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Four missense mutations of Rab7, a small GTPase of the Rab family involved in intracellular vesicular trafficking, are associated with the CMT2B phenotype. Despite a growing body of evidence concerning the gene structures responsible for genetically heterogenous CMT2B and other CMT2 neuropathies, little is known about the in vitro neuropathy model and how CMT2B\u2010associated mutation\u2010caused aberrant neuritogenesis is properly reversed. Here, we show that valproic acid (VPA), a classical mood\u2010stabilizing drug, improves defective neurite formation in N1E\u2010115 neuroblastoma cells regardless of which CMT2B\u2010associated Rab7 mutant protein is expressed. The effect is mediated by c\u2010Jun N\u2010terminal kinase (JNK) signaling, but not by deacetylase inhibition activity of VPA itself. Furthermore, VPA has similar effects in dorsal root ganglion (DRG) neurons expressing any of the four mutant Rab7 proteins. Thus, VPA has a previously unknown potential to improve defective neuritogenesis associated with CMT2B in vitro, indicating that JNK should be a potential therapeutic target for treatments aimed at improving neuritogenesis. \u00a9 2010 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jnr.22460","type":"journal-article","created":{"date-parts":[[2010,7,19]],"date-time":"2010-07-19T16:49:38Z","timestamp":1279558178000},"page":"3189-3197","source":"Crossref","is-referenced-by-count":46,"title":["The mood stabilizer valproic acid improves defective neurite formation caused by charcot\u2010marie\u2010tooth disease\u2010associated mutant Rab7 through the JNK signaling 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