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  • Title: A novel juxtamembrane deletion in rat TrkA blocks differentiative but not mitogenic cell signaling in response to nerve growth factor.
    Author: Meakin SO, MacDonald JI.
    Journal: J Neurochem; 1998 Nov; 71(5):1875-88. PubMed ID: 9798911.
    Abstract:
    We have generated a novel rat TrkA receptor mutant (TrkAS3) by deletion of five conserved residues (493IMENP497) in the juxtamembrane domain. TrkAS3 receptors cannot support nerve growth factor (NGF)-induced cell cycle arrest or neuronal differentiation but retain cell survival responses as well as Ras-dependent mitogenic signaling. Cells of the nnr5 line stably expressing TrkAS3 induce NGF-dependent SHC phosphorylation and phosphatidylinositol 3-kinase, phospholipase Cgamma-1, and prolonged mitogen-activated protein kinase activation to absolute levels comparable to those in PC12 cells. Although the stoichiometry of TrkAS3-SHC binding is reduced, cells overexpressing TrkAS3 exhibit NGF-dependent SHC-Grb-2/Sos binding, essential for Ras activation, as well as NGF-dependent SNT phosphorylation to absolute levels comparable to those in PC12 cells. Collectively, these data suggest that the TrkAS3 deletion either directly affects a novel Ras-independent TrkA binding protein or that the decrease in TrkAS3-SHC association affects a Ras-independent SHC binding protein essential for cell cycle arrest and/or neurite outgrowth.
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