New point mutations and deletions of the connexin 32 gene in x-linked charcot-marie-tooth neuropathy
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Cited by (33)
Gap junctions and neurological disorders of the central nervous system
2004, Biochimica et Biophysica Acta - BiomembranesCitation Excerpt :The function of gap junctions in oligodendrocytes is thought to be primarily metabolic to allow ions and nutrients to pass from the somata to all the layers of the myelin [104,105]. The importance of this channel has recently been realized by the reported mutations of Cx32 associated with X-linked Charcot–Marie–Tooth disease, a peripheral demyelinating disorder [106–110]. It was initially thought that human and rodent Schwann cells are susceptible to pathology, leading to peripheral nerve demyelination, while oligodendrocytes appeared not to be affected.
Functional analysis of connexin-32 mutants associated with X-linked dominant Charcot-Marie-Tooth disease
2004, Neurobiology of DiseaseChapter 4: Heteromultimeric Gap Junction Channels and Cardiac Disease
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1997, Neurobiology of DiseaseX-linked Charcot Marie Tooth mutations alter CO<inf>2</inf> sensitivity of connexin32 hemichannels
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