Mechanisms of mutant SOD1 induced mitochondrial toxicity in amyotrophic lateral sclerosis (Q26998585)

Jari Koistinaho

series ordinal

2

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Goldsteins Gundars

series ordinal

3

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language of work or name

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2014

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Frontiers in Cellular Neuroscience

published in

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volume

8

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page(s)

126

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VAPB interacts with the mitochondrial protein PTPIP51 to regulate calcium homeostasis

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Disulfide cross-linked protein represents a significant fraction of ALS-associated Cu, Zn-superoxide dismutase aggregates in spinal cords of model mice

21 March 2017

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The copper chaperone for superoxide dismutase

21 March 2017

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21 March 2017

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A disulfide relay system in the intermembrane space of mitochondria that mediates protein import

21 March 2017

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A fraction of yeast Cu,Zn-superoxide dismutase and its metallochaperone, CCS, localize to the intermembrane space of mitochondria. A physiological role for SOD1 in guarding against mitochondrial oxidative damage.

21 March 2017

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Mitochondrial Cu,Zn-superoxide dismutase mediates pulmonary fibrosis by augmenting H2O2 generation

21 March 2017

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

21 March 2017

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Copper chaperone for superoxide dismutase is essential to activate mammalian Cu/Zn superoxide dismutase

21 March 2017

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Motor neurons in Cu/Zn superoxide dismutase-deficient mice develop normally but exhibit enhanced cell death after axonal injury

21 March 2017

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

21 March 2017

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Unraveling the mechanisms involved in motor neuron degeneration in ALS

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ALS and neuromuscular disease: in search of the Holy Grail

28 September 2017

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Wild-type Cu/Zn superoxide dismutase stabilizes mutant variants by heterodimerization.

28 September 2017

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Distinctive features of the D101N and D101G variants of superoxide dismutase 1; two mutations that produce rapidly progressing motor neuron disease

28 September 2017

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Human superoxide dismutase 1 (hSOD1) maturation through interaction with human copper chaperone for SOD1 (hCCS)

28 September 2017

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Mutant superoxide dismutase-1 indistinguishable from wild-type causes ALS.

28 September 2017

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Localization of a toxic form of superoxide dismutase 1 protein to pathologically affected tissues in familial ALS

28 September 2017

1 reference

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Diacetylbis(N(4)-methylthiosemicarbazonato) copper(II) (CuII(atsm)) protects against peroxynitrite-induced nitrosative damage and prolongs survival in amyotrophic lateral sclerosis mouse model

28 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=4023018

Mutant SOD1 forms ion channel: implications for ALS pathophysiology

28 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=4023018

Mitochondrial Ccs1 contains a structural disulfide bond crucial for the import of this unconventional substrate by the disulfide relay system

28 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=4023018

Mia40-dependent oxidation of cysteines in domain I of Ccs1 controls its distribution between mitochondria and the cytosol

28 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=4023018

Copper depletion increases the mitochondrial-associated SOD1 in neuronal cells

28 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=4023018

SOD1 targeted to the mitochondrial intermembrane space prevents motor neuropathy in the Sod1 knockout mouse

28 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=4023018

Glutaredoxin 2 prevents aggregation of mutant SOD1 in mitochondria and abolishes its toxicity.

28 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=4023018

Mutant SOD1 in neuronal mitochondria causes toxicity and mitochondrial dynamics abnormalities

28 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=4023018

Wild-type Cu/Zn superoxide dismutase (SOD1) does not facilitate, but impedes the formation of protein aggregates of amyotrophic lateral sclerosis causing mutant SOD1.

28 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=4023018

Activation of Cu,Zn-superoxide dismutase in the absence of oxygen and the copper chaperone CCS.

28 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=4023018

Variation in aggregation propensities among ALS-associated variants of SOD1: correlation to human disease.

28 September 2017

1 reference

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Role of mutant SOD1 disulfide oxidation and aggregation in the pathogenesis of familial ALS

28 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=4023018

Oligomerization of mutant SOD1 in mitochondria of motoneuronal cells drives mitochondrial damage and cell toxicity

28 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=4023018

Wild-type SOD1 overexpression accelerates disease onset of a G85R SOD1 mouse.

28 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=4023018

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

28 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=4023018

Different regulation of wild-type and mutant Cu,Zn superoxide dismutase localization in mammalian mitochondria

28 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=4023018

Selective association of misfolded ALS-linked mutant SOD1 with the cytoplasmic face of mitochondria.

28 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=4023018

Heterodimer formation of wild-type and amyotrophic lateral sclerosis-causing mutant Cu/Zn-superoxide dismutase induces toxicity independent of protein aggregation

28 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=4023018

Amyotrophic lateral sclerosis models and human neuropathology: similarities and differences

28 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=4023018

Cysteine 111 affects aggregation and cytotoxicity of mutant Cu,Zn-superoxide dismutase associated with familial amyotrophic lateral sclerosis

28 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=4023018

Familial amyotrophic lateral sclerosis-linked SOD1 mutants perturb fast axonal transport to reduce axonal mitochondria content

28 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=4023018

Soluble misfolded subfractions of mutant superoxide dismutase-1s are enriched in spinal cords throughout life in murine ALS models

28 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=4023018

Disulfide bond mediates aggregation, toxicity, and ubiquitylation of familial amyotrophic lateral sclerosis-linked mutant SOD1.

28 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=4023018

Overexpression of CCS in G93A-SOD1 mice leads to accelerated neurological deficits with severe mitochondrial pathology

28 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=4023018

Familial ALS-superoxide dismutases associate with mitochondria and shift their redox potentials.

28 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=4023018

Conversion to the amyotrophic lateral sclerosis phenotype is associated with intermolecular linked insoluble aggregates of SOD1 in mitochondria

28 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=4023018

Destabilization of apoprotein is insufficient to explain Cu,Zn-superoxide dismutase-linked ALS pathogenesis.

28 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=4023018

Systematically perturbed folding patterns of amyotrophic lateral sclerosis (ALS)-associated SOD1 mutants

28 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=4023018

Copper-zinc superoxide dismutase and amyotrophic lateral sclerosis

28 September 2017

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Controlled elimination of intracellular H(2)O(2): regulation of peroxiredoxin, catalase, and glutathione peroxidase via post-translational modification

28 September 2017

1 reference

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Mechanisms for activating Cu- and Zn-containing superoxide dismutase in the absence of the CCS Cu chaperone

28 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=4023018

Familial amyotrophic lateral sclerosis mutants of copper/zinc superoxide dismutase are susceptible to disulfide reduction

28 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=4023018

Formation of high molecular weight complexes of mutant Cu, Zn-superoxide dismutase in a mouse model for familial amyotrophic lateral sclerosis.

28 September 2017

1 reference

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Redox activation of mitochondrial intermembrane space Cu,Zn-superoxide dismutase

28 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=4023018

Oxygen-induced maturation of SOD1: a key role for disulfide formation by the copper chaperone CCS.

31 May 2018

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Subcellular distribution of superoxide dismutases (SOD) in rat liver: Cu,Zn-SOD in mitochondria

31 May 2018

1 reference

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The copper chelator d-penicillamine delays onset of disease and extends survival in a transgenic mouse model of familial amyotrophic lateral sclerosis

31 May 2018

1 reference

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Mutant SOD1 from spinal cord of G93A rats is destabilized and binds to inner mitochondrial membrane

31 May 2018

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https://api.crossref.org/works/10.3389%2FFNCEL.2014.00126

Hypermetabolism in ALS patients: an early and persistent phenomenon.

21 January 2018

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Factors controlling the uptake of yeast copper/zinc superoxide dismutase into mitochondria.

21 January 2018

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Amyotrophic lateral sclerosis mutations have the greatest destabilizing effect on the apo- and reduced form of SOD1, leading to unfolding and oxidative aggregation.

21 January 2018

1 reference

https://api.crossref.org/works/10.3389%2FFNCEL.2014.00126

Expression of wild-type human superoxide dismutase-1 in mice causes amyotrophic lateral sclerosis.

21 January 2018

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https://api.crossref.org/works/10.3389%2FFNCEL.2014.00126

Oxidation and reduction of cysteines in the intermembrane space of mitochondria: multiple facets of redox control

21 January 2018

1 reference

https://api.crossref.org/works/10.3389%2FFNCEL.2014.00126

Human Cu/Zn superoxide dismutase (SOD1) overexpression in mice causes mitochondrial vacuolization, axonal degeneration, and premature motoneuron death and accelerates motoneuron disease in mice expressing a familial amyotrophic lateral sclerosis mut

21 January 2018

1 reference

https://api.crossref.org/works/10.3389%2FFNCEL.2014.00126

Toxicity of familial ALS-linked SOD1 mutants from selective recruitment to spinal mitochondria.

21 January 2018

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Mutated human SOD1 causes dysfunction of oxidative phosphorylation in mitochondria of transgenic mice.

21 January 2018

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https://api.crossref.org/works/10.3389%2FFNCEL.2014.00126

Mitochondrial protein oxidation in yeast mutants lacking manganese-(MnSOD) or copper- and zinc-containing superoxide dismutase (CuZnSOD): evidence that MnSOD and CuZnSOD have both unique and overlapping functions in protecting mitochondrial proteins

21 January 2018

1 reference

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Respiration and ROS production in brain and spinal cord mitochondria of transgenic rats with mutant G93a Cu/Zn-superoxide dismutase gene.

21 January 2018

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The disulfide relay system of mitochondria is required for the biogenesis of mitochondrial Ccs1 and Sod1.

21 January 2018

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Familial amyotrophic lateral sclerosis-associated mutations decrease the thermal stability of distinctly metallated species of human copper/zinc superoxide dismutase

21 January 2018

1 reference

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Dysregulation of intracellular copper homeostasis is common to transgenic mice expressing human mutant superoxide dismutase-1s regardless of their copper-binding abilities.

21 January 2018

1 reference

https://api.crossref.org/works/10.3389%2FFNCEL.2014.00126

Ammonium tetrathiomolybdate delays onset, prolongs survival, and slows progression of disease in a mouse model for amyotrophic lateral sclerosis

21 January 2018

1 reference

https://api.crossref.org/works/10.3389%2FFNCEL.2014.00126

Mia40 and MINOS act in parallel with Ccs1 in the biogenesis of mitochondrial Sod1.

21 January 2018

1 reference

https://api.crossref.org/works/10.3389%2FFNCEL.2014.00126

Copper-binding-site-null SOD1 causes ALS in transgenic mice: aggregates of non-native SOD1 delineate a common feature

21 January 2018

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https://api.crossref.org/works/10.3389%2FFNCEL.2014.00126

High molecular weight complexes of mutant superoxide dismutase 1: age-dependent and tissue-specific accumulation

21 January 2018

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Motor neuron disease in mice expressing the wild type-like D90A mutant superoxide dismutase-1

21 January 2018

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12 December 2020

Mutant SOD1 causes motor neuron disease independent of copper chaperone-mediated copper loading

1 reference

12 December 2020

Composition of soluble misfolded superoxide dismutase-1 in murine models of amyotrophic lateral sclerosis

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12 December 2020

The unusually stable quaternary structure of human Cu,Zn-superoxide dismutase 1 is controlled by both metal occupancy and disulfide status

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12 December 2020

The coupling between disulphide status, metallation and dimer interface strength in Cu/Zn superoxide dismutase

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12 December 2020

Mitochondrial superoxide simutase. Site of synthesis and intramitochondrial localization

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12 December 2020

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

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12 December 2020

Prevention of mutant SOD1 motoneuron degeneration by copper chelatorsin vitro

1 reference

12 December 2020

Deleterious role of superoxide dismutase in the mitochondrial intermembrane space

1 reference

12 December 2020

Stabilization of mutant Cu/Zn superoxide dismutase (SOD1) protein by coexpressed wild SOD1 protein accelerates the disease progression in familial amyotrophic lateral sclerosis mice

1 reference

12 December 2020

In yeast redistribution of Sod1 to the mitochondrial intermembrane space provides protection against respiration derived oxidative stress

1 reference

12 December 2020

Identifiers

DOI

10.3389/FNCEL.2014.00126

1 reference

872330

872330

1 reference

1 reference

1 reference