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j.bbrc.2009.12.154.pdf2.11 MBAdobe PDF見る/開く
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dc.contributor.authorShintani, Tomoyaen
dc.contributor.authorYamazaki, Fumiyoshien
dc.contributor.authorKatoh, Toshihikoen
dc.contributor.authorUmekawa, Midorien
dc.contributor.authorMatahira, Yoshiharuen
dc.contributor.authorHori, Seijien
dc.contributor.authorKakizuka, Akiraen
dc.contributor.authorTotani, Kazuhideen
dc.contributor.authorYamamoto, Kenjien
dc.contributor.authorAshida, Hisashien
dc.contributor.alternative芦田, 久ja
dc.date.accessioned2010-02-04T07:17:25Z-
dc.date.available2010-02-04T07:17:25Z-
dc.date.issued2010-01-22-
dc.identifier.issn1090-2104-
dc.identifier.urihttp://hdl.handle.net/2433/93625-
dc.description.abstractAutophagy is a cellular process that nonspecifically degrades cytosolic components and is involved in many cellular responses. We found that amino sugars with a free amino group such as glucosamine, galactosamine and mannosamine induced autophagy via an mTOR-independent pathway. Glucosamine-induced autophagy at concentrations of at least 500 microM to over 40 mM. In the presence of 40 mM glucosamine, autophagy induction was initiated at 6h and reached a plateau at 36 h. Glucosamine-induced autophagy could remove accumulated ubiquitin-conjugated proteins as well as 79-glutamine repeats. Therefore, orally administered glucosamine could contribute to the prevention of neurodegenerative diseases and promotion of antiaging effects.en
dc.language.isoeng-
dc.publisherElsevieren
dc.rights© 2010 Elsevier Inc. All rights reserved.en
dc.rightsこの論文は出版社版でありません。引用の際には出版社版をご確認ご利用ください。ja
dc.rightsThis is not the published version. Please cite only the published version.en
dc.subjectAutophagyen
dc.subjectChitinen
dc.subjectChitosanen
dc.subjectGlucosamineen
dc.subjectHexosamineen
dc.subjectPolyglutamine diseaseen
dc.titleGlucosamine induces autophagy via an mTOR-independent pathway.en
dc.typejournal article-
dc.type.niitypeJournal Article-
dc.identifier.jtitleBiochemical and biophysical research communicationsen
dc.identifier.volume391-
dc.identifier.issue4-
dc.identifier.spage1775-
dc.identifier.epage1779-
dc.relation.doi10.1016/j.bbrc.2009.12.154-
dc.textversionauthor-
dc.identifier.pmid20045674-
dcterms.accessRightsopen access-
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