Dynein mutations impair autophagic clearance of aggregate-prone proteins. - Wikidata - wikimedia - TriplyDB

Dynein mutations impair autophagic clearance of aggregate-prone proteins.

Dynein mutations impair autophagic clearance of aggregate-prone proteins.

http://www.wikidata.org/entity/Q34429194

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Dysregulation of the autophagy-endolysosomal system in amyotrophic lateral sclerosis and related motor neuron diseases p62/SQSTM1 is required for Parkin-induced mitochondrial clustering but not mitophagy; VDAC1 is dispensable for both SCAMP5 links endoplasmic reticulum stress to the accumulation of expanded polyglutamine protein aggregates via endocytosis inhibition Effects of ALS-related SOD1 mutants on dynein- and KIF5-mediated retrograde and anterograde axonal transport ZKSCAN3 is a master transcriptional repressor of autophagy Tau deletion exacerbates the phenotype of Niemann-Pick type C mice and implicates autophagy in pathogenesis.Development of autophagy inducers in clinical medicine Charcot-Marie-Tooth disease and intracellular traffic The emerging role of acetylation in the regulation of autophagy Why should autophagic flux be assessed?Autophagy and neurodegeneration Autophagy and disease: always two sides to a problem Autophagy in the physiology and pathology of the central nervous system Autophagy modulation as a potential therapeutic target for diverse diseases Axonal autophagosomes recruit dynein for retrograde transport through fusion with late endosomes.dnc-1/dynactin 1 knockdown disrupts transport of autophagosomes and induces motor neuron degeneration Cellular model of neuronal atrophy induced by DYNC1I1 deficiency reveals protective roles of RAS-RAF-MEK signaling.Autophagy in the Pathogenesis of Disease 14-3-3 protein targets misfolded chaperone-associated proteins to aggresomes Autophagosome dynamics in neurodegeneration at a glance Mutations in the tail domain of DYNC1H1 cause dominant spinal muscular atrophy.Aggresome formation and neurodegenerative diseases: therapeutic implications Retinoic acid-stimulated sequential phosphorylation, PML recruitment, and SUMOylation of nuclear receptor TR2 to suppress Oct4 expression The autophagy-related protein beclin 1 shows reduced expression in early Alzheimer disease and regulates amyloid beta accumulation in mice.The regulation of autophagosome dynamics by huntingtin and HAP1 is disrupted by expression of mutant huntingtin, leading to defective cargo degradation.Snapin-regulated late endosomal transport is critical for efficient autophagy-lysosomal function in neurons Autophagy as a Possible Underlying Mechanism of Nanomaterial Toxicity Regulation mechanisms and signaling pathways of autophagy New insights into behaviour using mouse ENU mutagenesis Role of microtubules in extracellular release of poliovirus Starvation-induced hyperacetylation of tubulin is required for the stimulation of autophagy by nutrient deprivation LC3 binding to the scaffolding protein JIP1 regulates processive dynein-driven transport of autophagosomes.Agent-based modeling of autophagy reveals emergent regulatory behavior of spatio-temporal autophagy dynamics.Retrograde transport of TrkB-containing autophagosomes via the adaptor AP-2 mediates neuronal complexity and prevents neurodegeneration Thiopurine S-methyltransferase pharmacogenetics: autophagy as a mechanism for variant allozyme degradation.BAG3 is involved in neuronal differentiation and migration.Autophagy: an overlooked mechanism of HIV-1 pathogenesis and neuroAIDS?Regulation of amyloid precursor protein processing by the Beclin 1 complex Protein Homeostasis in Amyotrophic Lateral Sclerosis: Therapeutic Opportunities?Dynein light chain 1 is required for autophagy, protein clearance, and cell death in Drosophila.

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Dynein mutations impair autophagic clearance of aggregate-prone proteins.

http://www.wikidata.org/entity/Q34429194

description

2005 nî lūn-bûn

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2005 թուականի Յունիսին հրատարակուած գիտական յօդուած

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2005 թվականի հունիսին հրատարակված գիտական հոդված

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2005年の論文

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2005年論文

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2005年論文

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2005年論文

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2005年論文

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2005年論文

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name

Dynein mutations impair autophagic clearance of aggregate-prone proteins.

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Dynein mutations impair autophagic clearance of aggregate-prone proteins.

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Dynein mutations impair autophagic clearance of aggregate-prone proteins.

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Dynein mutations impair autophagic clearance of aggregate-prone proteins.

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Dynein mutations impair autophagic clearance of aggregate-prone proteins.

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Dynein mutations impair autophagic clearance of aggregate-prone proteins.

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Dynein mutations impair autophagic clearance of aggregate-prone proteins.

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Dynein mutations impair autophagic clearance of aggregate-prone proteins.

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Dynein mutations impair autophagic clearance of aggregate-prone proteins.

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Nature Genetics

P1476

Dynein mutations impair autophagic clearance of aggregate-prone proteins.

@en

P2093

Brinda Ravikumar

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

Coralie Vacher

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

David C Rubinsztein

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Sara Imarisio

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Steve D M Brown

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Zdenek Berger

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P2860

LC3, a mammalian homologue of yeast Apg8p, is localized in autophagosome membranes after processing

In vivo analysis of autophagy in response to nutrient starvation using transgenic mice expressing a fluorescent autophagosome marker

Dynactin is required for microtubule anchoring at centrosomes

Inhibition of mTOR induces autophagy and reduces toxicity of polyglutamine expansions in fly and mouse models of Huntington disease

Mutant huntingtin impairs axonal trafficking in mammalian neurons in vivo and in vitro

Impaired degradation of mutant alpha-synuclein by chaperone-mediated autophagy

Aggregate-prone proteins with polyglutamine and polyalanine expansions are degraded by autophagy

From Charcot to SOD1: mechanisms of selective motor neuron death in ALS.

Microtubule-based transport systems in neurons: the roles of kinesins and dyneins.

SHIRPA, a protocol for behavioral assessment: validation for longitudinal study of neurological dysfunction in mice.

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771-776

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10.1038/NG1591

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7

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37

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Abraham Acevedo-Arozena

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2005-06-26T00:00:00Z

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7762688

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1036523260

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15980862

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