Please use this identifier to cite or link to this item: https://hdl.handle.net/11147/9462
Title: Deletion of Sialidase Neu3 Causes Progressive Neurodegeneration in Tay-Sachs Mice
Authors: Seyrantepe, Volkan
Publisher: Academic Press
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.
Description: 12th Annual WORLD Symposium -- FEB 29-MAR 04, 2016 -- San Diego, CA
URI: https://doi.org/10.1016/j.ymgme.2015.12.434
https://hdl.handle.net/11147/9462
ISSN: 1096-7192
1096-7206
Appears in Collections:Molecular Biology and Genetics / Moleküler Biyoloji ve Genetik
WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection

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