2026-06-01T20:29:03Zhttps://riubu.ubu.es/oai/requestoai:riubu.ubu.es:10259/82072023-12-15T12:59:34Zcom_10259_7130com_10259_5086com_10259_2604col_10259_7131
Repositorio Institucional de la Universidad de Burgos
author
Caño Espinel, Manuela del
author
Acebes, Judith R.
author
Sánchez, Diego
author
Ganfornina, María D.
2023-12-14T15:44:53Z
2023-12-14T15:44:53Z
2015
http://hdl.handle.net/10259/8207
10.1186/s13024-015-0009-8
1750-1326
A diverse set of neurodegenerative disorders are caused by abnormal extensions of polyglutamine (poly-Q) stretches in various, functionally unrelated proteins. A common feature of these diseases is altered proteostasis. Autophagy induction is part of the endogenous response to poly-Q protein expression. However, if autophagy is not resolved properly, clearance of toxic proteins or aggregates cannot occur effectively. Likewise, excessive autophagy induction can cause autophagic stress and neurodegeneration. The Lipocalins ApoD, Glial Lazarillo (GLaz) and Neural Lazarillo (NLaz) are neuroprotectors upon oxidative stress or aging. In this work we test whether these Lipocalins also protect against poly-Q-triggered deterioration of protein quality control systems.
eng
Atribución 4.0 Internacional
Autophagy
Neurodegeneration
Neuroprotection
Polyubiquitinated protein clearance
Drosophila
GLaz
NLaz
ApoD
GstS1
Atg1/ULK1
Atg4a
Atg8a/LC3
p62
Lazarillo-related Lipocalins confer long-term protection against type I Spinocerebellar Ataxia degeneration contributing to optimize selective autophagy
info:eu-repo/semantics/article
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URL
https://riubu.ubu.es/bitstream/10259/8207/1/Cano-mn_2015.pdf
File
MD5
12639f61caf02119c1becf323632381f
2195115
application/pdf
Cano-mn_2015.pdf