货号 | 7574S |
描述 | SignalSilence® HtrA2/Omi siRNA I from Cell Signaling Technology (CST) allows the researcher to specifically inhibit HtrA2/Omi 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 |
目标/特异性 | SignalSilence® HtrA2/Omi siRNA I inhibits human and monkey HtrA2/Omi expression. |
供应商 | CST |
背景 | High temperature requirement protein A2 (HtrA2)/Omi is a serine protease with homology to the E. coli HtrA protein (DegP) and is thought to be involved in apoptosis and stress-induced degradation of misfolded proteins (1). While HtrA2 was orignally identified to be present in either the nucleus (1) or endoplasmic reticulum (2), subsequent studies have shown that it localizes in mitochondria and is released during apoptosis (3-8). HtrA2 is produced as a 50 kDa zymogen that is cleaved to generate a 36 kDa mature protein that exposes an amino terminal motif (AVPS) resembling that of the IAP inhibitor Smac/Diablo (3-8). Like Smac, interaction between HtrA2 and IAP family members, such as XIAP, antagonizes their inhibition of caspase activity and protection from apoptosis (3-8). Interestingly, HtrA2 knock-out mice did not show signs of reduced apoptosis, but rather had a loss of neurons in the striatum and a Parkinsons-like phenotype, suggesting that HtrA2 might have a neuroprotective function (9-11). This activity is associated with the protease activity of HtrA2 (9). Furthermore, research studies have shown that loss of function mutations in the HtrA2 gene are associated with Parkinsons disease (12). |
存放说明 | -20C |
参考文献 | Gray, C.W. et al. (2000) Eur. J. Biochem. 267, 5699-5710. Faccio, L. et al. (2000) J. Biol. Chem. 275, 2581-2588. Suzuki, Y. et al. (2001) Mol. Cell 8, 613-621. Hegde, R. et al. (2002) J. Biol. Chem. 277, 432-438. Martins, L.M. et al. (2002) J. Biol. Chem. 277, 439-444. van Loo, G. et al. (2002) Cell Death Differ. 9, 20-26. Verhagen, A.M. et al. (2002) J. Biol. Chem. 277, 445-454. Jones, J.M. et al. (2003) Nature 425, 721-727. Vaux, D.L. and Silke, J. (2003) Cell 115, 251-253. Martins, L.M. et al. (2004) Mol. Cell Biol. 24, 9848-9862. Strauss, K.M. et al. (2005) Hum. Mol. Genet. 14, 2099-2111. |
Western blot analysis of extracts from 293T cells, transfected with 100 nM SignalSilence® Control siRNA (Unconjugated) #6568 (-) or SignalSilence® HtrA2/Omi siRNA I (+), using HtrA2/Omi (D20A5) Rabbit mAb #9745 (upper) or GAPDH (D16H11) XP® Rabbit mAb #5174 (lower). The HtrA2/Omi (D20A5) Rabbit mAb confirms silencing of HtrA2/Omi expression, while the GAPDH (D16H11) XP® Rabbit mAb is used as a loading control. Western blot方法检测293T细胞提取物,用100 nM SignalSilence® Control siRNA (Unconjugated) #6568 (-)或SignalSilence® HtrA2/Omi siRNA I (+)转染;使用HtrA2/Omi (D20A5) Rabbit mAb兔单抗#9745 (上图) 或GAPDH (D16H11) XP® Rabbit mAb兔单抗#5174 (下图)检测。HtrA2/Omi (D20A5) Rabbit mAb兔单抗确定HtrA2/Omi表达的沉默,GAPDH (D16H11) XP® Rabbit mAb兔单抗作为内参对照使用。 |