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  1. 原著論文

Loss of branched O-mannosyl glycans in astrocytes accelerates remyelination.

https://repo.qst.go.jp/records/46877
https://repo.qst.go.jp/records/46877
7a5f130d-3629-4063-b799-7cc7e33190c2
Item type 学術雑誌論文 / Journal Article(1)
公開日 2014-10-21
タイトル
タイトル Loss of branched O-mannosyl glycans in astrocytes accelerates remyelination.
言語
言語 eng
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_6501
資源タイプ journal article
アクセス権
アクセス権 metadata only access
アクセス権URI http://purl.org/coar/access_right/c_14cb
著者 Kanekiyo, Kenji

× Kanekiyo, Kenji

WEKO 467713

Kanekiyo, Kenji

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Inamori, Kei-ichiro

× Inamori, Kei-ichiro

WEKO 467714

Inamori, Kei-ichiro

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Kitazume, Shinobu

× Kitazume, Shinobu

WEKO 467715

Kitazume, Shinobu

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Sato, Keiko

× Sato, Keiko

WEKO 467716

Sato, Keiko

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Maeda, Jun

× Maeda, Jun

WEKO 467717

Maeda, Jun

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Higuchi, Makoto

× Higuchi, Makoto

WEKO 467718

Higuchi, Makoto

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Kizuka, Yasuhiko

× Kizuka, Yasuhiko

WEKO 467719

Kizuka, Yasuhiko

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Korekane, Hiroaki

× Korekane, Hiroaki

WEKO 467720

Korekane, Hiroaki

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Matsuo, Ichiro

× Matsuo, Ichiro

WEKO 467721

Matsuo, Ichiro

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Honke, Koichi

× Honke, Koichi

WEKO 467722

Honke, Koichi

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Taniguchi, Naoyuki

× Taniguchi, Naoyuki

WEKO 467723

Taniguchi, Naoyuki

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前田 純

× 前田 純

WEKO 467724

en 前田 純

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樋口 真人

× 樋口 真人

WEKO 467725

en 樋口 真人

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抄録
内容記述タイプ Abstract
内容記述 In demyelinating diseases such as multiple sclerosis, a critical problem is failure of remyelination, which is important for protecting axons against degeneration and restoring conduction deficits. However, the underlying mechanism of demyelination/remyelination remains unclear. N-acetylglucosaminyltransferase-IX (GnT-IX; also known as GnT-Vb) is a brain-specific glycosyltransferase that catalyzes the branched formation of O-mannosyl glycan structures. O-Mannosylation of α-dystroglycan is critical for its function as an extracellular matrix receptor, but the biological significance of its branched structures, which are exclusively found in the brain, is unclear. In this study, we found that GnT-IX formed branched O-mannosyl glycans on receptor protein tyrosine phosphatase β (RPTPβ) in vivo. Since RPTPβ is thought to play a regulatory role in demyelinating diseases, GnT-IX-deficient mice were subjected to cuprizone-induced demyelination. Cuprizone feeding for 8 weeks gradually promoted demyelination in wild-type mice. In GnT-IX-deficient mice, the myelin content in the corpus callosum was reduced after 4 weeks of treatment, but markedly increased at 8 weeks, suggesting enhanced remyelination under GnT-IX deficiency. Furthermore, astrocyte activation in the corpus callosum of GnT-IX-deficient mice was significantly attenuated, and an oligodendrocyte cell lineage analysis indicated that more oligodendrocyte precursor cells differentiated into mature oligodendrocytes. Together, branched O-mannosyl glycans in the corpus callosum in the brain are a necessary component of remyelination inhibition in the cuprizone-induced demyelination model, suggesting that modulation of O-mannosyl glycans is a likely candidate for therapeutic strategies.
書誌情報 The Journal of neuroscience : the official journal of the Society for Neuroscience

巻 33, 号 24, p. 10037-10047, 発行日 2013-06
出版者
出版者 Society for Neuroscience
ISSN
収録物識別子タイプ ISSN
収録物識別子 0270-6474
PubMed番号
識別子タイプ PMID
関連識別子 23761899
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