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Department of Physiological Sciences, State University of Londrina, Londrina, Brazil
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Biotechnology Unit, University of Ribeirao Preto, Ribeirao Preto, Brazil
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Department of Physiological Sciences, Biomedical Sciences Institute, Federal University of Alfenas, Alfenas, Brazil
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phosphatidylinositol 3-kinase (PI3K) and mitogen-activated protein kinase/extracellular-signal-regulated kinase (MAPK/ERK) signaling pathways mediate insulin effects in the CNS. The PI3K pathway is responsible for most metabolic effects of insulin, while the MAPK
Department of Biometry and Statistics, School of Public Health, University at Albany, SUNY, One University Place, Rensselaer, New York 12144, USA
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Department of Biometry and Statistics, School of Public Health, University at Albany, SUNY, One University Place, Rensselaer, New York 12144, USA
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; Lin et al. 1999 , Yen 2001 , D’Arezzo et al. 2004 ). Activation of the MAPK cascade by physiological concentrations of THs caused translocation of phosphorylated extracellular signal-regulated kinase (ERK) to the cell nucleus resulting in serine
Warwick Medical School, Interim Translational Research Institute, Department of Obstetrics and Gynaecology, Department of Histology and Embryology, Department of Endocrinology, 1st Medical Department, Department of Diabetes, Aston Medical Research Institute, University of Warwick, Coventry CV4 7AL, UK
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Warwick Medical School, Interim Translational Research Institute, Department of Obstetrics and Gynaecology, Department of Histology and Embryology, Department of Endocrinology, 1st Medical Department, Department of Diabetes, Aston Medical Research Institute, University of Warwick, Coventry CV4 7AL, UK
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Warwick Medical School, Interim Translational Research Institute, Department of Obstetrics and Gynaecology, Department of Histology and Embryology, Department of Endocrinology, 1st Medical Department, Department of Diabetes, Aston Medical Research Institute, University of Warwick, Coventry CV4 7AL, UK
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Warwick Medical School, Interim Translational Research Institute, Department of Obstetrics and Gynaecology, Department of Histology and Embryology, Department of Endocrinology, 1st Medical Department, Department of Diabetes, Aston Medical Research Institute, University of Warwick, Coventry CV4 7AL, UK
Warwick Medical School, Interim Translational Research Institute, Department of Obstetrics and Gynaecology, Department of Histology and Embryology, Department of Endocrinology, 1st Medical Department, Department of Diabetes, Aston Medical Research Institute, University of Warwick, Coventry CV4 7AL, UK
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signalling pathways in nesfatin-1 mediated H295R cell proliferation and apoptosis MAPK signalling pathways play a vital role in regulating cell proliferation and apoptosis ( Minden et al . 1994 , Xia et al . 1995 , Dhillon et al . 2007 ). We employed
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transcripts either play a direct role in insulin signaling (IRS-1 and ERK3) or have been implicated in insulin sensitivity/insulin resistance (PTP1B, LAR, p38 MAPK, IL6R1). The decline in IRS-1, a central element in insulin signaling, will severely inhibit
Shandong Provincial Key Laboratory of Endocrinology and Lipid Metabolism, Jinan, Shandong Province, China
Cheeloo College of Medicine, Shandong University, Jinan, Shandong Province, China
Department of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong Province, China
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Shandong Provincial Key Laboratory of Endocrinology and Lipid Metabolism, Jinan, Shandong Province, China
Cheeloo College of Medicine, Shandong University, Jinan, Shandong Province, China
Department of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong Province, China
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Shandong Provincial Key Laboratory of Endocrinology and Lipid Metabolism, Jinan, Shandong Province, China
Cheeloo College of Medicine, Shandong University, Jinan, Shandong Province, China
Department of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong Province, China
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Shandong Provincial Key Laboratory of Endocrinology and Lipid Metabolism, Jinan, Shandong Province, China
Cheeloo College of Medicine, Shandong University, Jinan, Shandong Province, China
Department of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong Province, China
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Shandong Provincial Key Laboratory of Endocrinology and Lipid Metabolism, Jinan, Shandong Province, China
Cheeloo College of Medicine, Shandong University, Jinan, Shandong Province, China
Department of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong Province, China
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Shandong Provincial Key Laboratory of Endocrinology and Lipid Metabolism, Jinan, Shandong Province, China
Cheeloo College of Medicine, Shandong University, Jinan, Shandong Province, China
Department of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong Province, China
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were treated with recombinant mouse FSH or vehicle. For MAPK signal analysis, PD98059 ERK inhibitor and SB203580 p38 inhibitor were purchased from Beyotime Biotechnology (Nanjing, China). ATDC5 cell line culture The mouse chondrogenic cell line
Departments of, Physiology and Biophysics, Pharmacology, Cell and Development of Biology, Department of Biological Sciences, Institute of Biomedical Sciences
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. Surprisingly, the LH levels in obese females treated for 180 days with high-fat diet were similar to controls. GNRH stimulates the secretory response of LH by a calcium-dependent signaling, and increases mRNA and protein synthesis of LH through the MAPK
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-phospho-AKT Ser473, anti-AKT, anti-p44/42 MAPK (anti-ERK1/2), anti-phospho-p44/42 MAPK Thr202/Tyr204 (anti-phospho-ERK1/2), anti-phospho-STAT3 Tyr705, anti-phospho-EGFR Tyr845, anti-cMyc, and anti-cFos antibodies were from Cell Signaling Technology, Inc. (Beverly
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phosphorylation (i.e. activation) of mitogen-activated protein kinase (MAPK, i.e. extracellular signal regulated kinase, ERK), a known PLC-activating cascade ( Montrose-Rafizadeh et al. 1999 ). Data in native human and mouse pancreatic islets conclusively
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effects observed with the osteoblast-specific deletion of FOXO1, none of the studies to date have addressed this question. Furthermore, osteoprogenitor-specific deletion of Pten led to FGF signaling-mediated activation of MAPK signaling showing that this
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, which mediates most of the effects of GH on skeletal metabolism, promotes chondrogenesis and increases bone formation by regulating the functions of the differentiated osteoblasts ( Giustina et al . 2008 ). Figure 1 GH and IGF1 signaling and action in