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

zu Verbundenen Objekten

Standort
Deutsche Nationalbibliothek Frankfurt am Main
ISSN
1750-1326
Umfang
Online-Ressource
Sprache
Englisch
Anmerkungen
online resource.

Erschienen in
A C9ORF72 BAC mouse model recapitulates key epigenetic perturbations of ALS/FTD ; volume:12 ; number:1 ; day:12 ; month:6 ; year:2017 ; pages:1-11 ; date:12.2017
Molecular neurodegeneration ; 12, Heft 1 (12.6.2017), 1-11, 12.2017

Schlagwort
Histologie
Cytologie

Urheber
Esanov, Rustam
Beteiligte Personen und Organisationen
Cabrera, Gabriela Toro
Andrade, Nadja S.
Gendron, Tania F.
Brown, Robert H.
Benatar, Michael
Wahlestedt, Claes
Mueller, Christian
Zeier, Zane
SpringerLink (Online service)

DOI
10.1186/s13024-017-0185-9
URN
urn:nbn:de:1111-201709063344
Rechteinformation
Der Zugriff auf das Objekt ist unbeschränkt möglich.
Letzte Aktualisierung
14.08.2025, 10:57 MESZ

Datenpartner

Dieses Objekt wird bereitgestellt von:
Deutsche Nationalbibliothek. Bei Fragen zum Objekt wenden Sie sich bitte an den Datenpartner.
Original beim Datenpartner anzeigen

Beteiligte

  • Esanov, Rustam
  • Cabrera, Gabriela Toro
  • Andrade, Nadja S.
  • Gendron, Tania F.
  • Brown, Robert H.
  • Benatar, Michael
  • Wahlestedt, Claes
  • Mueller, Christian
  • Zeier, Zane
  • SpringerLink (Online service)

Ähnliche Objekte (12)

A familial FTD associated with C9orf72 repeat expansion and dysplastic gangliocytoma

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

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

Nuclear lamina invaginations are not a pathological feature of C9orf72 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

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

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

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

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

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

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

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

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

The ALS/FTD-related C9orf72 hexanucleotide repeat expansion forms RNA condensates through multimolecular G-quadruplexes

The ALS/FTD-related C9orf72 hexanucleotide repeat expansion forms RNA condensates through multimolecular G-quadruplexes

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

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

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

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

Verbundene Objekte