Misfolded SOD1 associated with motor neuron mitochondria alters mitochondrial shape and distribution prior to clinical onset. - Wikidata - wikimedia - TriplyDB

Misfolded SOD1 associated with motor neuron mitochondria alters mitochondrial shape and distribution prior to clinical onset.

Misfolded SOD1 associated with motor neuron mitochondria alters mitochondrial shape and distribution prior to clinical onset.

http://www.wikidata.org/entity/Q33968208

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Dysregulated axonal RNA translation in amyotrophic lateral sclerosis Molecular motor proteins and amyotrophic lateral sclerosis Mitochondrial fission is an acute and adaptive response in injured motor neurons Emerging mechanisms of molecular pathology in ALS Mitochondrial dysfunction in neurodegenerative diseases Exploring new pathways of neurodegeneration in ALS: the role of mitochondria quality control FUS Interacts with HSP60 to Promote Mitochondrial Damage Axonal transport deficits and degeneration can evolve independently in mouse models of amyotrophic lateral sclerosis.Elevated PGC-1α activity sustains mitochondrial biogenesis and muscle function without extending survival in a mouse model of inherited ALS Abnormal mitochondrial transport and morphology are common pathological denominators in SOD1 and TDP43 ALS mouse models.Endo-MitoEGFP mice: a novel transgenic mouse with fluorescently marked mitochondria in microvascular endothelial cells.Abnormalities of Mitochondrial Dynamics in Neurodegenerative Diseases.Mechanisms, models and biomarkers in amyotrophic lateral sclerosis Macrophage migration inhibitory factor as a chaperone inhibiting accumulation of misfolded SOD1.Mitochondrial dynamic abnormalities in amyotrophic lateral sclerosis.ALS-linked misfolded SOD1 species have divergent impacts on mitochondria.A novel phenotype for the dynein heavy chain mutation Loa: altered dendritic morphology, organelle density, and reduced numbers of trigeminal motoneurons.Endogenous macrophage migration inhibitory factor reduces the accumulation and toxicity of misfolded SOD1 in a mouse model of ALS.Mitochondrial damage revealed by immunoselection for ALS-linked misfolded SOD1.Protein misdirection inside and outside motor neurons in Amyotrophic Lateral Sclerosis (ALS): a possible clue for therapeutic strategies Neurodegeneration as a consequence of failed mitochondrial maintenance.Misfolded SOD1 and ALS: zeroing in on mitochondria.Review: Axon pathology in age-related neurodegenerative disorders.Amyotrophic lateral sclerosis: new genes, new models, and new mechanisms.Selective vulnerability of motoneuron and perturbed mitochondrial calcium homeostasis in amyotrophic lateral sclerosis: implications for motoneurons specific calcium dysregulation.Targeting mitochondrial metal dyshomeostasis for the treatment of neurodegeneration.Neurobiology of axonal transport defects in motor neuron diseases: Opportunities for translational research?Motoneuron Disease: Basic Science.Mitochondrial quality control in amyotrophic lateral sclerosis: towards a common pathway?Enhancing mitochondrial calcium buffering capacity reduces aggregation of misfolded SOD1 and motor neuron cell death without extending survival in mouse models of inherited amyotrophic lateral sclerosis Atomic structure of a toxic, oligomeric segment of SOD1 linked to amyotrophic lateral sclerosis (ALS).Constitutive downregulation protein kinase C epsilon in hSOD1G93A astrocytes influences mGluR5 signaling and the regulation of glutamate uptake.The mito::mKate2 mouse: A far-red fluorescent reporter mouse line for tracking mitochondrial dynamics in vivo.Inhibition of Drp1/Fis1 interaction slows progression of amyotrophic lateral sclerosis.Phrenic Motor Neuron Loss in Aged Rats.Releasing Syntaphilin Removes Stressed Mitochondria from Axons Independent of Mitophagy under Pathophysiological Conditions.The voltage-gated calcium channel blocker lomerizine is neuroprotective in motor neurons expressing mutant SOD1, but not TDP-43.Impact of aging on diaphragm muscle function in male and female Fischer 344 rats.Amyotrophic lateral sclerosis

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Misfolded SOD1 associated with motor neuron mitochondria alters mitochondrial shape and distribution prior to clinical onset.

http://www.wikidata.org/entity/Q33968208

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2011 nî lūn-bûn

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2011 թուականի Յուլիսին հրատարակուած գիտական յօդուած

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2011年の論文

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Andre Zandona

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Christian S Lobsiger

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Christine Vande Velde

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Jean-Pierre Julien

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Karli K McDonald

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Melissa McAlonis-Downes

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Samar Bel Hadj

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Sameer B Shah

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Yasmin Boukhedimi

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P2860

ALS-associated mutant SOD1G93A causes mitochondrial vacuolation by expansion of the intermembrane space and by involvement of SOD1 aggregation and peroxisomes

Mitochondria: dynamic organelles in disease, aging, and development

Amyotrophic lateral sclerosis-associated SOD1 mutant proteins bind and aggregate with Bcl-2 in spinal cord mitochondria

Requirement for the homeobox gene Hb9 in the consolidation of motor neuron identity

ALS: a disease of motor neurons and their nonneuronal neighbors

Wild-type and mutant SOD1 share an aberrant conformation and a common pathogenic pathway in ALS.

Drosophila Porin/VDAC affects mitochondrial morphology.

Axonal mitochondrial clusters containing mutant SOD1 in transgenic models of ALS.

Misfolded mutant SOD1 directly inhibits VDAC1 conductance in a mouse model of inherited ALS

ALS-linked mutant superoxide dismutase 1 (SOD1) alters mitochondrial protein composition and decreases protein import.

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Don W Cleveland

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