4.7 Article

Modifiers of C9orf72 dipeptide repeat toxicity connect nucleocytoplasmic transport defects to FTD/ALS

期刊

NATURE NEUROSCIENCE
卷 18, 期 9, 页码 1226-+

出版社

NATURE PUBLISHING GROUP
DOI: 10.1038/nn.4085

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资金

  1. US National Institutes of Health (NIH) [NS069375]
  2. NIH [1R01NS065317, 1R01NS073660, K99/R00, NS091538]
  3. Packard Center for ALS Research at Johns Hopkins
  4. Stanford University
  5. Target ALS
  6. Target ALS Springboard Fellowship
  7. JPB Foundation
  8. Helmsley Foundation
  9. Mathers Foundation
  10. KU Leuven
  11. European Research Council (ERC) [340429]
  12. Fund for Scientific Research Flanders (FWO-Vlaanderen) [G.0983.14N]
  13. Interuniversity Attraction Poles Programme [P7/16]
  14. Belgian Science Policy Office
  15. Association Belge contre les Maladies Neuro-Musculaires (ABMM)
  16. ALS Liga (Belgium)
  17. Opening the Future fund
  18. Agency for Innovation by Science and Technology IWT
  19. FWO-Vlaanderen
  20. E. von Behring Chair for Neuromuscular and Neurodegenerative Disorders

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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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