货号 | 12407S |
描述 | SignalSilence® FLIP siRNA II from Cell Signaling Technology (CST) allows the researcher to specifically inhibit FLIP expression using RNA interference, a method whereby gene expression can be selectively silenced through the delivery of double stranded RNA molecules into the cell. All SignalSilence® siRNA products from CST are rigorously tested in-house and have been shown to reduce target protein expression by western analysis. |
反应种属 | Human |
应用 | TFN |
供应商 | CST |
背景 | Cellular FLIP (FLICE inhibitory protein) is a regulator of apoptosis that has various names, such as c-FLIP (1), Casper (2), CLARP (3), FLAME (4), I-FLICE (5), MRIT (6), CASH (7), and Usurpin (8). FLIP is expressed as two alternative splice isoforms, FLIP short (FLIPS) and FLIP long (FLIPL). FLIPS contains two death effector domains (DEDs) like those found on the death receptor adaptor protein FADD and the pro-domain of caspase-8. FLIPL shares significant homology with caspase-8 (FLICE), and contains an additional death effector domain, but FLIPL lacks the catalytic active site of the caspases and does not have protease activity. Both FLIP isoforms have been reported to interact with FADD and pro-caspase-8. The role of FLIP in apoptosis is controversial as some research studies have reported it to be anti-apoptotic, while others claim that it is pro-apoptotic. Overexpression of FLIPL can lead to caspase-8 heterodimers that produce an active protease, resulting in apoptosis. However, at physiological levels, it is thought that the binding of FLIP to the DED of FADD results in inhibition of caspase-8 processing. Reduction of FLIP by siRNA or gene targeting sensitizes cells to death receptor-mediated apoptosis. FLIP has also been implicated in the resistance of cancer cells to apoptosis and is upregulated in some cancer types including Hodgkins lymphoma and ovarian and colon carcinomas (9). |
存放说明 | -20C |
参考文献 | Irmler, M. et al. (1997) Nature 388, 190-195. Shu, H. B. et al. (1997) Immunity 6, 751-763. Inohara, N. et al. (1997) Proc. Natl. Acad. Sci. USA 94, 10717-10722. Srinivasula, S. M. et al. (1997) J. Biol. Chem. 272, 18542-18545. Hu, S. et al. (1997) J. Biol. Chem. 272, 17255-17257. Han, D. K. et al. (1997) Proc. Natl. Acad. Sci. USA 94, 11333-11338. Dita, R. M. et al. (1998) Cell Death Differ. 5, 271-288. Goltsev, Y. V. et al. (1997) J. Biol. Chem. 272, 19641-19644. Kataoka, T. (2005) Crit. Rev. Immunol. 25, 31-58. |
Western blot analysis of extracts from A549 cells, transfected with 100 nM SignalSilence® Control siRNA (Unconjugated) #6568 (-), SignalSilence® FLIP siRNA I #12372 (+), or SignalSilence® FLIP siRNA II (+), using FLIP (D16A8) Rabbit mAb #8510 (upper) or β-Actin (D6A8) Rabbit mAb #8457 (lower). The FLIP (D16A8) Rabbit mAb confirms silencing of FLIP expression, while the β-Actin (D6A8) Rabbit mAb is used as a loading control. Western blot方法检测A549细胞提取物,用100 nM SignalSilence® Control siRNA (Unconjugated) #6568 (-)、SignalSilence® FLIP siRNA I #12372 (+)或SignalSilence® FLIP siRNA II(+)转染;使用FLIP (D16A8) Rabbit mAb兔单抗#8510 (上图) 或β-Actin (D6A8) Rabbit mAb兔单抗#8457 (下图)检测。FLIP (D16A8) Rabbit mAb兔单抗确定FLIP表达的沉默,β-Actin (D6A8) Rabbit mAb兔单抗作为内参对照使用。 |