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binds and activates activin type 2B receptors to promote phosphorylation of Smad2/3 ( Rebbapragada et al. 2003 ), while IGF1 activates the IGF1 receptor and phosphorylates PI3 kinase (PI3K) and AKT ( Rommel et al. 2001 ). The PI3K/AKT pathway is
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Embryotoxicology Laboratory, Environmental Toxicology Group, CSIR-Indian Institute of Toxicology Research (CSIR-IITR), Vishvigyan Bhavan, Lucknow, Uttar Pradesh, India
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intervention within the brain ( Garcia-Huerta et al. 2016 ). Growth factor signal transduction pathways often stimulate PI3K-AKT-mTOR mechanism and inhibit neuronal autophagy ( Kalkman & Feuerbach 2017 ). Although primarily studied in glial cells, epidermal
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AKT ( Rommel et al. 2001 ). The PI3K/AKT pathway is common to both factors and there is considerable cross-regulation between the two, wherein myostatin inhibits AKT to block IGF1-induced hypertrophy of myotubes ( Morissette et al. 2009 ), IGF1
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Burnett School of Biomedical Sciences, Department of Head and Neck Surgery, College of Medicine, University of Central Florida, 6900 Lake Nona Boulevard, Orlando, Florida 32827, USA
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Introduction AKT, a serine/threonine kinase, is downstream of phosphatidylinositol-3-kinase (PI3K) and growth factor receptors (e.g. epidermal growth factor receptor), and is a hallmark signaling protein predominantly recognized for regulation of
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Introduction Akt is a serine/threonine protein kinase bearing multiple cellular processes such as glucose metabolism, apoptosis, cell proliferation, transcription, and cell migration. Akt includes three closely related isoforms Akt1, Akt2, and Akt3
UMR859, INSERM UMR859, INSERM UMR837, CHU Lille, Faculty of Medicine, Université Lille Nord de France, 1 Place de Verdun, F-59000 Lille, France
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UMR859, INSERM UMR859, INSERM UMR837, CHU Lille, Faculty of Medicine, Université Lille Nord de France, 1 Place de Verdun, F-59000 Lille, France
UMR859, INSERM UMR859, INSERM UMR837, CHU Lille, Faculty of Medicine, Université Lille Nord de France, 1 Place de Verdun, F-59000 Lille, France
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UMR859, INSERM UMR859, INSERM UMR837, CHU Lille, Faculty of Medicine, Université Lille Nord de France, 1 Place de Verdun, F-59000 Lille, France
UMR859, INSERM UMR859, INSERM UMR837, CHU Lille, Faculty of Medicine, Université Lille Nord de France, 1 Place de Verdun, F-59000 Lille, France
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& Sonenberg 2004 , Wullschleger et al . 2006 ). mTORC1 and mTORC2 are two distinct complexes sharing mTOR as a catalytic subunit. mTORC1 is composed of mTOR, regulated associated protein of mTOR (raptor), proline-rich Akt substrate of 40 kDa (PRAS40), and G
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factor 2 receptor (IGF-2R) and angiotensin II type 1 receptor (AT 1 R)-mediated Akt signaling as molecular foundations for the association between low birth weight and cardiovascular disease in adulthood. Cardiomyocyte development during fetal life
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the Ser/Thr protein kinase, Akt (also called protein kinase B) ( Chan et al. 1999 , Datta et al. 1999 ). Akt activation can stimulate changes in gene transcription, cell survival, cell division, and cell differentiation. In the present
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be triggered by activation of its upstream molecules phosphatidylinositol 3 (PI-3) kinase and the serine/threonine kinase PKB/Akt ( Hornberger et al. 2004 , Oudit et al. 2004 ). Meanwhile, increased levels of nutrients, growth factors such as
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/2, AKT and PKCε activation ( Brar et al . 2002 , 2004 , Lawrence et al . 2005 ). UCN2 and CRFR2 are both expressed in mouse skeletal muscle ( Chen et al . 2004 , Keipert et al . 2013 ), where they inhibit atrophy and promote hypertrophy ( Hinkle