Stable transgenic C9orf72 zebrafish model key aspects of the ALS/FTD phenotype and reveal novel pathological features

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Location: Deutsche Nationalbibliothek Frankfurt am Main

ISSN: 2051-5960

Extent: Online-Ressource

Language: Englisch

Notes: online resource.

Bibliographic citation: Stable transgenic C9orf72 zebrafish model key aspects of the ALS/FTD phenotype and reveal novel pathological features ; volume:6 ; number:1 ; day:19 ; month:11 ; year:2018 ; pages:1-16 ; date:12.2018
Acta Neuropathologica Communications ; 6, Heft 1 (19.11.2018), 1-16, 12.2018

Creator: Shaw, Matthew P.
Higginbottom, Adrian
McGown, Alexander
Castelli, Lydia M.
James, Evlyn
Hautbergue, Guillaume M.
Shaw, Pamela J.
Ramesh, Tennore M.

Contributor: SpringerLink (Online service)

DOI: 10.1186/s40478-018-0629-7

URN: urn:nbn:de:101:1-2019010221170952315631

Rights: Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.

Last update: 14.08.2025, 10:50 AM CEST

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Shaw, Matthew P.
Higginbottom, Adrian
McGown, Alexander
Castelli, Lydia M.
James, Evlyn
Hautbergue, Guillaume M.
Shaw, Pamela J.
Ramesh, Tennore M.
SpringerLink (Online service)

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Stable transgenic C9orf72 zebrafish model key aspects of the ALS/FTD phenotype and reveal novel pathological features

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Other Objects (12)

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

A new inducible transgenic mouse model for C9orf72-associated GGGGCC repeat expansion supports a gain-of-function mechanism in C9orf72-associated ALS and FTD

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

Retraction Note to: A new inducible transgenic mouse model for C9orf72-associated GGGGCC repeat expansion supports a gain-of-function mechanism in C9orf72-associated ALS and FTD

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

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

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

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

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

A new inducible transgenic mouse model for C9orf72-associated GGGGCC repeat expansion supports a gain-of-function mechanism in C9orf72-associated ALS and FTD

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

Retraction Note to: A new inducible transgenic mouse model for C9orf72-associated GGGGCC repeat expansion supports a gain-of-function mechanism in C9orf72-associated ALS and FTD

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

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

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

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

Phenylalanine-tRNA aminoacylation is compromised by ALS/FTD-associated C9orf72 C4G2 repeat RNA

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A new inducible transgenic mouse model for C9orf72-associated GGGGCC repeat expansion supports a gain-of-function mechanism in C9orf72-associated ALS and FTD

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

Retraction Note to: A new inducible transgenic mouse model for C9orf72-associated GGGGCC repeat expansion supports a gain-of-function mechanism in C9orf72-associated ALS and FTD

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

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

Phenylalanine-tRNA aminoacylation is compromised by ALS/FTD-associated C9orf72 C4G2 repeat RNA

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