ALS-associated mutant SOD1G93A causes mitochondrial vacuolation by expansion of the intermembrane space and by involvement of SOD1 aggregation and peroxisomes
- Location
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Deutsche Nationalbibliothek Frankfurt am Main
- ISSN
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1471-2202
- Extent
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Online-Ressource
- Language
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Englisch
- Notes
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online resource.
- Bibliographic citation
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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 ; volume:4 ; number:1 ; day:15 ; month:7 ; year:2003 ; pages:1-14 ; date:12.2003
BMC neuroscience ; 4, Heft 1 (15.7.2003), 1-14, 12.2003
- Creator
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Higgins, Cynthia MJ
- Contributor
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Jung, Cheolwha
Xu, Zuoshang
SpringerLink (Online service)
- DOI
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10.1186/1471-2202-4-16
- URN
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urn:nbn:de:1111-2016032050434
- Rights
-
Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Last update
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14.08.2025, 10:56 AM CEST
Data provider
This object is provided by:
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Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Associated
- Higgins, Cynthia MJ
- Jung, Cheolwha
- Xu, Zuoshang
- SpringerLink (Online service)
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Tryptophan 32-mediated SOD1 aggregation is attenuated by pyrimidine-like compounds in living cells
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Peripheral administration of SOD1 aggregates does not transmit pathogenic aggregation to the CNS of SOD1 transgenic mice
Impaired ATF3 signaling involves SNAP25 in SOD1 mutant ALS patients
Correction to: Better survival in female SOD1-mutant patients with ALS: a study of SOD1-related natural history
ALS mutant SOD1 interacts with G3BP1 and affects stress granule dynamics
Tissue-specific roles of peroxisomes revealed by expression meta-analysis
Cellular analysis of SOD1 protein-aggregation propensity and toxicity: a case of ALS with slow progression harboring homozygous SOD1-D92G mutation
Differential induction of mutant SOD1 misfolding and aggregation by tau and α-synuclein pathology
Increased surface P2X4 receptors by mutant SOD1 proteins contribute to ALS pathogenesis in SOD1-G93A mice
Widespread aggregation of mutant VAPB associated with ALS does not cause motor neuron degeneration or modulate mutant SOD1 aggregation and toxicity in mice
Tryptophan 32-mediated SOD1 aggregation is attenuated by pyrimidine-like compounds in living cells
Peroxisomes
Better survival in female SOD1-mutant patients with ALS: a study of SOD1-related natural history
Peripheral administration of SOD1 aggregates does not transmit pathogenic aggregation to the CNS of SOD1 transgenic mice
Impaired ATF3 signaling involves SNAP25 in SOD1 mutant ALS patients
Correction to: Better survival in female SOD1-mutant patients with ALS: a study of SOD1-related natural history
ALS mutant SOD1 interacts with G3BP1 and affects stress granule dynamics
Tissue-specific roles of peroxisomes revealed by expression meta-analysis