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POSH promotes cell survival in Drosophila and in human RASF cells
Author(s) -
Tsuda Manabu,
Kawaida Reimi,
Kobayashi Kyoko,
Shinagawa Akira,
Sawada Tetsuji,
Yamada Ryo,
Yamamoto Kazuhiko,
Aigaki Toshiro
Publication year - 2010
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2010.10.048
Subject(s) - programmed cell death , apoptosis , microbiology and biotechnology , tumor necrosis factor alpha , schneider 2 cells , rna interference , necrosis , cell , kinase , cell culture , biology , chemistry , immunology , gene , genetics , rna
In Drosophila , Eiger, a tumor necrosis factor α (TNFα) 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.