POSH promotes cell survival in Drosophila and in human RASF cells
POSH promotes cell survival in Drosophila and in human RASF cells
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DOI：
10.1016/j.febslet.2010.10.048
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发表时间：
2010-11
期刊：
影响因子：
3.5
通讯作者：
M. Tsuda;R. Kawaida;Kyoko Kobayashi;A. Shinagawa;T. Sawada;R. Yamada;Kazuhiko Yamamoto;T. Aigaki
中科院分区：
文献类型：
--
作者：
M. Tsuda;R. Kawaida;Kyoko Kobayashi;A. Shinagawa;T. Sawada;R. Yamada;Kazuhiko Yamamoto;T. Aigaki
在果蝇中，Eiger 是一种肿瘤坏死因子 α (TNFα) 超家族配体，通过激活 c-Jun N 末端激酶 (JNK) 途径诱导细胞死亡。在这里，我们报告 Plenty of SH3s (POSH) 的过度表达抑制艾格峰诱导的细胞死亡并产生高度变形的组织。这些结果意味着高水平的 POSH 可以保护组织免于细胞死亡。在人类中，类风湿性关节炎滑膜成纤维细胞（RASF）通常对细胞凋亡具有抵抗力。我们发现 POSH 在 RASF 中以相对较高的水平表达，并且 RNAi 降低 POSH 使这些细胞对 Fas 介导的细胞凋亡敏感。因此，我们证明 POSH 促进果蝇和人类 RASF 的细胞存活。
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.