ALS-linked mutant SOD1 damages mitochondria by promoting conformational changes in Bcl-2. - Wikidata - wikimedia - TriplyDB

ALS-linked mutant SOD1 damages mitochondria by promoting conformational changes in Bcl-2.

ALS-linked mutant SOD1 damages mitochondria by promoting conformational changes in Bcl-2.

http://www.wikidata.org/entity/Q33980322

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SOD1 misplacing and mitochondrial dysfunction in amyotrophic lateral sclerosis pathogenesis Mitochondrial dysfunction in amyotrophic lateral sclerosis - a valid pharmacological target?Calcium dysregulation links ALS defective proteins and motor neuron selective vulnerability The complex molecular biology of amyotrophic lateral sclerosis (ALS)Exploring new pathways of neurodegeneration in ALS: the role of mitochondria quality control Elevated PGC-1α activity sustains mitochondrial biogenesis and muscle function without extending survival in a mouse model of inherited ALS SOD1, an unexpected novel target for cancer therapy New Therapeutics to Modulate Mitochondrial Function in Neurodegenerative Disorders.Role of mitochondria in mutant SOD1 linked amyotrophic lateral sclerosis Angiogenin inhibits nuclear translocation of apoptosis inducing factor in a Bcl-2-dependent manner.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.Mechanisms, models and biomarkers in amyotrophic lateral sclerosis Pathogenic role of BECN1/Beclin 1 in the development of amyotrophic lateral sclerosis.Macrophage migration inhibitory factor as a chaperone inhibiting accumulation of misfolded SOD1.In vivo pathogenic role of mutant SOD1 localized in the mitochondrial intermembrane space Bcl-2 is a novel interacting partner for the 2-oxoglutarate carrier and a key regulator of mitochondrial glutathione.Mitochondria as a therapeutic target for aging and neurodegenerative diseases.An over-oxidized form of superoxide dismutase found in sporadic amyotrophic lateral sclerosis with bulbar onset shares a toxic mechanism with mutant SOD1 The mitochondrial calcium regulator cyclophilin D is an essential component of oestrogen-mediated neuroprotection in amyotrophic lateral sclerosis Nonnative SOD1 trimer is toxic to motor neurons in a model of amyotrophic lateral sclerosis.Mitochondrial dynamics and bioenergetic dysfunction is associated with synaptic alterations in mutant SOD1 motor neurons.Mitochondrial glutathione transport is a key determinant of neuronal susceptibility to oxidative and nitrosative stress.Small peptides against the mutant SOD1/Bcl-2 toxic mitochondrial complex restore mitochondrial function and cell viability in mutant SOD1-mediated ALS Reduced activity of AMP-activated protein kinase protects against genetic models of motor neuron disease.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.Characterization of early pathogenesis in the SOD1(G93A) mouse model of ALS: part I, background and methods.A new zebrafish model produced by TILLING of SOD1-related amyotrophic lateral sclerosis replicates key features of the disease and represents a tool for in vivo therapeutic screening.Dysregulation of axonal transport and motorneuron diseases.Neuroprotective effects of creatine.Cerebral microvascular endothelium and the pathogenesis of neurodegenerative diseases.Proteostasis and movement disorders: Parkinson's disease and amyotrophic lateral sclerosis.In vivo and in vitro determination of cell death markers in neurons.Using yeast models to probe the molecular basis of amyotrophic lateral sclerosis.SOD1 and mitochondria in ALS: a dangerous liaison.Endoplasmic reticulum stress and the ER mitochondrial calcium cycle in amyotrophic lateral sclerosis.An emerging role for misfolded wild-type SOD1 in sporadic ALS pathogenesis.The ER mitochondria calcium cycle and ER stress response as therapeutic targets in amyotrophic lateral sclerosis.Mitochondria and endoplasmic reticulum crosstalk in amyotrophic lateral sclerosis.

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P2860

ALS-linked mutant SOD1 damages mitochondria by promoting conformational changes in Bcl-2.

http://www.wikidata.org/entity/Q33980322

description

2010 nî lūn-bûn

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2010 թուականի Մայիսին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի մայիսին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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name

ALS-linked mutant SOD1 damages mitochondria by promoting conformational changes in Bcl-2.

@ast

ALS-linked mutant SOD1 damages mitochondria by promoting conformational changes in Bcl-2.

@en

type

label

ALS-linked mutant SOD1 damages mitochondria by promoting conformational changes in Bcl-2.

@ast

ALS-linked mutant SOD1 damages mitochondria by promoting conformational changes in Bcl-2.

@en

prefLabel

ALS-linked mutant SOD1 damages mitochondria by promoting conformational changes in Bcl-2.

@ast

ALS-linked mutant SOD1 damages mitochondria by promoting conformational changes in Bcl-2.

@en

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Human Molecular Genetics

P1476

ALS-linked mutant SOD1 damages mitochondria by promoting conformational changes in Bcl-2.

@en

P2093

Azadeh Kia

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

Daniela Sau

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

Davide Trotti

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

Marina Bogush

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

Nicole Naniche

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

Piera Pasinelli

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

Stefania Guareschi

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Steve Pedrini

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P2860

Direct activation of Bax by p53 mediates mitochondrial membrane permeabilization and apoptosis

A short Nur77-derived peptide converts Bcl-2 from a protector to a killer

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

Mutations in Cu/Zn superoxide dismutase gene are associated with familial amyotrophic lateral sclerosis

Conversion of Bcl-2 from protector to killer by interaction with nuclear orphan receptor Nur77/TR3

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

Structure-function analysis of Bcl-2 family proteins. Regulators of programmed cell death

Mutant Cu, Zn superoxide dismutase that causes motoneuron degeneration is present in mitochondria in the CNS

Mitochondrial membrane permeabilization in cell death

Unraveling the mechanisms involved in motor neuron degeneration in ALS

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2974-2986

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scholarly article

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10.1093/HMG/DDQ202

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15

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19

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2010-05-11T00:00:00Z

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44589998

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20460269

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P921

amyotrophic lateral sclerosis

P932

2901139

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