Cell
Volume 71, Issue 4, 13 November 1992, Pages 565-576
ArticleMouse P0 gene disruption leads to hypomyelination, abnormal expression of recognition molecules, and degeneration of myelin and axons
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Beta-subunit-eliminated eHAP expression (BeHAPe) cells reveal subunit regulation of the cardiac voltage-gated sodium channel
2023, Journal of Biological ChemistryMechanisms and Treatments in Demyelinating CMT
2021, NeurotherapeuticsNew evidence for secondary axonal degeneration in demyelinating neuropathies
2021, Neuroscience LettersMyelin protein zero gene dose dependent axonal ion-channel dysfunction in a family with Charcot-Marie-Tooth disease
2020, Clinical NeurophysiologyTargeting the programmed axon degeneration pathway as a potential therapeutic for Charcot-Marie-Tooth disease
2020, Brain ResearchCitation Excerpt :CMT1B is caused by numerous different point mutations that are predominantly localized within the extracellular domain of the MPZ protein (Sanmaneechai et al., 2015). Several mutations have been suggested to be pathogenic due to loss of function, which is supported by the presence of CMT1B-like symptoms in MPZ knockout mice (Giese et al., 1992; Martini et al., 1995). These mice exhibit demyelination, impaired nerve conduction, axon degeneration and abnormal motor function similar to CMT1B patients (Giese et al., 1992; Martini et al., 1995; Martini, 1999).
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