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Fas engagement induces neurite growth through ERK activation and p35 upregulation
Author(s): Desbarats J, Birge RB, Mimouni-Rongy M, Weinstein DE, Palerme JS, Newell MK
Source: NATURE CELL BIOLOGY    Volume: 5    Issue: 2    Pages: 118-125    Published: FEB 2003  
Times Cited: 127     References: 50     
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.
Document Type: Article
Language: English
Reprint Address: Desbarats, J (reprint author), McGill Univ, Dept Physiol, 3655 Drummond St, Montreal, PQ H3G 1Y6 Canada
Addresses:
1. McGill Univ, Dept Physiol, Montreal, PQ H3G 1Y6 Canada
2. Rockefeller Univ, Oncol Mol Lab, New York, NY 10021 USA
3. Univ Colorado, Dept Biol, Colorado Springs, CO 80918 USA
4. Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Biochem & Mol Biol, Newark, NJ 07103 USA
5. Yeshiva Univ Albert Einstein Coll Med, Dept Neurosci, Bronx, NY 10461 USA
6. Yeshiva Univ Albert Einstein Coll Med, Dept Pathol, Bronx, NY 10461 USA
Publisher: NATURE PUBLISHING GROUP, MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
Subject Category: Cell Biology
IDS Number: 642KF
ISSN: 1465-7392
DOI: 10.1038/ncb916
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