The roles of MAGE-D1 in the neuronal functions and pathology of the central nervous system

Akihiro Mouri, Yukihiro Noda, Ken Watanabe, Toshitaka Nabeshima

Research output: Contribution to journalArticle

11 Citations (Scopus)

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 ROR α , 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.

Original languageEnglish
Pages (from-to)61-70
Number of pages10
JournalReviews in the Neurosciences
Volume24
Issue number1
DOIs
Publication statusPublished - 01-02-2013
Externally publishedYes

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Melanoma-Specific Antigens
Central Nervous System
Pathology
Prader-Willi Syndrome
Nerve Growth Factor Receptor
Serotonin Plasma Membrane Transport Proteins
Bone Morphogenetic Proteins
Ubiquitination
Nerve Growth Factors
Brain
Circadian Rhythm
Mesenchymal Stromal Cells
Knockout Mice
Genes
Carrier Proteins
Stem Cells
Embryonic Structures
Phosphorylation
Depression

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)

Cite this

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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 ROR α , 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.",
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The roles of MAGE-D1 in the neuronal functions and pathology of the central nervous system. / Mouri, Akihiro; Noda, Yukihiro; Watanabe, Ken; Nabeshima, Toshitaka.

In: Reviews in the Neurosciences, Vol. 24, No. 1, 01.02.2013, p. 61-70.

Research output: Contribution to journalArticle

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