- Location
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Deutsche Nationalbibliothek Frankfurt am Main
- Extent
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Online-Ressource, 1 online resource.
- Language
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Englisch
- Bibliographic citation
-
Cortical glia in SOD1(G93A) mice are subtly affected by ALS-like pathology ; volume:13 ; number:1 ; day:21 ; month:4 ; year:2023 ; pages:1-15 ; date:12.2023
Scientific reports ; 13, Heft 1 (21.4.2023), 1-15, 12.2023
- Creator
-
Filipi, Tereza
Matusova, Zuzana
Abaffy, Pavel
Vanatko, Ondrej
Tureckova, Jana
Benesova, Sarka
Kubiskova, Monika
Kirdajova, Denisa
Zahumensky, Jakub
Valihrach, Lukas
Anderova, Miroslava
- Contributor
-
SpringerLink (Online service)
- DOI
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10.1038/s41598-023-33608-y
- URN
-
urn:nbn:de:101:1-2023090121050950950150
- Rights
-
Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Last update
-
14.08.2025, 10:45 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
- Filipi, Tereza
- Matusova, Zuzana
- Abaffy, Pavel
- Vanatko, Ondrej
- Tureckova, Jana
- Benesova, Sarka
- Kubiskova, Monika
- Kirdajova, Denisa
- Zahumensky, Jakub
- Valihrach, Lukas
- Anderova, Miroslava
- SpringerLink (Online service)
Other Objects (12)
Misfolded SOD1 pathology in sporadic Amyotrophic Lateral Sclerosis
Aß Pathology and Neuron–Glia Interactions: A Synaptocentric View
RNS60 exerts therapeutic effects in the SOD1 ALS mouse model through protective glia and peripheral nerve rescue
Widespread CNS pathology in amyotrophic lateral sclerosis homozygous for the D90A SOD1 mutation
Differential induction of mutant SOD1 misfolding and aggregation by tau and α-synuclein pathology
Afadin controls cell polarization and mitotic spindle orientation in developing cortical radial glia
Primary glia expressing the G93A-SOD1 mutation present a neuroinflammatory phenotype and provide a cellular system for studies of glial inflammation
A small-molecule inhibitor of SOD1-Derlin-1 interaction ameliorates pathology in an ALS mouse model
Mass spectrometry imaging of SOD1 protein-metal complexes in SOD1G93A transgenic mice implicates demetalation with pathology
Meningeal and cortical grey matter pathology in multiple sclerosis
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
Misfolded SOD1 pathology in sporadic Amyotrophic Lateral Sclerosis
Aß Pathology and Neuron–Glia Interactions: A Synaptocentric View
RNS60 exerts therapeutic effects in the SOD1 ALS mouse model through protective glia and peripheral nerve rescue
Widespread CNS pathology in amyotrophic lateral sclerosis homozygous for the D90A SOD1 mutation
Differential induction of mutant SOD1 misfolding and aggregation by tau and α-synuclein pathology
Afadin controls cell polarization and mitotic spindle orientation in developing cortical radial glia
Primary glia expressing the G93A-SOD1 mutation present a neuroinflammatory phenotype and provide a cellular system for studies of glial inflammation
A small-molecule inhibitor of SOD1-Derlin-1 interaction ameliorates pathology in an ALS mouse model
Mass spectrometry imaging of SOD1 protein-metal complexes in SOD1G93A transgenic mice implicates demetalation with pathology
Meningeal and cortical grey matter pathology in multiple sclerosis
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
Misfolded SOD1 pathology in sporadic Amyotrophic Lateral Sclerosis
Aß Pathology and Neuron–Glia Interactions: A Synaptocentric View
RNS60 exerts therapeutic effects in the SOD1 ALS mouse model through protective glia and peripheral nerve rescue
Widespread CNS pathology in amyotrophic lateral sclerosis homozygous for the D90A SOD1 mutation
Differential induction of mutant SOD1 misfolding and aggregation by tau and α-synuclein pathology
Afadin controls cell polarization and mitotic spindle orientation in developing cortical radial glia
Primary glia expressing the G93A-SOD1 mutation present a neuroinflammatory phenotype and provide a cellular system for studies of glial inflammation
A small-molecule inhibitor of SOD1-Derlin-1 interaction ameliorates pathology in an ALS mouse model
Mass spectrometry imaging of SOD1 protein-metal complexes in SOD1G93A transgenic mice implicates demetalation with pathology
Meningeal and cortical grey matter pathology in multiple sclerosis
Der Einfluss einer wildtypischen SOD1-Untereinheit auf Konformation und Stabilität mutanter SOD1-Heterodimere