Studies on cellular signal transduction of PNS demyelination
| Project/Area Number |
19500340
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neurochemistry/Neuropharmacology
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| Research Institution | National Research Institute for Child Health and Development |
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Principal Investigator |
YAMAUCHI Junji National Research Institute for Child Health and Development, 薬剤治療研究部, 室長 (20335483)
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| Project Period (FY) |
2007 – 2009
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| Project Status |
Completed (Fiscal Year 2009)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2009: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2008: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2007: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 末梢神経 / 神経栄養因子 / ミエリン化 / 脱髄疾病 / 低分子量GTP結合蛋白質 / ミエリン / 脱ミエリン / PMP22 / MAPキナーゼ |
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| Research Abstract |
Charcot-Marie-Tooth (CMT) disease is the most common inherited neuropathy of the peripheral nervous system (PNS) and is genetically and clinically heterogenous. CMT disease is characterized by progressive sensory neuron loss and by weakness, beginning in the legs and manifesting later in the hands. Based on nerve electrophysiology, most patients with CMT are categorized into two major types : CMT disease type 1 (CMT1) and CMT disease type 2 (CMT2). While many of the genes and mutations responsible for CMT disease have been identified, we still do not know what compound protects against nerve fiber loss, nor how it may be reversed. Hre, we have found that some small compounds (inhibitors for neurotrophin receptors and Rho family small GTPases) impaits demyelination in in vitro CMT1A model (the responsible gene : PMP22) and have now tried to applied to the effects on in vivo model. Thus, these results have a previously unknown potential to improve defective mylinogenesis associated with CMT1A in vitro, indicating that their associated signaling pathways (primarily in the new gene dock7) should be a potential therapeutic targets for treatments aimed at improving defective mylinogenesis.
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Report
(4 results)
Research Products
(22 results)
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[Journal Article] Valproic acid-inducible Arl4D and cytohesin-2/ARNO, acting through the downstream Arf6, regulate neurite outgrowth in N1E-115 cells.2009
Author(s)
Junji Yamauchi, Yuki Miyamoto, Tomohiro Torii, Reiko Mizutani, Kazuaki Nakamura, Atsushi Sanbe, Hiroshi Koide, Shinji Kusakawa, Akito Tanoue
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Journal Title
Exp. Cell Res 315巻
Pages: 2043-2052
Related Report
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[Journal Article] Valproic acid-inducible Arl4D and cytohesin-2/ARNO, acting through the downstream Arf6, regulate neurite outgrowth in N1E-115 cells2009
Author(s)
Junji Yamauchi, Yuki Miyamoto, Tomohiro Torii, Reiko Mizutani, Kazuaki Nakamura, Atsushi Sanbe, Hiroshi Koide, Shinji Kusakawa, Akito Tanoue
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Journal Title
Exp.Cell Res. 315
Pages: 2043-2052
Related Report
Peer Reviewed
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[Journal Article] Neurofibromatosis 2 tumor suppressor, the gene induced by valproic acid, mediates neurite outgrowth through interaction with paxillin2008
Author(s)
Junji Yamauchi, Yuki Miyamoto, Shinji Kusakawa, Tomohiro Torii, Reiko Mizutani, Atsushi Sanbe, Hideki Nakajima, Nobutaka Kiyokawa, Akito Tanoue
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Journal Title
Exp. Cell Res. 314
Pages: 2279-2288
Related Report
Peer Reviewed
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[Journal Article] Neurofibromatosis 2 tumor suppressor, the gene induced by valproic acid, mediates neurite outgrowth through interaction with paxillin.
Author(s)
Junji Yamauchi, Yuki Miyamoto, Shinji Kusakawa, Tomohiro Torii, Reiko Mizutani, Atsushi Sanbe, Hideki Nakajima, Nobutaka Kiyokawa, Akito Tanoue
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Journal Title
Exp. Cell Res 314巻
Pages: 2279-2288
Related Report
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