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 | |
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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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