Interaction of CRMP1 and Filamin-A regulates F-actin-cytoskeleton.
Project/Area Number |
24500443
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Neurochemistry/Neuropharmacology
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Research Institution | Yokohama City University |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
ARITA Kyohei 横浜市立大学, 生命ナノシステム科学研究科, 准教授 (40549648)
YAMASHITA Naoya 横浜市立大学, 医学研究科, 客員講師 (40508793)
HASHIMOTO Hiroshi 静岡県立大学, 薬学部, 教授 (40336590)
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Project Period (FY) |
2012-04-01 – 2015-03-31
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Project Status |
Completed (Fiscal Year 2014)
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Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
Keywords | 神経回路形成 / 細胞骨格 / アクチン / セマフォリン / Sema3A / CRMP1 / Filamin-A / リン酸化 / Filamin / フィラミン / 線虫 |
Outline of Final Research Achievements |
Sema3A, an axon guidance molecule, repels neurite outgrowth. This action accompanies the collapse of actin-cytoskeleton in the neuronal growth cones. We found that CRMP1, an intracellular mediator for Sema3A-signaling, interacts with Filamin-A, an actin binding protein. In C. elegans, Filamin-1 (Filamin-A homologue) is involved in DD/VD motoneuron guidance with UNC-33 (CRMP1 homologue). CRMP1 binds N- and C-termini of Filamin-A and alters its ternary structure. We determined the interaction residues in Filamin-A and CRMP1. Overexpression of the point-mutants of those residues in cultured neurons interferes Sema3A-response. Sema3A induces phosphorylation of CRMP1. A phospho-mimicking mutant of CRMP1 binds Filamin-A with higher affinity than wildtype. The phospho-mimicking CRMP1 interferes the actin cytoskeleton weaved with F-actin and Filamin-A. These results suggest that phosphorylated CRMP1 removes Filamin-A from actin-cytoskeleton in turn to bring the collapse in Sema3A-signaling.
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Report
(4 results)
Research Products
(13 results)
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[Journal Article] Amino and carboxyl terminal domains of Filamin-A interact with CRMP1 to mediate Sema3A-signaling2014
Author(s)
Fumio Nakamura, Kosuke Kumeta, Tomonobu Hida, Toshinari Isono, Yuichi Nakayama, Emiko Kuramata-Matsuoka, Naoya Yamashita, Yutaka Uchida, Ken-ichi Ogura, Keiko Gengyo-Ando, Shohei Mitani, Toshio Ogino, and Yoshio Goshima
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Journal Title
Nat. Commun.
Volume: 5 5325
Issue: 1
Pages: 1-14
DOI
Related Report
Peer Reviewed / Acknowledgement Compliant
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[Journal Article] The protein Ocular albinism 1 is the orphan GPCR GPR143 and mediates depressor and bradycardic responses to DOPA in the nucleus tractus solitarii.2014
Author(s)
Hiroshima Y, Miyamoto H, Nakamura F, Masukawa D, Yamamoto T, Muraoka H, Kamiya M, Yamashita N, Suzuki T, Matsuzaki S, Endo I, Goshima Y
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Journal Title
British Journal of Pharmacology
Volume: 171
Issue: 2
Pages: 403-414
DOI
Related Report
Peer Reviewed
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[Journal Article] lexinA4-dependent retrograde Semaphorin3A signaling regulates the dendritic localization of GluA2-containing AMPA receptors.2014
Author(s)
1) Yamashita, N., Usui, H., Nakamura, F., Chen, S., Sasaki, Y., Hida, T., Suto, F., Taniguchi, M., Takei, K., Goshima, Y.
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Journal Title
Nature Communications
Volume: 5
Issue: 1
Pages: 3424-3424
DOI
Related Report
Peer Reviewed / Open Access
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[Journal Article] Amyloid-β25–35 induces impairment of cognitive function andlong-term potentiation through phosphorylation of collapsinresponse mediator protein 2.2013
Author(s)
Isono T, Yamashita N, Obara M, Araki T, Nakamura F, Kamiya Y, Alkam T, Nitta A, Nabeshima T, Mikoshiba K, Ohshima T, Goshima Y
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Journal Title
Neurosci Res
Volume: 77
Issue: 3
Pages: 180-185
DOI
Related Report
Peer Reviewed
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[Journal Article] Decreased Expression of Semaphorin-3A, a Neurite-Collapsing Factor, is Associated With Itch in PsoriaticSkin.2012
Author(s)
Kou K, Nakamura F,Aihara M, Chen H, Seto K, Komori-Yamaguchi J, Kambara T, Nagashima Y,Goshima Y, Ikezawa Z
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Journal Title
Acta Derm Venereol
Volume: 92
Issue: 5
Pages: 521-528
DOI
Related Report
Peer Reviewed
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