| 货号 | 11968S |
| 描述 | SignalSilence® ADAM9 siRNA I from Cell Signaling Technology (CST) allows the researcher to specifically inhibit ADAM9 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® ADAM9 siRNA I inhibits human and monkey ADAM9 expression. |
| 供应商 | CST |
| 背景 | The ADAM (A Disintegrin and A Metalloprotease) family of multidomain membrane proteins influences cell signaling and adhesion by shedding cell surface proteins such as cytokines and growth factors, by influencing cell adhesion to the extracellular matrix (ECM), and by directly remodeling the ECM. Conserved domains in ADAM family members include a prodomain, a zinc-dependent metalloprotease domain, a disintegrin domain, a cysteine-rich domain, an EGF-like sequence, and a short cytoplasmic tail (1,2). The prodomain is thought to aid in protein folding. Disintegrin and cysteine-rich domains mediate adhesion, at least in part, through binding to integrins. Phosphorylation of the cytoplasmic tail as well as its interaction with other signaling proteins may influence intra- and extracellular signaling (1). ADAM9 is widely distributed and has been shown to affect migration in skin keratinocytes (3,4). Research studies have shown that ADAM9 is overexpressed in prostate cancer (5), pancreatic cancer (6), gastric cancer (7), and has been linked to invasion and metastasis in small cell lung cancer (8). Research has also shown that an alternatively spliced short (50 kDa) form of ADAM9 containing protease activity is involved in tumor cell invasion (9). |
| 存放说明 | -20C |
| 参考文献 | N. M. Hooper and U. Lendeckel. . The Netherlands: Springer, 2005 Schlöndorff, J. and Blobel, C.P. (1999) J Cell Sci 112 ( Pt 21), 3603-17. Franzke, C.W. et al. (2002) EMBO J 21, 5026-35. Zigrino, P. et al. (2007) J Biol Chem 282, 30785-93. Fritzsche, F.R. et al. (2008) Eur Urol 54, 1097-106. Grützmann, R. et al. (2004) Br J Cancer 90, 1053-8. Carl-McGrath, S. et al. (2005) Int J Oncol 26, 17-24. Shintani, Y. et al. (2004) Cancer Res 64, 4190-6. Mazzocca, A. et al. (2005) Cancer Res 65, 4728-38. |
Western blot analysis of extracts from HeLa cells, transfected with 100 nM SignalSilence® Control siRNA (Unconjugated) #6568 (-), SignalSilence® ADAM9 siRNA I (+), or SignalSilence® ADAM9 siRNA II #12085 (+), using ADAM9 (D64B5) Rabbit mAb #4151 (upper) or β-Actin (D6A8) Rabbit mAb #8457 (lower). The ADAM9 (D64B5) Rabbit mAb confirms silencing of ADAM9 expression, while the β-Actin (D6A8) Rabbit mAb is used as a loading control.Western blot检测转染100 nM SignalSilence® Control siRNA (Unconjugated) #6568 (-)，SignalSilence® ADAM9 siRNA I (+)或者SignalSilence® ADAM9 siRNA II #12085 (+)后的HeLa细胞提取物，采用的抗体是ADAM9 (D64B5) Rabbit mAb #4151 (上图)或者β-Actin (D6A8) Rabbit mAb #8457 (下图)。ADAM9 (D64B5) Rabbit mAb证实了ADAM9的沉默表达，β-Actin (D6A8) Rabbit mAb为内参。 |
