期刊
NATURE NEUROSCIENCE
卷 18, 期 9, 页码 1226-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nn.4085
关键词
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资金
- US National Institutes of Health (NIH) [NS069375]
- NIH [1R01NS065317, 1R01NS073660, K99/R00, NS091538]
- Packard Center for ALS Research at Johns Hopkins
- Stanford University
- Target ALS
- Target ALS Springboard Fellowship
- JPB Foundation
- Helmsley Foundation
- Mathers Foundation
- KU Leuven
- European Research Council (ERC) [340429]
- Fund for Scientific Research Flanders (FWO-Vlaanderen) [G.0983.14N]
- Interuniversity Attraction Poles Programme [P7/16]
- Belgian Science Policy Office
- Association Belge contre les Maladies Neuro-Musculaires (ABMM)
- ALS Liga (Belgium)
- Opening the Future fund
- Agency for Innovation by Science and Technology IWT
- FWO-Vlaanderen
- E. von Behring Chair for Neuromuscular and Neurodegenerative Disorders
C9orf72 mutations are the most common cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Dipeptide repeat proteins (DPRs) produced by unconventional translation of the C9orf72 repeat expansions cause neurodegeneration in cell culture and in animal models. We performed two unbiased screens in Saccharomyces cerevisiae and identified potent modifiers of DPR toxicity, including karyopherins and effectors of Ran-mediated nucleocytoplasmic transport, providing insight into potential disease mechanisms and therapeutic targets.
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