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Updated: Aug 5, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
Fas engagement induces neurite growth through ERK activation and p35 upregulation
Julie Desbarats1, Raymond B Birge, Manuelle Mimouni-Rongy
1Department of Physiology, McGill University, Montréal, Quebec, Canada, H3G 1Y6. Julie@desbarats.mcgill.ca
Abstract:
Fas (also known as CD95), a member of the tumour-necrosis receptor factor family 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 recovery after sciatic nerve injury 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.
Insights
Fas receptor engagement promotes neurite growth in sensory neurons by activating the ERK pathway. This signaling also accelerates nerve regeneration and functional recovery after injury in vivo.
Area of Science:
- Neuroscience
- Cell Biology
- Immunology
Background:
- Fas (CD95) is a death receptor involved in apoptosis and growth signaling.
- The role of Fas in neuronal growth and regeneration is not fully understood.
Purpose of the Study:
- To investigate the role of Fas in primary sensory neuron growth and nerve regeneration.
- To elucidate the molecular mechanisms underlying Fas-mediated neurite outgrowth.
Main Methods:
- Crosslinking Fas on primary sensory neurons in vitro.
- Analyzing the extracellular-signal regulated kinase (ERK) pathway activation and p35 upregulation.
- Assessing sciatic nerve injury recovery in Fas-deficient (lpr) mice and with anti-Fas antibody treatment in vivo.
Main Results:
- Fas crosslinking induced neurite growth via sustained ERK pathway activation and p35 upregulation.
- Fas-deficient mice showed delayed functional recovery after sciatic nerve injury.
- Administration of anti-Fas antibodies accelerated nerve regeneration and functional recovery.
Conclusions:
- Fas acts as an inducer of neurite growth in primary sensory neurons.
- Fas signaling contributes to nerve regeneration and functional recovery after injury in vivo.
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