Journal
FEBS LETTERS
Volume 584, Issue 22, Pages 4689-4694Publisher
WILEY
DOI: 10.1016/j.febslet.2010.10.048
Keywords
Plenty of SH3s; Eiger; Tumor necrosis factor; Rheumatoid arthritis synovial fibroblasts; Fas-mediated apoptosis; Pro-survival function
Funding
- Ministry of Education, Culture, Sports, Science and Technology of Japan
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In Drosophila, Eiger, a tumor necrosis factor a (TNF alpha) superfamily ligand, induces cell death by activating the c-Jun N-terminal kinase (JNK) pathway. Here, we report that overexpression of Plenty of SH3s (POSH) suppresses Eiger-induced cell death and produces highly deformed tissues. These results imply that high levels of POSH protect tissues from cell death. In humans, rheumatoid arthritis synovial fibroblasts (RASF) are generally resistant to apoptosis. We show that POSH is expressed at relatively high levels in RASF, and its reduction by RNAi sensitizes these cells to Fas-mediated apoptosis. Thus, we demonstrate that POSH promotes cell survival in Drosophila and in human RASF. (C) 2010 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.
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