Deleterious effects of neuronal accumulation of glycogen in flies and mice - sprookjes - yvandenbroek - TriplyDB

Deleterious effects of neuronal accumulation of glycogen in flies and mice

Deleterious effects of neuronal accumulation of glycogen in flies and mice

http://www.wikidata.org/entity/Q36386453

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Genetics of Lafora progressive myoclonic epilepsy: current perspectives Loss of GABAergic cortical neurons underlies the neuropathology of Lafora disease Contributions of glycogen to astrocytic energetics during brain activation.Neuroglobin Overexpression Inhibits AMPK Signaling and Promotes Cell Anabolism.Neurons have an active glycogen metabolism that contributes to tolerance to hypoxia.Does abnormal glycogen structure contribute to increased susceptibility to seizures in epilepsy?Allele copy number and underlying pathology are associated with subclinical severity in equine type 1 polysaccharide storage myopathy (PSSM1)Neuronal glycogen synthesis contributes to physiological aging.Adipose tissue glycogen accumulation is associated with obesity-linked inflammation in humans.Alternative mitochondrial electron transfer for the treatment of neurodegenerative diseases and cancers: Methylene blue connects the dots.Hyperglycaemia induces metabolic dysfunction and glycogen accumulation in pancreatic β-cells.The metabolic response to excitotoxicity - lessons from single-cell imaging.Changing shapes of glycogen-autophagy nexus in neurons: perspective from a rare epilepsy.Pathogenesis of Lafora Disease: Transition of Soluble Glycogen to Insoluble Polyglucosan.Is Type 2 Diabetes a Glycogen Storage Disease of Pancreatic β Cells?Over-expression of muscle glycogen synthase in human diabetic nephropathy.Muscle glycogen synthase isoform is responsible for testicular glycogen synthesis: glycogen overproduction induces apoptosis in male germ cells.Insights into Brain Glycogen Metabolism: THE STRUCTURE OF HUMAN BRAIN GLYCOGEN PHOSPHORYLASE.Inhibitory properties of 1,4-dideoxy-1,4-imino-d-arabinitol (DAB) derivatives acting on glycogen metabolising enzymes.Genetic models rule out a major role of beta cell glycogen in the control of glucose homeostasis.Immunohistochemical localization of glycogen synthase and GSK3β: control of glycogen content in retina.Insect models of central nervous system energy metabolism and its links to behavior.The unique evolution of the carbohydrate-binding module CBM20 in laforin.PTG protein depletion rescues malin-deficient Lafora disease in mouse.Regulation of Carbohydrate Energy Metabolism in Drosophila melanogaster.Glycogen synthase protects neurons from cytotoxicity of mutant huntingtin by enhancing the autophagy flux.Glycogen accumulation underlies neurodegeneration and autophagy impairment in Lafora disease.

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Deleterious effects of neuronal accumulation of glycogen in flies and mice

http://www.wikidata.org/entity/Q36386453

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2012 nî lūn-bûn

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2012年の論文

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2012年学术文章

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2012年学术文章

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2012年学术文章

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2012年学术文章

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name

Deleterious effects of neuronal accumulation of glycogen in flies and mice

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Deleterious effects of neuronal accumulation of glycogen in flies and mice

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Deleterious effects of neuronal accumulation of glycogen in flies and mice

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Deleterious effects of neuronal accumulation of glycogen in flies and mice

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Deleterious effects of neuronal accumulation of glycogen in flies and mice

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Deleterious effects of neuronal accumulation of glycogen in flies and mice

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EMBO Molecular Medicine

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Deleterious effects of neuronal accumulation of glycogen in flies and mice

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Joan J Guinovart

http://www.w3.org/2001/XMLSchema#string

Joaquim Calbó

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Jordi Duran

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María Florencia Tevy

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P2860

Bioconductor: open software development for computational biology and bioinformatics

Laforin, defective in the progressive myoclonus epilepsy of Lafora type, is a dual-specificity phosphatase associated with polyribosomes

Insights into Lafora disease: malin is an E3 ubiquitin ligase that ubiquitinates and promotes the degradation of laforin.

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

Cerebellar neurodegeneration in the absence of microRNAs

Targeted gene expression as a means of altering cell fates and generating dominant phenotypes

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

Targeted disruption of the Epm2a gene causes formation of Lafora inclusion bodies, neurodegeneration, ataxia, myoclonus epilepsy and impaired behavioral response in mice

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

Brain glycogen re-awakened.

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719-729

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scholarly article

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10.1002/EMMM.201200241

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8

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4

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Mar García-Rocha

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2012-05-02T00:00:00Z

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224879114

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22549942

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3494072

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