| 货号 | 12519S |
| 描述 | SignalSilence® BRCA1 siRNA I from Cell Signaling Technology (CST) allows the researcher to specifically inhibit BRCA1 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.Cell Signaling Technology (CST) 公司的SignalSilence® BRCA1 siRNA I帮助研究人员使用RNA干扰技术特异性抑制BRCA1表达，该技术通过向细胞内导入双链RNA分子以选择性的抑制某些基因的表达。所有CST公司的SignalSilence® siRNA都经过了严格的内部测试，western分析显示能够能够降低目标蛋白的表达。Quality Control |
| 反应种属 | Human |
| 应用 | TFN |
| 供应商 | CST |
| 背景 | The breast cancer susceptibility proteins BRCA1 and BRCA2 are frequently mutated in cases of hereditary breast and ovarian cancers and have roles in multiple processes related to DNA damage, repair, cell cycle progression, transcription, ubiquitination, and apoptosis (1-4). BRCA2 has been shown to be required for localization of Rad51 to sites of double stranded breaks (DSBs) in DNA, and cells lacking BRCA1 and BRCA2 cannot repair DSBs through the Rad51-dependent process of homologous recombination (HR) (5). Numerous DNA damage-induced phosphorylation sites on BRCA1 have been identified, including Ser988, 1189, 1387, 1423, 1457, 1524 and 1542, and kinases activated in a cell cycle-dependent manner, including Aurora A and CDK2, can also phosphorylate BRCA1 at Ser308 and Ser1497, respectively (6-10). Cell cycle-dependent phosphorylation of BRCA2 at Ser3291 by CDKs has been proposed as a mechanism to switch off HR as cells progress beyond S-phase by blocking the carboxy terminal Rad51 binding site (11).乳腺癌易感蛋白BRCA1和BRCA2在遗传性乳腺癌和卵巢癌病人体内经常会发生突变，在DNA损伤，修复，细胞周期进程，转录，泛素化和细胞凋亡等多个过程中都发挥了作用（1-4）。已经发现BRCA2对于Rad51定位到双链损伤（DSBs）区域是必须的，细胞缺乏BRCA1和BRCA2不能通过Rad51依赖的同源重组（HR）修复DSBs（5）。已经在BRCA1蛋白上发现了多个DNA损伤诱导的磷酸化位点，包括Ser988, 1189, 1387, 1423, 1457, 1524 和1542，并且激酶以一种细胞周期依赖的方式被激活，包括Aurora A 和 CDK2,都可以分别磷酸化BRCA1的308和1497位丝氨酸（6-10）。BRCA1 的3291位丝氨酸发生的细胞周期依赖的磷酸化是通过CDKs进行的，已经被认为是一种阻止羧基末端Rad51结合区域以促进细胞通过S期中止HR的机制（11）。 |
| 存放说明 | -20C |
| 参考文献 | Rahman, N. and Stratton, M.R. (1998) Annu Rev Genet 32, 95-121. Gayther, S.A. et al. (1999) Am J Hum Genet 65, 1021-9. Kerr, P. and Ashworth, A. (2001) Curr Biol 11, R668-76. Scully, R. and Livingston, D.M. (2000) Nature 408, 429-32. Tutt, A. and Ashworth, A. (2002) Trends Mol Med 8, 571-6. Okada, S. and Ouchi, T. (2003) J Biol Chem 278, 2015-20. Cortez, D. et al. (1999) Science 286, 1162-6. Xu, B. et al. (2002) Cancer Res 62, 4588-91. Ouchi, M. et al. (2004) J Biol Chem 279, 19643-8. Ruffner, H. et al. (1999) Mol Cell Biol 19, 4843-54. Esashi, F. et al. (2005) Nature 434, 598-604. |
Western blot analysis of extracts from 293T cells, transfected with 100 nM SignalSilence® Control siRNA (Unconjugated) #6568 (-), SignalSilence® BRCA1 siRNA I (+), or SignalSilence® BRCA1 siRNA II #12642 (+), using BRCA1 Antibody #9010 (upper) or β-Actin (D6A8) Rabbit mAb #8457 (lower). The BRCA1 Antibody confirms silencing of BRCA1 expression, while the β-Actin (D6A8) Rabbit mAb is used as a loading control.转染100 nM SignalSilence®对照siRNA(未标记) #6568 (-),SignalSilence® BRCA1 siRNA I (+),或SignalSilence® BRCA1 siRNA II #12642 (+)的293T细胞提取物，使用BRCA1 抗体#9010 (上)或β-Actin (D6A8) Rabbit mAb #8457 (下)进行western blot分析。BRCA1 抗体可以确认BRCA1表达受抑制，β-Actin (D6A8) Rabbit mAb用于确认上样量一致。 |
