Loss of function of C9orf72 causes motor deficits in a zebrafish model of amyotrophic lateral sclerosis.

  title={Loss of function of C9orf72 causes motor deficits in a zebrafish model of amyotrophic lateral sclerosis.},
  author={Sorana Ciura and Serena Lattante and I Le Ber and Morwena Latouche and Herv{\'e} Tostivint and Alexis Brice and Edor Kabashi},
  journal={Annals of neurology},
  volume={74 2},
OBJECTIVE To define the role that repeat expansions of a GGGGCC hexanucleotide sequence of the C9orf72 gene play in the pathogenesis of amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). A genetic model for ALS was developed to determine whether loss of function of the zebrafish orthologue of C9orf72 (zC9orf72) leads to abnormalities in neuronal development. METHODS C9orf72 mRNA levels were quantified in brain and lymphoblasts derived from FTLD and ALS/FTLD… CONTINUE READING
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Calcium channel agonists protect against neuromuscular dysfunction in a genetic model of TDP-43 mutation in ALS.

The Journal of neuroscience : the official journal of the Society for Neuroscience • 2013
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Unconventional translation of C 9 ORF 72 GGGGCC expansion generates insoluble polypeptides specific to c 9 FTD = ALS

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