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<field name="value">Caño Espinel, Manuela del</field>
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<field name="value">Acebes, Judith R.</field>
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<field name="value">Sánchez, Diego</field>
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<field name="value">Ganfornina, María D.</field>
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<field name="value">2023-12-14T15:44:53Z</field>
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<field name="value">2015</field>
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<field name="value">10.1186/s13024-015-0009-8</field>
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<field name="value">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.</field>
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<field name="value">This work was supported by grants to MDG and DS: Junta de Castilla y León (JCyL) grant VA180A11-2, and Ministerio de Ciencia e Innovación (MICINN) grants BFU2008-01170 and BFU2011-23978. MdC-E was supported by a University of Valladolid, predoctoral fellowship.</field>
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<field name="value">eng</field>
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<field name="value">Molecular Neurodegeneration. 2015, V. 10, n. 11, p. 1-18</field>
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<field name="value">https://doi.org/10.1186/s13024-015-0009-8</field>
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<field name="value">Atribución 4.0 Internacional</field>
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<field name="value">Autophagy</field>
<field name="value">Neurodegeneration</field>
<field name="value">Neuroprotection</field>
<field name="value">Polyubiquitinated protein clearance</field>
<field name="value">Drosophila</field>
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<field name="value">GLaz</field>
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<field name="value">Neurology</field>
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<field name="value">Lazarillo-related Lipocalins confer long-term protection against type I Spinocerebellar Ataxia degeneration contributing to optimize selective autophagy</field>
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