The effect of ATF6 deletion on ALS pathology
Project/Area Number |
26430069
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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 | Kanazawa University |
Principal Investigator |
Hori Osamu 金沢大学, 医学系, 教授 (60303947)
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Co-Investigator(Renkei-kenkyūsha) |
TAKARADA Mika 金沢大学, 医学系, 助教 (40565412)
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Project Period (FY) |
2014-04-01 – 2017-03-31
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Project Status |
Completed (Fiscal Year 2016)
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Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
Keywords | 神経変性 / 小胞体ストレス |
Outline of Final Research Achievements |
To dissect the role of the unfolded protein response (UPR) in the pathology of amyotrophic lateral sclerosis (ALS), we crossed ALS (SOD G93A Tg) mice with Atf6α-/- mice, the latter of which lack ATF6a, a major sensor in the UPR. Analysis using ALS and ALS/Atf6α-/- mice revealed the onset time of ALS was significantly earlier in ALS/Atf6α-/- mice, but the life span was not significantly different between two genotypes. Consistent with these results, higher levels of SOD aggregation was observed in ALS/Atf6α-/- mice before the onset, while lower levels of activation was observed in Atf6α-/- mouse-derived microglia, compared with wild-type mouse-derived microglia. These results suggest the time- and cell type-specific regulation of ATF6 may play the important role in the pathology of ALS.
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Report
(4 results)
Research Products
(21 results)
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[Journal Article] CD38 positively regulates postnatal development of astrocytes cell-autonomously and oligodendrocytes non-cell-autonomously.2017
Author(s)
Hattori T, Kaji M, Ishii H, Jureepon R, Takarada-Iemata M, Ta HM, Le TM, Konno A, Hirai H, Shiraishi Y, Ozaki N, Yamamoto Y, Okamoto H, Yokoyama S, Higashida H, Kitao Y, Hori O.
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Journal Title
Glia
Volume: 印刷中
Issue: 6
Pages: 974-989
DOI
Related Report
Peer Reviewed / Int'l Joint Research / Acknowledgement Compliant
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[Journal Article] Atf6α deficiency suppresses microglial activation and ameliorates pathology of experimental autoimmune encephalomyelitis.2016
Author(s)
Ta HM, Le TM, Ishii H, Takarada-Iemata M, Hattori T, Hashida K, Yamamoto Y, Mori K, Takahashi R, Kitao Y, Hori O.
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Journal Title
Journal of Neurochemistry
Volume: 139
Issue: 6
Pages: 1124-1137
DOI
Related Report
Peer Reviewed / Int'l Joint Research / Acknowledgement Compliant
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[Journal Article] Deletion of Atf6α impairs astroglial activation and enhances neuronal death after brain ischemia in mice.2015
Author(s)
Yoshikawa A, KamideT, Hashida K, Ta HM, Inahata Y, Takarada-Iemata M, Hattori T, Mori K, Takahashi R, Matsuyama T, Hayashi Y, Kitao Y, Hori O
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Journal Title
J Neurochem.
Volume: 132(3)
Issue: 3
Pages: 342-53
DOI
Related Report
Peer Reviewed / Acknowledgement Compliant
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[Journal Article] Anxiety- and depression-like behavior in mice lacking the CD157/BST1 gene, a risk factor for Parkinson's disease.2014
Author(s)
Lopatina O, Yoshihara T, Nishimura T, Zhong J, Akther S, Fakhrul AA, Liang M, Higashida C, Sumi K, Furuhara K, Inahata Y, Huang JJ, Koizumi K, Yokoyama S, Tsuji T, Petugina Y, Sumarokov A, Salmina AB, Hashida K, Kitao Y, Hori O, Asano M, Kitamura Y, Kozaka T, Shiba K, Zhong F, Xie MJ, Sato M, Ishihara K, Higashida H.
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Journal Title
Front Behav Neurosci
Volume: 8
Pages: 1-18
DOI
Related Report
Peer Reviewed / Open Access
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