Article
Functional abnormalities in P0-deficient mice resemble human hereditary neuropathies linked to P0 gene mutations.
Muscle & nerve - 1 Aug 1996
Zielasek J, Martini R, Toyka K V
Abstract excerpt
Mutations in the gene encoding the transmembranous cell adhesion molecule, myelin protein zero (P0), have been reported in patients with Charcot-Marie-Tooth disease types 1B and 3 (Déjérine-Sottas disease). We have previously shown that the targeted deletion of the P0 gene in mice results in impairment of sciatic nerve conduction, and we now extend our detailed electrophysiologic investigation to the facial...
Read the complete abstract on PubMedTopics
Share this publication in a Topic to start or enrich a Post.