The death receptor antagonist FAIM promotes neurite outgrowth by a mechanism that depends on ERK and NF-kapp B signaling

Sole, Carme and Dolcet, Xavier and Segura, Miguel F. and Gutierrez, Humberto and Diaz-Meco, Maria-Teresa and Gozzelino, Raffaella and Sanchis, Daniel and Bayascas, Jose R. and Gallego, Carme and Moscat, Jorge and Davies, Alun M. and Comella, Joan X. (2004) The death receptor antagonist FAIM promotes neurite outgrowth by a mechanism that depends on ERK and NF-kapp B signaling. The Journal of Cell Biology, 167 (3). pp. 479-92. ISSN 0021-9525

Full content URL: http://dx.doi.org/10.1083/jcb.200403093

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Item Type:Article
Item Status:Live Archive

Abstract

Fas apoptosis inhibitory molecule (FAIM) is a protein identified as an antagonist of Fas-induced cell death. We show that FAIM overexpression fails to rescue neurons from trophic factor deprivation, but exerts a marked neurite growth-promoting action in different neuronal systems. Whereas FAIM overexpression greatly enhanced neurite outgrowth from PC12 cells and sympathetic neurons grown with nerve growth factor (NGF), reduction of endogenous FAIM levels by RNAi decreased neurite outgrowth in these cells. FAIM overexpression promoted NF-kappa B activation, and blocking this activation by using a super-repressor I kappa B alpha or by carrying out experiments using cortical neurons from mice that lack the p65 NF-kappa B subunit prevented FAIM-induced neurite outgrowth. The effect of FAIM on neurite outgrowth was also blocked by inhibition of the Ras-ERK pathway. Finally, we show that FAIM interacts with both Trk and p75 neurotrophin receptor NGF receptors in a ligand-dependent manner. These results reveal a new function of FAIM in promoting neurite outgrowth by a mechanism involving activation of the Ras-ERK pathway and NF-kappa B.

Keywords:Neuronal Development
Subjects:C Biological Sciences > C141 Developmental Biology
Divisions:College of Science > School of Life Sciences
ID Code:7862
Deposited On:23 Mar 2013 18:54

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