Clayton, Victoria, Australia
Department of Molecular and Translational Sciences, Monash University, Clayton, Victoria, Australia

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-inflammatory pathways in macrophages ( Armanini et al. 1987 , Wehling et al. 1991 ). Mitogen-activated protein kinase (MAPK) signalling is a rapid-acting, critical signal transduction pathway for myeloid cell differentiation and behaviour ( Miranda et al. 2005

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-20-0161
Volume/Issue:
Volume 246: Issue 2
Restricted access