(Q50480523)

14 March 2018

title

Glycogen accumulation underlies neurodegeneration and autophagy impairment in Lafora disease. (English)

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14 March 2018

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author name string

Jordi Duran

1

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14 March 2018

Agnès Gruart

2

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14 March 2018

José M Delgado-García

4

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Joan J Guinovart

5

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14 March 2018

publication date

22 January 2014

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14 March 2018

published in

Human Molecular Genetics

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14 March 2018

volume

23

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issue

12

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14 March 2018

page(s)

3147-3156

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14 March 2018

Cytochemical identification of cerebral glycogen and glucose-6-phosphatase activity under normal and experimental conditions. II. Choroid plexus and ependymal epithelia, endothelia and pericytes

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Lafora bodies and neurological defects in malin-deficient mice correlate with impaired autophagy

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Laforin, the most common protein mutated in Lafora disease, regulates autophagy

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Dysfunctions in endosomal-lysosomal and autophagy pathways underlie neuropathology in a mouse model for Lafora disease.

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Neurodegeneration and functional impairments associated with glycogen synthase accumulation in a mouse model of Lafora disease

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Impairment in long-term memory formation and learning-dependent synaptic plasticity in mice lacking glycogen synthase in the brain

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21 January 2018

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Disruption of the glucocorticoid receptor gene in the nervous system results in reduced anxiety

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Brain region- and age-dependent dysregulation of p62 and NBR1 in a mouse model of Huntington's disease

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NBR1 cooperates with p62 in selective autophagy of ubiquitinated targets.

21 January 2018

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PTG depletion removes Lafora bodies and rescues the fatal epilepsy of Lafora disease

21 January 2018

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Loss of autophagy in the central nervous system causes neurodegeneration in mice

21 January 2018

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Suppression of basal autophagy in neural cells causes neurodegenerative disease in mice

21 January 2018

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Genetic depletion of the malin E3 ubiquitin ligase in mice leads to lafora bodies and the accumulation of insoluble laforin

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NBR1 and p62 as cargo receptors for selective autophagy of ubiquitinated targets

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21 January 2018

Identifiers

DOI

10.1093/HMG/DDU024

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14 March 2018

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14 March 2018