Deletion of a conserved juxtamembrane sequence in Trk abolishes NGF-promoted neuritogenesis
1995; Cell Press; Volume: 15; Issue: 2 Linguagem: Inglês
10.1016/0896-6273(95)90043-8
ISSN1097-4199
AutoresPeng Xing, Lloyd A. Greene, David R. Kaplan, Robert M. Stephens,
Tópico(s)Protein Kinase Regulation and GTPase Signaling
ResumoDeletion of a conserved juxtamembrane sequence (KFG) in the Trk NGF receptor resulted in impaired neurite outgrowth, somatic hypertrophy, and induction of c-fos, c-jun, and TIS1 immediate-early genes. In contrast, these receptors retained the ability to mediate NGF-promoted survival and TIS8 and TIS11 immediate-early gene induction. The mutated receptor also mediated unimpaired autophosphorylation; SHC, PLC-gamma 1, and ERK tyrosine phosphorylation; and PI-3 kinase and ERK activation. However, SNT protein tyrosine phosphorylation, which wild-type receptors mediate via a ras-independent pathway, was undetectable. These findings indicate that the KFG sequence is indispensable for activating a ras-independent NGF signaling pathway involved in promoting neuronal differentiation and highlight potential roles of non-tyrosine-containing receptor domains in growth factor signal transduction.
Referência(s)