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Article: PIKE is essential for oligodendroglia development and CNS myelination

TitlePIKE is essential for oligodendroglia development and CNS myelination
Authors
Issue Date2014
Citation
Proceedings of the National Academy of Sciences of the United States of America, 2014, v. 111, n. 5, p. 1993-1998 How to Cite?
AbstractOligodendrocyte (OL) differentiation and myelin development are complex events regulated by numerous signal transduction factors. Here, we report that phosphoinositide-3 kinase enhancer L (PIKE-L) is required for OL development and myelination. PIKE-L expression is up-regulated when oligodendrocyte progenitor cells commit to differentiation. Conversely, depleting phosphoinositide- 3 kinase enhancer (PIKE) expression by shRNA prevents oligodendrocyte progenitor cell differentiation. In both conventional PIKE knockout (PIKE-/-) and OL-specific PIKE knockout mice, the number of OLs is reduced in the corpus callosum. PIKE-/- OLs also display defects when forming myelin sheath on neuronal axons during neonatal development, which is partially rescued when PTEN is ablated. In addition, Akt/mTOR signaling is impaired in OL-enriched tissues of the PIKE-/- mutant, leading to reduced expression of critical proteins for myelin development and hypomyelination. Moreover, myelin repair of lysolecithin-induced lesions is delayed in PIKE-/- brain. Thus, PIKE plays pivotal roles to advance OL development and myelinogenesis through Akt/mTOR activation.
Persistent Identifierhttp://hdl.handle.net/10722/219886
ISSN
2015 Impact Factor: 9.423
2015 SCImago Journal Rankings: 6.883

 

DC FieldValueLanguage
dc.contributor.authorChan, Chi Bun-
dc.contributor.authorLiu, Xia-
dc.contributor.authorZhao, Lixia-
dc.contributor.authorLiu, Guanglu-
dc.contributor.authorLee, Chi Wai-
dc.contributor.authorFeng, Yue-
dc.contributor.authorYe, Keiqang-
dc.date.accessioned2015-09-24T04:44:16Z-
dc.date.available2015-09-24T04:44:16Z-
dc.date.issued2014-
dc.identifier.citationProceedings of the National Academy of Sciences of the United States of America, 2014, v. 111, n. 5, p. 1993-1998-
dc.identifier.issn0027-8424-
dc.identifier.urihttp://hdl.handle.net/10722/219886-
dc.description.abstractOligodendrocyte (OL) differentiation and myelin development are complex events regulated by numerous signal transduction factors. Here, we report that phosphoinositide-3 kinase enhancer L (PIKE-L) is required for OL development and myelination. PIKE-L expression is up-regulated when oligodendrocyte progenitor cells commit to differentiation. Conversely, depleting phosphoinositide- 3 kinase enhancer (PIKE) expression by shRNA prevents oligodendrocyte progenitor cell differentiation. In both conventional PIKE knockout (PIKE-/-) and OL-specific PIKE knockout mice, the number of OLs is reduced in the corpus callosum. PIKE-/- OLs also display defects when forming myelin sheath on neuronal axons during neonatal development, which is partially rescued when PTEN is ablated. In addition, Akt/mTOR signaling is impaired in OL-enriched tissues of the PIKE-/- mutant, leading to reduced expression of critical proteins for myelin development and hypomyelination. Moreover, myelin repair of lysolecithin-induced lesions is delayed in PIKE-/- brain. Thus, PIKE plays pivotal roles to advance OL development and myelinogenesis through Akt/mTOR activation.-
dc.languageeng-
dc.relation.ispartofProceedings of the National Academy of Sciences of the United States of America-
dc.titlePIKE is essential for oligodendroglia development and CNS myelination-
dc.typeArticle-
dc.description.natureLink_to_subscribed_fulltext-
dc.identifier.doi10.1073/pnas.1318185111-
dc.identifier.pmid24449917-
dc.identifier.scopuseid_2-s2.0-84893463527-
dc.identifier.volume111-
dc.identifier.issue5-
dc.identifier.spage1993-
dc.identifier.epage1998-
dc.identifier.eissn1091-6490-

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