ArticleNeurobiology of disease2009
Redox susceptibility of SOD1 mutants is associated with the differential response to CCS over-expression in vivo.
Article in Neurobiology of disease, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- A pathological link between dysregulated copper binding in Cu/Zn-superoxide dismutase and amyotrophic lateral sclerosis.Journal of clinical biochemistry and nutrition · 2022Article
- Molecular and pharmacological chaperones for SOD1.Biochemical Society transactions · 2020Review
- Does wild-type Cu/Zn-superoxide dismutase have pathogenic roles in amyotrophic lateral sclerosis?Translational neurodegeneration · 2020Review
- Exploring the Extended Biological Functions of the Human Copper Chaperone of Superoxide Dismutase 1.The protein journal · 2019Review
- Long-lived rodents reveal signatures of positive selection in genes associated with lifespan.PLoS genetics · 2018Article
- Ionic Homeostasis Maintenance in ALS: Focus on New Therapeutic Targets.Frontiers in neuroscience · 2018Review
- Proteinopathies and OXPHOS dysfunction in neurodegenerative diseases.The Journal of cell biology · 2017Review
- S-acylation of SOD1, CCS, and a stable SOD1-CCS heterodimer in human spinal cords from ALS and non-ALS subjects.Scientific reports · 2017Article
- Copper Homeostasis as a Therapeutic Target in Amyotrophic Lateral Sclerosis with SOD1 Mutations.International journal of molecular sciences · 2016Review
- SOD1 misplacing and mitochondrial dysfunction in amyotrophic lateral sclerosis pathogenesis.Frontiers in cellular neuroscience · 2015Review
- Aggregation propensities of superoxide dismutase G93 hotspot mutants mirror ALS clinical phenotypes.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Is SOD1 loss of function involved in amyotrophic lateral sclerosis?Brain : a journal of neurology · 2013Review
- Biochemical properties and in vivo effects of the SOD1 zinc-binding site mutant (H80G).Journal of neurochemistry · 2011Article
- Decreased glutathione accelerates neurological deficit and mitochondrial pathology in familial ALS-linked hSOD1(G93A) mice model.Neurobiology of disease · 2011Article
- Aggregation modulating elements in mutant human superoxide dismutase 1.Archives of biochemistry and biophysics · 2010Article
- Import, maturation, and function of SOD1 and its copper chaperone CCS in the mitochondrial intermembrane space.Antioxidants & redox signaling · 2010Review
- Cellular copper distribution: a mechanistic systems biology approach.Cellular and molecular life sciences : CMLS · 2010Review
- Regulation of the copper chaperone CCS by XIAP-mediated ubiquitination.Molecular and cellular biology · 2010Article
- The right to choose: multiple pathways for activating copper,zinc superoxide dismutase.The Journal of biological chemistry · 2009Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Over-expression of CCS in G93A SOD1 mice accelerates neurological disease and enhances mitochondrial pathology. We studied the effect of CCS over-expression in transgenic mice expressing G37R, G86R or L126Z SOD1 mutations in order to understand factors which influence mitochondrial dysfunction. Over-expression of CCS markedly decreased survival and produced mitochondrial vacuolation in G37R SOD1 mice but not in G86R or L126Z SOD1 mice. Moreover, CCS/G37R SOD1 spinal cord showed specific reductions in mitochondrial complex IV subunits consistent with an isolated COX deficiency, while no such reductions were detected in CCS/G86R or CCS/L126Z SOD1 mice. CCS over-expression increased the ratio of reduced to oxidized SOD1 monomers in the spinal cords of G37R SOD1 as well as G93A SOD1 mice, but did not influence the redox state of G86R or L126Z SOD1 monomers. The effects of CCS on disease are SOD1 mutation dependent and correlate with SOD1 redox susceptibility.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.