| 货号 | 6598S |
| 描述 | SignalSilence® p16 INK4A siRNA I from Cell Signaling Technology (CST) allows the researcher to specifically inhibit p16 INK4A 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.CST的SignalSilence® p16 INK4A siRNA I使得研究人员可以使用RNA干扰的方法特异性抑制p16 INK4A的表达，RNA干扰是一种通过将双链RNA分子转入细胞从而选择性沉默基因表达的方法。CST的所有SignalSilence® siRNA产品都通过了严格的内部测试，并使用western blot方法检测其减少目标蛋白表达的效用。Quality Control |
| 反应种属 | Human |
| 应用 | TFN |
| 供应商 | CST |
| 背景 | Cyclin-dependent kinases (CDKs) are activated in part by forming complexes with cyclins. For example, CDK4 and CDK6 associate with the D-type cyclins and phosphorylate the retinoblastoma protein. This phosphorylation is a necessary event for cells to enter S-phase (1). The inhibitors of CDK4 (INK4) family include p15 INK4B, p16 INK4A, p18 INK4C and p19 INK4D. p18 has been shown to function as a haploinsufficient tumor suppressor in vivo (2). All INK4 proteins are composed of 32 amino acid ankyrin motifs and selectively inhibit CDK4/6 activity. Mutational analyses of p18 implicate the third and the amino-terminal portion of the fourth ankyrin repeat in mediating binding to CDK4/6 (3). The interaction of INK4 family members can be a binary complex with CDK4/6 or ternary complex with cyclin D-bound CDK4/6 and ultimately results in the inhibition of cell cycle progression (4,5).细胞周期依赖性蛋白激酶(CDKs)的激活部分经由周期蛋白复合体的形成。例如，CDK4和CDK6联合D-型周期蛋白并磷酸化Rb蛋白。这种磷酸化使细胞进入S期的必需事件(1)。CDK4 (INK4)家族抑制剂包括p15 INK4B，p16 INK4A，p18 INK4C 和p19 INK4D。p18被认为在体能够发挥单纯不充分肿瘤抑制基因的功能(2)。所有的INK4蛋白是由32个氨基酸锚蛋白模体组成并可以选择性抑制CDK4/6的活性。P18的突变分析表明第三个锚蛋白和第四个锚蛋白重复序列的氨基末端部分介导了CDK4/6的结合(3)。INK4家族成员的相互作用可能是通过与CDK4/6形成的二元复合物或者是与周期蛋白-D结合的CDK4/6形成的三元复合物，最终导致细胞周期进程的抑制(4,5)。 |
| 存放说明 | -20C |
| 参考文献 | Lukas, J. et al. (1996) Mol. Cell. Biol. 16, 6917-6925. Bai, F. et al. (2003) Mol. Cell. Biol. 23, 1269-1277. Noh, S.J. et al. (1999) Cancer Res. 59, 558-564. Guan, K.L. et al. (1994) Genes Dev. 8, 2939-2952. Hirai, H. et al. (1995) Mol. Cell. Biol. 15, 2672-2681. Sherr, C.J. (2001) Nat Rev Mol Cell Biol 2, 731-7. Lowe, S.W. and Sherr, C.J. (2003) Curr Opin Genet Dev 13, 77-83. |
Western blot analysis of extracts from HeLa cells, transfected with 100 nM SignalSilence® Control siRNA (Unconjugated) #6568 (-) or SignalSilence® p16 INK4A siRNA I (+), using p16 INK4A Antibody #4824 (upper) or α-Tubulin (11H10) Rabbit mAb #2125 (lower). The p16 INK4A Antibody confirms silencing of p16 INK4A expression, while the α-Tubulin (11H10) Rabbit mAb is used as a loading control.Western blot方法分析Hela细胞提取物。分别用100 nM SignalSilence® Control siRNA (Unconjugated) #6568 (-)或 SignalSilence® p16 INK4A siRNA I (+)转染HeLa细胞。使用的抗体为p16 INK4A Antibody #4824 (上图), 和α-Tubulin (11H10) Rabbit mAb #2125 (下图)。和对照抗体α-Tubulin (11H10) Rabbit mAb #2125相比，p16 INK4A Antibody #4824的检测结果证实p16 INK4A的表达被有效沉默。 |
