2026-06-01T21:29:19Zhttps://riubu.ubu.es/oai/request

oai:riubu.ubu.es:10259/82072023-12-15T12:59:34Zcom_10259_7130com_10259_5086com_10259_2604col_10259_7131

Caño Espinel, Manuela del Acebes, Judith R. Sánchez, Diego 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 http://creativecommons.org/licenses/by/4.0/ info:eu-repo/semantics/openAccess 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