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Radicicol Potentiates Neurotrophin‐Mediated Neurite Outgrowth and Survival of Cultured Sensory Neurons from Chick Embryo
Author(s) -
Sano Mamoru,
Yoshida Minoru,
Fukui Shigeyuki,
Kitajima Satoko
Publication year - 1999
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1999.0722256.x
Subject(s) - trk receptor , neurotrophin , biology , neurite , microbiology and biotechnology , tyrosine kinase , receptor tyrosine kinase , kinase , signal transduction , receptor , biochemistry , in vitro
Radicicol, an antifungal antibiotic with markedly lowtoxicity, is a potent inhibitor of the Src family of protein tyrosine kinasesand causes morphological reversion of v‐ src ‐transformed fibroblasts. Recently, this antibiotic was also found to inhibit Raf kinase. In the present study, we found that nanomolar concentrations of radicicol (10 ng/ml) enhanced the survival and neurite outgrowth of neurons from embryonic chick dorsal root ganglia (DRGs) and sympathetic ganglia. It potentiated the trophic effects of nerve growth factor, brain‐derived neurotrophic factor, and neurotrophin‐3 on the cultured DRG neurons. This concentration of radicicol did not alter the tyrosine phosphorylation of Trk receptors or the activity of mitogen‐activated protein (MAP) kinases. Wortmannin, an inhibitor of phosphatidylinositol 3‐kinase (P13‐kinase), did not inhibit radicicol, excluding the involvement of P13‐kinase in the radicicol‐dependent trophic actions. These results suggest that radicicol mediates neuronal growth presumably via a mechanism not involving the activation of Trk receptors, MAP kinase, or P13‐kinase.