In Vivo Modelling of ATP1A3 G316S-Induced Ataxia in C. elegans Using CRISPR/Cas9-Mediated Homologous Recombination Reveals Dominant Loss of Function Defects-Reference-Cited by-同舟云学术

In Vivo Modelling of ATP1A3 G316S-Induced Ataxia in C. elegans Using CRISPR/Cas9-Mediated Homologous Recombination Reveals Dominant Loss of Function Defects

Published:2016-12-09 Issue:12 Volume:11 Page:e0167963
ISSN:1932-6203
Container-title:PLOS ONE
language:en
Short-container-title:PLoS ONE

Author:

Sorkaç Altar,Alcantara Ivan C.,Hart Anne C.^ORCID

Funder

National Institute of Neurological Disorders and Stroke

Brown University

Publisher

Public Library of Science (PLoS)

Subject

Multidisciplinary

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4. Distinct neurological disorders with ATP1A3 mutations;EL Heinzen;The Lancet Neurology,2014

5. Mutations in the Na+/K+ -ATPase alpha3 gene ATP1A3 are associated with rapid-onset dystonia parkinsonism;P de Carvalho Aguiar;Neuron,2004

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