Fas engagement induces neurite growth through ERK activation and p35 upregulation.
作者： Julie Desbarats , Raymond B. Birge , Manuelle Mimouni-Rongy , David E. Weinstein , Jean-Sébastien Palerme
DOI: 10.1038/NCB916
关键词: Cell biology 、 Sciatic nerve injury 、 Receptor 、 Neurite 、 Downregulation and upregulation 、 Fas receptor 、 Nerve injury 、 MAPK/ERK pathway 、 Chemistry 、 Apoptosis
摘要: Fas (also known as CD95), a member of the tumour-necrosis receptor factor family 'death receptors', can induce apoptosis or, conversely, deliver growth stimulatory signals. Here we report that crosslinking on primary sensory neurons induces neurite through sustained activation extracellular-signal regulated kinase (ERK) pathway and consequent upregulation p35, mediator outgrowth. In addition, functional recovery after sciatic nerve injury is delayed in Fas-deficient lpr mice accelerated by local administration antibodies against Fas, which indicates engagement may contribute to regeneration vivo. Our findings define role for an inducer both vitro
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