Deletion of Sialidase Neu3 Causes Progressive Neurodegeneration in Tay-Sachs Mice

dc.contributor.author Seyrantepe, Volkan
dc.coverage.doi 10.1016/j.ymgme.2015.12.434
dc.date.accessioned 2020-07-25T22:12:34Z
dc.date.available 2020-07-25T22:12:34Z
dc.date.issued 2016
dc.description 12th Annual WORLD Symposium -- FEB 29-MAR 04, 2016 -- San Diego, CA en_US
dc.description.abstract Tay-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.identifier.doi 10.1016/j.ymgme.2015.12.434 en_US
dc.identifier.issn 1096-7192
dc.identifier.issn 1096-7206
dc.identifier.uri https://doi.org/10.1016/j.ymgme.2015.12.434
dc.identifier.uri https://hdl.handle.net/11147/9462
dc.language.iso en en_US
dc.publisher Academic Press en_US
dc.relation.ispartof Molecular Genetics and Metabolism en_US
dc.rights info:eu-repo/semantics/openAccess en_US
dc.title Deletion of Sialidase Neu3 Causes Progressive Neurodegeneration in Tay-Sachs Mice en_US
dc.type Conference Object en_US
dspace.entity.type Publication
gdc.author.institutional Seyrantepe, Volkan
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gdc.description.department İzmir Institute of Technology. Molecular Biology and Genetics en_US
gdc.description.endpage S104 en_US
gdc.description.issue 2 en_US
gdc.description.publicationcategory Konferans Öğesi - Uluslararası - Kurum Öğretim Elemanı en_US
gdc.description.scopusquality Q2
gdc.description.startpage S104 en_US
gdc.description.volume 117 en_US
gdc.description.wosquality Q2
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gdc.oaire.sciencefields 0301 basic medicine
gdc.oaire.sciencefields 03 medical and health sciences
gdc.oaire.sciencefields 0302 clinical medicine
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