Neurofibromin negatively regulates neurotrophin signaling through p21(ras) in embryonic sensory neurons

Kristine S. Vogel, Mary El-Afandi, Luis F. Parada

Research output: Contribution to journalArticle

14 Scopus citations

Abstract

Embryonic sensory and sympathetic neurons that lack neurofibromin, the protein product of the neurofibromatosis type 1 (Nfl) gene, survive and extend neurites in the absence of neurotrophins. To determine whether neurofibromin negatively regulates neurotrophin signaling through its interaction with p21(ras), we used Fab antibody fragments to block Ras function in DRG, trigeminal, nodose, and SCG neurons isolated from Nfl-/- and wild-type mouse embryos. We show that introduction of anti-Ras Fab fragments significantly reduces the ability of neurofibromin-deficient neurons to survive in the absence of neurotrophins. Moreover, addition of H-ras protein enhances the survival of Nfl-/-, but not wild-type, DRG neurons. Our results are consistent with a major role for neurofibromin in modulating Trk signaling through p21(ras) during neuronal development.

Original languageEnglish (US)
Pages (from-to)398-407
Number of pages10
JournalMolecular and Cellular Neurosciences
Volume15
Issue number4
DOIs
StatePublished - Apr 2000

ASJC Scopus subject areas

  • Molecular Biology
  • Cellular and Molecular Neuroscience
  • Cell Biology

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