Please use this identifier to cite or link to this item: https://hdl.handle.net/11147/9462
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dc.contributor.authorSeyrantepe, Volkan-
dc.date.accessioned2020-07-25T22:12:34Z-
dc.date.available2020-07-25T22:12:34Z-
dc.date.issued2016-
dc.identifier.issn1096-7192-
dc.identifier.issn1096-7206-
dc.identifier.urihttps://doi.org/10.1016/j.ymgme.2015.12.434-
dc.identifier.urihttps://hdl.handle.net/11147/9462-
dc.description12th Annual WORLD Symposium -- FEB 29-MAR 04, 2016 -- San Diego, CAen_US
dc.description.abstractTay-Sachs disease is a severe lysosomal disorder caused by mutations in the HEXA gene coding for α subunit of lysosomal βhexosaminidase A which converts GM2 to GM3 ganglioside. HexA-/-mice, depleted of β-hexosaminidase A gene, remains asymptomatic to 1 year of age, owing to the ability of these mice to catabolise stored GM2 ganglioside via sialidase(s) removing sialic acid into glycolipid GA2 which further processed by β-Hexosaminidase B, thereby bypassing the HexA defect.en_US
dc.language.isoenen_US
dc.publisherAcademic Pressen_US
dc.relation.ispartofMolecular Genetics and Metabolismen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.titleDeletion of sialidase NEU3 causes progressive neurodegeneration in Tay-Sachs miceen_US
dc.typeConference Objecten_US
dc.institutionauthorSeyrantepe, Volkan-
dc.departmentİzmir Institute of Technology. Molecular Biology and Geneticsen_US
dc.identifier.volume117en_US
dc.identifier.issue2en_US
dc.identifier.startpageS104en_US
dc.identifier.endpageS104en_US
dc.identifier.wosWOS:000370888100277en_US
dc.relation.publicationcategoryKonferans Öğesi - Uluslararası - Kurum Öğretim Elemanıen_US
dc.identifier.doi10.1016/j.ymgme.2015.12.434-
dc.relation.doi10.1016/j.ymgme.2015.12.434en_US
dc.coverage.doi10.1016/j.ymgme.2015.12.434en_US
dc.identifier.wosqualityQ2-
dc.identifier.scopusqualityQ3-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextWith Fulltext-
item.openairetypeConference Object-
item.languageiso639-1en-
item.cerifentitytypePublications-
item.grantfulltextopen-
crisitem.author.dept04.03. Department of Molecular Biology and Genetics-
Appears in Collections:Molecular Biology and Genetics / Moleküler Biyoloji ve Genetik
WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection
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