Fas engagement induces neurite growth through ERK activation and p35 upregulation

Julie Desbarats, Raymond B. Birge, Manuelle Mimouni-Rongy, David E. Weinstein, Jean Sébastien Palerme, M. Karen Newell

Research output: Contribution to journalReview articlepeer-review

268 Scopus citations


Fas (also known as CD95), a member of the tumour-necrosis receptor factor of 'death receptors', can induce apoptosis or, conversely, can deliver growth stimulatory signals. Here we report that crosslinking Fas on primary sensory neurons induces neurite growth through sustained activation of the extracellular-signal regulated kinase (ERK) pathway and the consequent upregulation of p35, a mediator of neurite outgrowth. In addition, functional of antibodies after sciatic nerve is delayed in Fas-deficient lpr mice and accelerated by local administration of antibodies against Fas, which indicates that Fas engagement may contribute to nerve regeneration in vivo. Our findings define a role for Fas as an inducer of both neurite growth in vitro and accelerated recovery after nerve injury in vivo.

Original languageEnglish (US)
Pages (from-to)118-125
Number of pages8
JournalNature Cell Biology
Issue number2
StatePublished - Feb 1 2003

All Science Journal Classification (ASJC) codes

  • Cell Biology


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