Transneuronal propagation of mutant huntingtin contributes to non–cell autonomous pathology in neurons-Reference-Cited by-同舟云学术

Transneuronal propagation of mutant huntingtin contributes to non–cell autonomous pathology in neurons

Published:2014-07-13 Issue:8 Volume:17 Page:1064-1072
ISSN:1097-6256
Container-title:Nature Neuroscience
language:en
Short-container-title:Nat Neurosci

Author:

Pecho-Vrieseling Eline,Rieker Claus,Fuchs Sascha,Bleckmann Dorothee,Esposito Maria Soledad,Botta Paolo,Goldstein Chris,Bernhard Mario,Galimberti Ivan,Müller Matthias,Lüthi Andreas,Arber Silvia,Bouwmeester Tewis,van der Putten Herman,Di Giorgio Francesco Paolo

Publisher

Springer Science and Business Media LLC

Subject

General Neuroscience

Link

http://www.nature.com/articles/nn.3761.pdf

Reference59 articles.

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3. Landles, C. et al. Proteolysis of mutant huntingtin produces an exon 1 fragment that accumulates as an aggregated protein in neuronal nuclei in Huntington disease. J. Biol. Chem. 285, 8808–8823 (2010).

4. Sathasivam, K. et al. Aberrant splicing of HTT generates the pathogenic exon 1 protein in Huntington disease. Proc. Natl. Acad. Sci. USA 110, 2366–2370 (2013).

5. Mangiarini, L. et al. Exon 1 of the HD gene with an expanded CAG repeat is sufficient to cause a progressive neurological phenotype in transgenic mice. Cell 87, 493–506 (1996).

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