RNAi mechanisms in Huntington’s disease therapy: siRNA versus shRNA-Reference-Cited by-同舟云学术

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RNAi mechanisms in Huntington’s disease therapy: siRNA versus shRNA

Published:2017-11-27 Issue:1 Volume:6 Page:
ISSN:2047-9158
Container-title:Translational Neurodegeneration
language:en
Short-container-title:Transl Neurodegener

Author:

Aguiar Sebastian^ORCID,van der Gaag Bram,Cortese Francesco Albert Bosco

Funder

Universiteit van Amsterdam (NL)

Biogerontology Research Foundation (BGRF), Oxford

Publisher

Springer Science and Business Media LLC

Subject

Cellular and Molecular Neuroscience,Cognitive Neuroscience,Neurology (clinical)

Link

http://link.springer.com/content/pdf/10.1186/s40035-017-0101-9.pdf

Reference61 articles.

1. Sorensen SA, Fenfer K, Olsen JH. Significantly lower incidence of cancer among patients with Huntington’s disease: an apoptotic effect of an expanded polyglutamine tract? Cancer. 1999;86:1342–6.

2. Bae BI, Xu H, Igarashi S, Fujimuro M, Agrawal N, Taya Y, et al. P53 mediates cellular dysfunction and behavioral abnormalities in Huntington’s disease. Neuron. 2005; doi: 10.1016/j.neuron.2005.06.005 .

3. Harjes P, Wanker EE. The hunt for huntingtin function: interaction partners tell many different stories. Trends Biochem Sci. 2003; doi: 10.1016/S0968-0004(03)00168-3 .

4. Squitieri F, Gellera C, Cannella M, Mariotti C, Cislaghi G, Rubinsztein DC, et al. Homozygosity for CAG mutation in Huntington’s disease is associated with a more severe clinical course. Brain. 2003;126(Pt 4):946–55.

5. Vonsattel JP, DiFiglia M. Huntington disease. J Neuropathol Exp Neurol. 1998; doi: 10.1016/S0968-0004(03)00168-3 .

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