Dipeptide repeat proteins inhibit homology-directed DNA double strand break repair in C9ORF72 ALS/FTD

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Location: Deutsche Nationalbibliothek Frankfurt am Main

ISSN: 1750-1326

Extent: Online-Ressource

Language: Englisch

Notes: online resource.

Bibliographic citation: Dipeptide repeat proteins inhibit homology-directed DNA double strand break repair in C9ORF72 ALS/FTD ; volume:15 ; number:1 ; day:24 ; month:2 ; year:2020 ; pages:1-18 ; date:12.2020
Molecular neurodegeneration ; 15, Heft 1 (24.2.2020), 1-18, 12.2020

Creator: Andrade, Nadja S.
Ramic, Melina
Esanov, Rustam
Liu, Wenjun
Rybin, Mathew J.
Gaidosh, Gabriel
Abdallah, Abbas
Del’Olio, Samuel
Huff, Tyler C.
Chee, Nancy T.
Anatha, Sadhana
Gendron, Tania F.
Wahlestedt, Claes
Zhang, Yanbin
Benatar, Michael
Mueller, Christian
Zeier, Zane

Contributor: SpringerLink (Online service)

DOI: 10.1186/s13024-020-00365-9

URN: urn:nbn:de:101:1-2020051906054239988186

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

Last update: 14.08.2025, 10:49 AM CEST

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Associated

Andrade, Nadja S.
Ramic, Melina
Esanov, Rustam
Liu, Wenjun
Rybin, Mathew J.
Gaidosh, Gabriel
Abdallah, Abbas
Del’Olio, Samuel
Huff, Tyler C.
Chee, Nancy T.
Anatha, Sadhana
Gendron, Tania F.
Wahlestedt, Claes
Zhang, Yanbin
Benatar, Michael
Mueller, Christian
Zeier, Zane
SpringerLink (Online service)

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Antibodies inhibit transmission and aggregation of C9orf72 poly‐ GA dipeptide repeat proteins

CUG initiation and frameshifting enable production of dipeptide repeat proteins from ALS/FTD C9ORF72 transcripts

Poly‐ GP in cerebrospinal fluid links C9orf72 ‐associated dipeptide repeat expression to the asymptomatic phase of ALS/FTD

C9orf72-Associated Dipeptide Repeat Expansions Perturb ER-Golgi Vesicular Trafficking, Inducing Golgi Fragmentation and ER Stress, in ALS/FTD

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Antibodies inhibit transmission and aggregation of C9orf72 poly‐ GA dipeptide repeat proteins

CUG initiation and frameshifting enable production of dipeptide repeat proteins from ALS/FTD C9ORF72 transcripts

Poly‐ GP in cerebrospinal fluid links C9orf72 ‐associated dipeptide repeat expression to the asymptomatic phase of ALS/FTD

C9orf72-Associated Dipeptide Repeat Expansions Perturb ER-Golgi Vesicular Trafficking, Inducing Golgi Fragmentation and ER Stress, in ALS/FTD

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

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Dipeptide repeat proteins inhibit homology-directed DNA double strand break repair in C9ORF72 ALS/FTD

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Other Objects (12)

C9orf72 ALS/FTD dipeptide repeat protein levels are reduced by small molecules that inhibit PKA or enhance protein degradation

Antibodies inhibit transmission and aggregation of C9orf72 poly‐ GA dipeptide repeat proteins

CUG initiation and frameshifting enable production of dipeptide repeat proteins from ALS/FTD C9ORF72 transcripts

Poly‐ GP in cerebrospinal fluid links C9orf72 ‐associated dipeptide repeat expression to the asymptomatic phase of ALS/FTD

C9orf72-Associated Dipeptide Repeat Expansions Perturb ER-Golgi Vesicular Trafficking, Inducing Golgi Fragmentation and ER Stress, in ALS/FTD

CRISPR deletion of the C9ORF72 promoter in ALS/FTD patient motor neurons abolishes production of dipeptide repeat proteins and rescues neurodegeneration

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

C9orf72 ALS/FTD dipeptide repeat protein levels are reduced by small molecules that inhibit PKA or enhance protein degradation

Antibodies inhibit transmission and aggregation of C9orf72 poly‐ GA dipeptide repeat proteins

CUG initiation and frameshifting enable production of dipeptide repeat proteins from ALS/FTD C9ORF72 transcripts

Poly‐ GP in cerebrospinal fluid links C9orf72 ‐associated dipeptide repeat expression to the asymptomatic phase of ALS/FTD

C9orf72-Associated Dipeptide Repeat Expansions Perturb ER-Golgi Vesicular Trafficking, Inducing Golgi Fragmentation and ER Stress, in ALS/FTD

CRISPR deletion of the C9ORF72 promoter in ALS/FTD patient motor neurons abolishes production of dipeptide repeat proteins and rescues neurodegeneration

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

C9orf72 ALS/FTD dipeptide repeat protein levels are reduced by small molecules that inhibit PKA or enhance protein degradation

Antibodies inhibit transmission and aggregation of C9orf72 poly‐ GA dipeptide repeat proteins

CUG initiation and frameshifting enable production of dipeptide repeat proteins from ALS/FTD C9ORF72 transcripts

Poly‐ GP in cerebrospinal fluid links C9orf72 ‐associated dipeptide repeat expression to the asymptomatic phase of ALS/FTD

C9orf72-Associated Dipeptide Repeat Expansions Perturb ER-Golgi Vesicular Trafficking, Inducing Golgi Fragmentation and ER Stress, in ALS/FTD

CRISPR deletion of the C9ORF72 promoter in ALS/FTD patient motor neurons abolishes production of dipeptide repeat proteins and rescues neurodegeneration

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

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