Poly-GA triggers TDP-43 pathology by inhibiting the proteasome and nucleocytoplasmic import in C9orf72 ALS/FTD

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Location: Deutsche Nationalbibliothek Frankfurt am Main

Extent: Online-Ressource

Language: Englisch

Notes: München, Ludwig-Maximilians-Universität, Dissertation, 2021

Keyword: Pathology

Event: Veröffentlichung

(where): München

(who): Universitätsbibliothek der Ludwig-Maximilians-Universität

(when): 2021

Creator: Khosravi, Bahram

Contributor: Edbauer, Dieter

DOI: 10.5282/edoc.28991

URN: urn:nbn:de:bvb:19-289917

Rights: Der Zugriff auf das Objekt ist unbeschränkt möglich.

Last update: 15.08.2025, 7:26 AM CEST

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Associated

Khosravi, Bahram
Edbauer, Dieter
Universitätsbibliothek der Ludwig-Maximilians-Universität

Time of origin

2021

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Divergence, Convergence, and Therapeutic Implications: A Cell Biology Perspective of C9ORF72-ALS/FTD

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Disulfide cross-linked multimers of TDP-43 and spinal motoneuron loss in a TDP-43A315T ALS/FTD mouse model

TDP-43 pathology disrupts nuclear pore complexes and nucleocytoplasmic transport in ALS/FTD

SUMOylation Regulates TDP-43 Splicing Activity and Nucleocytoplasmic Distribution

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Disulfide cross-linked multimers of TDP-43 and spinal motoneuron loss in a TDP-43A315T ALS/FTD mouse model

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Poly-GA triggers TDP-43 pathology by inhibiting the proteasome and nucleocytoplasmic import in C9orf72 ALS/FTD

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Other Objects (12)

TDP-43 pathology disrupts nuclear pore complexes and nucleocytoplasmic transport in ALS/FTD

SUMOylation Regulates TDP-43 Splicing Activity and Nucleocytoplasmic Distribution

A familial FTD associated with C9orf72 repeat expansion and dysplastic gangliocytoma

Roadmap for C9ORF72 in Frontotemporal Dementia and Amyotrophic Lateral Sclerosis: Report on the C9ORF72 FTD/ALS Summit

A C9ORF72 BAC mouse model recapitulates key epigenetic perturbations of ALS/FTD

Nuclear lamina invaginations are not a pathological feature of C9orf72 ALS/FTD

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RNA dependent suppression of C9orf72 ALS/FTD associated neurodegeneration by Matrin-3

Targeting RNA G‐quadruplexes as new treatment strategy for C9orf72 ALS/FTD

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Specific biomarkers for C9orf72 FTD/ALS could expedite the journey towards effective therapies

Disulfide cross-linked multimers of TDP-43 and spinal motoneuron loss in a TDP-43A315T ALS/FTD mouse model

TDP-43 pathology disrupts nuclear pore complexes and nucleocytoplasmic transport in ALS/FTD

SUMOylation Regulates TDP-43 Splicing Activity and Nucleocytoplasmic Distribution

A familial FTD associated with C9orf72 repeat expansion and dysplastic gangliocytoma

Roadmap for C9ORF72 in Frontotemporal Dementia and Amyotrophic Lateral Sclerosis: Report on the C9ORF72 FTD/ALS Summit

A C9ORF72 BAC mouse model recapitulates key epigenetic perturbations of ALS/FTD

Nuclear lamina invaginations are not a pathological feature of C9orf72 ALS/FTD

Aktive und passive anti-GA Immuntherapie für C9orf72 ALS/FTD im Mausmodell

RNA dependent suppression of C9orf72 ALS/FTD associated neurodegeneration by Matrin-3

Targeting RNA G‐quadruplexes as new treatment strategy for C9orf72 ALS/FTD

Divergence, Convergence, and Therapeutic Implications: A Cell Biology Perspective of C9ORF72-ALS/FTD

Specific biomarkers for C9orf72 FTD/ALS could expedite the journey towards effective therapies

Disulfide cross-linked multimers of TDP-43 and spinal motoneuron loss in a TDP-43A315T ALS/FTD mouse model

TDP-43 pathology disrupts nuclear pore complexes and nucleocytoplasmic transport in ALS/FTD

SUMOylation Regulates TDP-43 Splicing Activity and Nucleocytoplasmic Distribution

A familial FTD associated with C9orf72 repeat expansion and dysplastic gangliocytoma

Roadmap for C9ORF72 in Frontotemporal Dementia and Amyotrophic Lateral Sclerosis: Report on the C9ORF72 FTD/ALS Summit

A C9ORF72 BAC mouse model recapitulates key epigenetic perturbations of ALS/FTD

Nuclear lamina invaginations are not a pathological feature of C9orf72 ALS/FTD

Aktive und passive anti-GA Immuntherapie für C9orf72 ALS/FTD im Mausmodell

RNA dependent suppression of C9orf72 ALS/FTD associated neurodegeneration by Matrin-3

Targeting RNA G‐quadruplexes as new treatment strategy for C9orf72 ALS/FTD

Divergence, Convergence, and Therapeutic Implications: A Cell Biology Perspective of C9ORF72-ALS/FTD

Specific biomarkers for C9orf72 FTD/ALS could expedite the journey towards effective therapies

Disulfide cross-linked multimers of TDP-43 and spinal motoneuron loss in a TDP-43A315T ALS/FTD mouse model

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