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. 1998 Jun 29;141(7):1625–1636. doi: 10.1083/jcb.141.7.1625

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Model of signal transduction and cross-talks of the Rho–ROCK pathway in the neurite remodeling. p160ROCK is activated downstream of Rho in response to agonist stimulation, and in turn induces the actomyosin-based contractility and the disassembly of the microtubules and the intermediate filaments, leading to the neurite retraction. p160ROCK also transmits a negative signal to the Cdc42/Rac pathways and suppresses the neurite outgrowth by tonically inhibiting their actions. The activation of the cAMP–A kinase pathway is likely to inhibit the Rho–ROCK pathway and to release the suppression of neurite outgrowth. Disassembly of intermediate filaments may be caused by direct phosphorylation by p160ROCK at specific amino acid residue(s) of this cytoskeletal proteins as shown for GFAP (Kosako et al., 1997) or may well be a secondary consequence of ROCK's effect on the actomyosin system.