The roles of MAGE-D1 in the neuronal functions and pathology of the central nervous system
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Akihiro Mouri
Akihiro Mouri , PhD, Division of Clinical Sciences and Neuropsychopharmacology, Graduate School of Pharmacy, Meijo University.Professor Yukihiro Noda , PhD, Division of Clinical Sciences and Neuropsychopharmacology, Graduate School of Pharmacy, Meijo University.Ken Watanabe , PhD, Department of Bone and Joint Disease, National Center for Geriatrics and Gerontology (NCGG).Professor Toshitaka Nabeshima , PhD, Department of Regional Pharmaceutical Care and Sciences, Faculty of Pharmacy, Meijo University.
Abstract
Melanoma-associated antigen-D1 (MAGE-D1) was discovered in bone marrow stromal cells. MAGE-D1 is detected in progenitor cells in the neuroepithelia and subventricular regions as well as in the postmitotic neuronal cells in the entire brain in the developing embryo and is also detected in most adult tissues, predominantly in the brain. Herein, we provide an overview of the roles of MAGE-D1 in the central nervous system. MAGE-D1 participates in neurotrophin-induced neuronal differentiation and survival by modulating Trk-dependent phosphorylation. MAGE-D1 regulates Dlx-dependent migration-related transcription by binding to necdin or praja-1. MAGE-D1 regulates a number of apoptotic pathways, each caused by distinct input signals, such as bone morphogenetic protein, p75 neurotrophin receptor, and uncoordinated gene-5 homologue. MAGE-D1 knockout mice show depressive behavior and impairments of circadian rhythm caused by decreased ubiquitylation of serotonin transporter and regulated transcription of RORα, respectively. The gene for necdin, a MAGE-D1-binding protein, has been described as responsible for Prader-Willi syndrome. In conclusion, MAGE-D1 plays important roles in the central nervous system in both developmental and adult stages and would be an invaluable target in the development of novel diagnostic and therapeutic agents for depression and Prader-Willi syndrome and also for providing new insights into the pathogenesis/pathophysiology of these diseases.
About the authors
Akihiro Mouri, PhD, Division of Clinical Sciences and Neuropsychopharmacology, Graduate School of Pharmacy, Meijo University.
Professor Yukihiro Noda, PhD, Division of Clinical Sciences and Neuropsychopharmacology, Graduate School of Pharmacy, Meijo University.
Ken Watanabe, PhD, Department of Bone and Joint Disease, National Center for Geriatrics and Gerontology (NCGG).
Professor Toshitaka Nabeshima, PhD, Department of Regional Pharmaceutical Care and Sciences, Faculty of Pharmacy, Meijo University.
©2013 by Walter de Gruyter Berlin Boston
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- Dissecting circuit mechanisms by genetic manipulation of specific neural pathways
- The basal ganglia: motor and cognitive relationships in a clinical neurobehavioral context
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