Mutant SOD1 protein increases Nav1.3 channel excitability
نویسندگان
چکیده
منابع مشابه
SOD1 mutant increases microglial neurotoxicity - 1 - Expression of ALS-linked SOD1 mutant increases the neurotoxic potential of microglia via TLR2
Amyotrophic lateral sclerosis (ALS) is a progressive motor neuron disease, in which activated microglia overexpressing ALS-linked SOD1 mutants (mSOD1) are known to contribute to neuronal death. However, it is unclear how mSOD1 expression affects micoglial activation and subsequently damage neurons. In this study, we created mSOD1overexpressing BV-2 microglial cell lines. Following TLR2, but not...
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Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder characterized by the progressive loss of motor neurons leading to paralysis and death. Mutations of the human Cu/Zn superoxide dismutase (SOD1) are found in some cases of familial ALS (fALS). Recent evidences suggest the accumulation of intracellular calcium is one of the primary mechanisms of motor neuronal degeneration. In th...
متن کاملHeat shock protein 70 protects motor neuronal cells expressing mutant Cu/Zn superoxide dismutase (SOD1) against altered calcium homeostasis
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder characterized by the progressive loss of motor neurons leading to paralysis and death. Mutations of the human Cu/Zn superoxide dismutase (SOD1) are found in some cases of familial ALS (fALS). Recent evidences suggest the accumulation of intracellular calcium is one of the primary mechanisms of motor neuronal degeneration. In th...
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Amyotrophic lateral sclerosis (ALS) is a progressive motor neuron disease, in which activated microglia overexpressing ALS-linked SOD1 mutants (mSOD1) are known to contribute to neuronal death. However, it is unclear how mSOD1 expression affects micoglial activation and subsequently damage neurons. In this study, we created mSOD1overexpressing BV-2 microglial cell lines. Following TLR2, but not...
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ژورنال
عنوان ژورنال: Journal of Biological Physics
سال: 2016
ISSN: 0092-0606,1573-0689
DOI: 10.1007/s10867-016-9411-x