Journal
NATURE NEUROSCIENCE
Volume 22, Issue 9, Pages 1383-+Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41593-019-0455-7
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Funding
- National Institutes of Health (NIH) [R35NS097263, AI099506, AG064690, R35NS097273, P01NS099114, R01NS097850]
- Target ALS
- US Department of Defense
- Muscular Dystrophy Association [2T32HG000044-21 NIHGRI]
- Brain Rejuvenation Project of the Wu Tsai Neurosciences Institute
- European Research Council [ERC-2014-CoG-648716]
- Alzheimer's Research UK
- Medical Research Council
- Robert Packard Center for ALS Research at Johns Hopkins
- MRC [UKDRI-1006] Funding Source: UKRI
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Nucleotide repeat expansions in the C9orf72 gene are the most common cause of amyotrophic lateral sclerosis and frontotemporal dementia. Unconventional translation (RAN translation) of C9orf72 repeats generates dipeptide repeat proteins that can cause neurodegeneration. We performed a genetic screen for regulators of RAN translation and identified small ribosomal protein subunit 25 (RPS25), presenting a potential therapeutic target for C9orf72-related amyotrophic lateral sclerosis and frontotemporal dementia and other neurodegenerative diseases caused by nucleotide repeat expansions.
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