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Insulin and IGF-1 improve mitochondrial function in a PI-3K/Akt-dependent manner and reduce mitochondrial generation of reactive oxygen species in Huntington’s disease knock-in striatal cells
Institution:1. CNC-Center for Neuroscience and Cell Biology, University of Coimbra, 3004-504 Coimbra, Portugal;2. Faculty of Medicine, University of Coimbra, 3004-504 Coimbra, Portugal;1. Grupos de Neurociencias y Muerte Celular, Facultad de Medicina e Instituto de Genética, Universidad Nacional de Colombia, Bogotá, Colombia;2. Laboratory of Neurogenetics, National Institute of Aging, National Institutes of Health, Bethesda, MD, USA;1. Department of Pharmacology, J.S.S College of Pharmacy, Jagadguru Sri Shivarathreeswara University, S.S Nagar, Mysuru, 570015 KA, India;2. Department of Biotechnology, Dr. M.G.R. Educational and Research Institute University, Chennai 600095, TN, India;3. Research and Development Centre, Bharathiar University, Coimbatore 641046, India;4. Central Inter - Disciplinary Research Facility, Sri Balaji Vidyapeeth University, Puducherry 605014, India;5. CEFT, Sri Ramachandra University, Chennai 116, TN, India;1. The Stroke Unit, The First People’s Hospital of Shangqiu, Shangqiu City, 476100, Henan Province, PR China;2. Department of Neurosurgery, The First People’s Hospital of Shangqiu, Shangqiu City, 476100, Henan Province, PR China;1. Department of Neurosurgery, Xijing Hospital, The Fourth Military Medical University, 127 Changle West Road, Xi’an 710032, China;2. Department of Biomedical Engineering, The Fourth Military Medical University, 169 Changle West Road, Xi’an 710032, China;3. Department of Scientific Research, The Fourth Military Medical University, 169 Changle West Road, Xi’an 710032, China
Abstract:
Keywords:Huntington disease  Oxidative stress  Insulin/IGF-1 signaling  Nrf2  Mitochondria  Reactive oxygen species  Striatal cells  Akt
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