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

Files in This Item:
File SizeFormat 
1-s2.0-S1096719215006198-main.pdf50.95 kBAdobe PDFView/Open
Show full item record



CORE Recommender

Page view(s)

112
checked on Mar 25, 2024

Download(s)

24
checked on Mar 25, 2024

Google ScholarTM

Check




Altmetric


Items in GCRIS Repository are protected by copyright, with all rights reserved, unless otherwise indicated.