Cellular analysis of SOD1 protein-aggregation propensity and toxicity: a case of ALS with slow progression harboring homozygous SOD1-D92G mutation
- Location
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Deutsche Nationalbibliothek Frankfurt am Main
- ISSN
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2045-2322
- 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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Cellular analysis of SOD1 protein-aggregation propensity and toxicity: a case of ALS with slow progression harboring homozygous SOD1-D92G mutation ; volume:12 ; number:1 ; day:25 ; month:7 ; year:2022 ; pages:1-10 ; date:12.2022
Scientific reports ; 12, Heft 1 (25.7.2022), 1-10, 12.2022
- Creator
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Sawamura, Masanori
Imamura, Keiko
Hikawa, Rie
Enami, Takako
Nagahashi, Ayako
Yamakado, Hodaka
Ichijo, Hidenori
Fujisawa, Takao
Yamashita, Hirofumi
Minamiyama, Sumio
Kaido, Misako
Wada, Hiromi
Urushitani, Makoto
Inoue, Haruhisa
Egawa, Naohiro
Takahashi, Ryosuke
- Contributor
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SpringerLink (Online service)
- DOI
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10.1038/s41598-022-16871-3
- URN
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urn:nbn:de:101:1-2022100619542749855483
- Rights
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Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Last update
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15.08.2025, 7:30 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
- Sawamura, Masanori
- Imamura, Keiko
- Hikawa, Rie
- Enami, Takako
- Nagahashi, Ayako
- Yamakado, Hodaka
- Ichijo, Hidenori
- Fujisawa, Takao
- Yamashita, Hirofumi
- Minamiyama, Sumio
- Kaido, Misako
- Wada, Hiromi
- Urushitani, Makoto
- Inoue, Haruhisa
- Egawa, Naohiro
- Takahashi, Ryosuke
- SpringerLink (Online service)
Other Objects (12)
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Widespread CNS pathology in amyotrophic lateral sclerosis homozygous for the D90A SOD1 mutation
Der Einfluss einer wildtypischen SOD1-Untereinheit auf Konformation und Stabilität mutanter SOD1-Heterodimere
Der Einfluss einer wildtypischen SOD1-Untereinheit auf Konformation und Stabilität mutanter SOD1-Heterodimere
Die Beteiligung von wildtypischer SOD1 an der Pathogenese der SOD1-vermittelten amyotrophen Lateralsklerose (ALS1)
Features of wild-type human SOD1 limit interactions with misfolded aggregates of mouse G86R Sod1
Better survival in female SOD1-mutant patients with ALS: a study of SOD1-related natural history
Increased surface P2X4 receptors by mutant SOD1 proteins contribute to ALS pathogenesis in SOD1-G93A mice
A novel homozygous p.Ser69Pro SOD1 mutation causes severe young-onset ALS with decreased enzyme activity
Tryptophan 32-mediated SOD1 aggregation is attenuated by pyrimidine-like compounds in living cells
Differential induction of mutant SOD1 misfolding and aggregation by tau and α-synuclein pathology
Correction to: 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
Widespread CNS pathology in amyotrophic lateral sclerosis homozygous for the D90A SOD1 mutation
Der Einfluss einer wildtypischen SOD1-Untereinheit auf Konformation und Stabilität mutanter SOD1-Heterodimere
Der Einfluss einer wildtypischen SOD1-Untereinheit auf Konformation und Stabilität mutanter SOD1-Heterodimere
Die Beteiligung von wildtypischer SOD1 an der Pathogenese der SOD1-vermittelten amyotrophen Lateralsklerose (ALS1)
Features of wild-type human SOD1 limit interactions with misfolded aggregates of mouse G86R Sod1
Better survival in female SOD1-mutant patients with ALS: a study of SOD1-related natural history
Increased surface P2X4 receptors by mutant SOD1 proteins contribute to ALS pathogenesis in SOD1-G93A mice
A novel homozygous p.Ser69Pro SOD1 mutation causes severe young-onset ALS with decreased enzyme activity
Tryptophan 32-mediated SOD1 aggregation is attenuated by pyrimidine-like compounds in living cells
Differential induction of mutant SOD1 misfolding and aggregation by tau and α-synuclein pathology