Calcium dysregulation, mitochondrial pathology and protein aggregation in a culture model of amyotrophic lateral sclerosis: Mechanistic relationship and differential sensitivity to intervention (Q57041407)

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scientific article published on February 3, 2011

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English	Calcium dysregulation, mitochondrial pathology and protein aggregation in a culture model of amyotrophic lateral sclerosis: Mechanistic relationship and differential sensitivity to intervention	scientific article published on February 3, 2011

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Calcium dysregulation, mitochondrial pathology and protein aggregation in a culture model of amyotrophic lateral sclerosis: mechanistic relationship and differential sensitivity to intervention (English)

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Calcium dysregulation, mitochondrial pathology and protein aggregation in a culture model of amyotrophic lateral sclerosis: Mechanistic relationship and differential sensitivity to intervention (English)

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10.1016/J.NBD.2011.01.016

https://api.crossref.org/works/10.1016/J.NBD.2011.01.016

23 November 2024

amyotrophic lateral sclerosis

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based on heuristic

inferred from title

protein aggregation

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based on heuristic

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Sandra Minotti

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Miranda L. Tradewell

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Europe PubMed Central

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https://www.ebi.ac.uk/europepmc/webservices/rest/search?resulttype=core&format=json&query=SRC%3AMED%20AND%20EXT_ID%3A21296666

23 November 2024

Laura A. Cooper

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Europe PubMed Central

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https://www.ebi.ac.uk/europepmc/webservices/rest/search?resulttype=core&format=json&query=SRC%3AMED%20AND%20EXT_ID%3A21296666

23 November 2024

Heather D. Durham

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Europe PubMed Central

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June 2011

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3 February 2011

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23 November 2024

full work available at URL

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10.1016/J.NBD.2011.01.016

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https://api.elsevier.com/content/article/PII:S0969996111000283?httpAccept=text/plain

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10.1016/J.NBD.2011.01.016

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Neurobiology of Disease

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42

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3

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265-75

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The role of calcium-binding proteins in selective motoneuron vulnerability in amyotrophic lateral sclerosis

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

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Induction of multiple heat shock proteins and neuroprotection in a primary culture model of familial amyotrophic lateral sclerosis

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Parvalbumin overexpression alters immune-mediated increases in intracellular calcium, and delays disease onset in a transgenic model of familial amyotrophic lateral sclerosis

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Impairment of the ubiquitin-proteasome system by protein aggregation

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Overloading of stable and exclusion of unstable human superoxide dismutase-1 variants in mitochondria of murine amyotrophic lateral sclerosis models

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Expression of mutant SOD1 in astrocytes induces functional deficits in motoneuron mitochondria

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Excitability properties of mouse motor axons in the mutant SOD1(G93A) model of amyotrophic lateral sclerosis

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Mitochondrial enzyme activity in amyotrophic lateral sclerosis: implications for the role of mitochondria in neuronal cell death

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Up-regulation of protein chaperones preserves viability of cells expressing toxic Cu/Zn-superoxide dismutase mutants associated with amyotrophic lateral sclerosis

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Expression of a Cu,Zn superoxide dismutase typical of familial amyotrophic lateral sclerosis induces mitochondrial alteration and increase of cytosolic Ca2+ concentration in transfected neuroblastoma SH-SY5Y cells

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Fluorescence and bioluminescence measurement of cytoplasmic free calcium

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Amyotrophic lateral sclerosis: from current developments in the laboratory to clinical implications

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Neural mitochondrial Ca2+ capacity impairment precedes the onset of motor symptoms in G93A Cu/Zn-superoxide dismutase mutant mice

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

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CuZn superoxide dismutase (SOD1) accumulates in vacuolated mitochondria in transgenic mice expressing amyotrophic lateral sclerosis-linked SOD1 mutations

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Cu/Zn superoxide dismutase typical for familial amyotrophic lateral sclerosis increases the vulnerability of mitochondria and perturbs Ca2+ homeostasis in SOD1G93A mice

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Altered axonal excitability properties in amyotrophic lateral sclerosis: impaired potassium channel function related to disease stage

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