ALS/FTD-Linked Mutation in FUS Suppresses Intra-axonal Protein Synthesis and Drives Disease Without Nuclear Loss-of-Function of FUS

(Neuron 100, 816–830.e1–e7; November 21, 2018) In the original publication of this paper, the concentration of the puromycin was incorrectly reported. In both panel A of Figure 7 and the “In vivo protein synthesis labeling” section of the STAR Methods, the amount was listed as 10 μg/kg. The correct concentration should be 10 mg/kg. The authors apologize for this error. ALS/FTD-Linked Mutation in FUS Suppresses Intra-axonal Protein Synthesis and Drives Disease Without Nuclear Loss-of-Function of FUSLópez-Erauskin et al.NeuronOctober 18, 2018In BriefMutations in FUS are causative of ALS and frontotemporal dementia (FTD). López-Erauskin et al. show that disease-causing mutant FUS inhibits intra-axonal protein synthesis and provokes hippocampal synaptic loss and dysfunction without loss of nuclear FUS function or FUS aggregation. Full-Text PDF Open Access