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). Concerning the differentiation of thyroid cells, the activation of PI3K by IGF1 inhibits the expression of NIS that is stimulated by TSH and cAMP ( Garcia & Santisteban 2002 ). Moreover, TSH stimulates AKT phosphorylation in a PI3K-dependent and cAMP
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; Tremblay & Marette 2001 ). In contrast, mTORC2 is a positive regulator of insulin signal transduction through its phosphorylation of protein kinase B/Akt on its serine 473 activation site ( Hresko & Mueckler 2005 , Sarbassov et al . 2005 ). Its ability to
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.05). Additionally, we verified that despite unchanged total AKT content, insulin increased ( P < 0.001) the AKT phosphorylation ( Fig. 1A and B ). GLUT4 and GLUT1 staining revealed that both were present in luteal cells; however, only GLUT4 showed a qualitative
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PI3K/AKT pathway is a key regulator of insulin signaling ( Whiteman et al . 2002 ). In adipose and muscle cells, AKT (AKT1) overexpression results in an increased insulin-sensitive glucose transporter GLUT4 translocation and glucose uptake ( Kohn et
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Department of Psychiatry and Behavioral Neurobiology, St Vincent Health System, Department of Animal Sciences, Division of Molecular and Cellular Pathology, Veterans Affairs Medical Center, The University of Alabama at Birmingham, 1720 University Boulevard, Birmingham, Alabama 35294, USA
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Department of Psychiatry and Behavioral Neurobiology, St Vincent Health System, Department of Animal Sciences, Division of Molecular and Cellular Pathology, Veterans Affairs Medical Center, The University of Alabama at Birmingham, 1720 University Boulevard, Birmingham, Alabama 35294, USA
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Department of Psychiatry and Behavioral Neurobiology, St Vincent Health System, Department of Animal Sciences, Division of Molecular and Cellular Pathology, Veterans Affairs Medical Center, The University of Alabama at Birmingham, 1720 University Boulevard, Birmingham, Alabama 35294, USA
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). The protein concentrations of tissue lysates were determined by the BCA method (Pierce, Rockford, IL, USA). For immunoblotting, protein was separated by SDS–PAGE and analyzed by specific antibodies including anti-phosphothreonine 308-AKT, anti
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-pERK (αpERK/Tyr 204, detecting pERK42 and pERK44), anti-Akt1, and anti-phospho [Ser 473 ]Akt1 were from Santa Cruz Biotechnology (Santa Cruz, CA, USA). Rabbit anti-p85/phosphatidylinositol-3 kinase (PI3-kinase) antiserum was from UBI (Lake Placid, NY, USA
School of Pharmacy, University of Chinese Academy of Sciences, Beijing, China
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School of Pharmacy, University of Chinese Academy of Sciences, Beijing, China
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School of Pharmacy, University of Chinese Academy of Sciences, Beijing, China
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School of Pharmacy, University of Chinese Academy of Sciences, Beijing, China
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School of Pharmacy, University of Chinese Academy of Sciences, Beijing, China
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School of Pharmacy, University of Chinese Academy of Sciences, Beijing, China
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School of Pharmacy, University of Chinese Academy of Sciences, Beijing, China
School of Medicine and Life Sciences, Nanjing University of Chinese Medicine, Nanjing, China
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-coupled receptors, Akt, IRS2, PTEN, Fas/FasL, NF-κb, Bcl2 family, caspase family, ion channels and so on are tightly associated with β-cell apoptosis ( Anuradha et al . 2014 , Reimann & Gribble 2016 ), and some of the β-cell apoptosis-related proteins have been
Departamento de Farmacologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil
Departamento de Clínica Médica, Divisão de Nefrologia, Laboratório de Hipertensão Experimental da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil
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Departamento de Farmacologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil
Departamento de Clínica Médica, Divisão de Nefrologia, Laboratório de Hipertensão Experimental da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil
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Departamento de Farmacologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil
Departamento de Clínica Médica, Divisão de Nefrologia, Laboratório de Hipertensão Experimental da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil
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Departamento de Farmacologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil
Departamento de Clínica Médica, Divisão de Nefrologia, Laboratório de Hipertensão Experimental da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil
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Departamento de Farmacologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil
Departamento de Clínica Médica, Divisão de Nefrologia, Laboratório de Hipertensão Experimental da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil
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Departamento de Farmacologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil
Departamento de Clínica Médica, Divisão de Nefrologia, Laboratório de Hipertensão Experimental da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil
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Departamento de Farmacologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil
Departamento de Clínica Médica, Divisão de Nefrologia, Laboratório de Hipertensão Experimental da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil
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Departamento de Farmacologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil
Departamento de Clínica Médica, Divisão de Nefrologia, Laboratório de Hipertensão Experimental da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil
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2002 ). Following tyrosine phosphorylation, IRS-1 and IRS-2 bind and activate the enzyme phosphatidylinositol 3-kinase (PI3-K) ( Folli et al. 1992 , Saltiel & Pessin 2002 ). The activation of PI3-K increases serine phosphorylation of Akt (protein
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FAK activity, which in turn acts as a scaffold in focal adhesions and activates various downstream signaling pathways, such as AKT and ERK ( Parsons 2003 ). In β-cells, FAK has been shown to convey signals from the extracellular matrix ( Hammar et al
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Department of Biochemistry, Department of Clinical Biochemistry, Endocrinology and Metabolism Research Centre, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Islamic Republic of Iran
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carried out through overnight incubation at 4 °C with 5% nonfat dry milk in TBS with 0.5% Tween 20. Blots were incubated with antibodies against LAR, p-IRS1 (Tyr632), and IRS1 (Santa Cruz Biotechnology); Akt and phospho-Akt (Ser473) (Cell Signaling