Temporal manipulation of KCC3 expression in juvenile or adult mice suggests irreversible developmental deficit in hereditary motor sensory neuropathy with agenesis of the corpus callosum

Eitemau Tebyg

• Deletion of KCC3 in parvalbumin neurons leads to locomotor deficit in a conditional mouse model of peripheral neuropathy associated with agenesis of the corpus callosum
  gan: Ding, Jinlong, et al.
  Cyhoeddwyd: (2014)
• Loss of Neuronal Potassium/Chloride Cotransporter 3 (KCC3) Is Responsible for the Degenerative Phenotype in a Conditional Mouse Model of Hereditary Motor and Sensory Neuropathy Associated with Agenesis of the Corpus Callosum
  gan: Shekarabi, Masoud, et al.
  Cyhoeddwyd: (2012)
• Transit Defect of Potassium-Chloride Co-transporter 3 Is a Major Pathogenic Mechanism in Hereditary Motor and Sensory Neuropathy with Agenesis of the Corpus Callosum
  gan: Salin-Cantegrel, Adèle, et al.
  Cyhoeddwyd: (2011)
• Agenesis of the Corpus Callosum
  gan: Harcourt-Webster, J. N., et al.
  Cyhoeddwyd: (1965)
• Agenesis of the corpus callosum
  gan: Singh, Sangram, et al.
  Cyhoeddwyd: (2010)