| 货号 | 2896T |
| 同种亚型 | Mouse IgG2a |
| 反应种属 | Human, |
| 来源宿主 | Mouse IgG2a |
| 应用 | WB, IP |
| 目标/特异性 | The p18 INK4C (DCS118) Mouse mAb detects endogenous levels of p18 INK4C protein. The antibody does not cross-react with other proteins of the INK4 family. |
| 使用方法 | WB(1:1000) IP (1:50) |
| 供应商 | CST |
| 灵敏度 | Endogenous |
| 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).周期蛋白依赖性激酶(CDKs)的激活部分经由和周期蛋白形成复合体。例如，CDK4和CDK6联合D-型周期蛋白并磷酸化Rb蛋白。该磷酸化过程是细胞进入S期必不可少的事件(1)。CDK4(INK4)抑制剂家族包括p15 INK4B, p16 INK4A, p18 INK4C和p19 INK4D。p18被认为是一个在体的单纯不足的肿瘤抑制基因(2)。所有的INK4蛋白都是由32个氨基酸残基铆钉蛋白模体组成并能够选择性的抑制CDK4/6的活性。p18的突变分析表明第四个锚定蛋白的第三个氨基末端部分介导CDK4/6的结合(3)。INK4家族成员的相互作用可能是通过与CDK4/6形成的二元复合体或者是周期蛋白D结合CDK4/6形成的三元复合体并最终导致细胞周期进程的抑制(4,5)。 |
| 存放说明 | -20C |
| 计算分子量 | 18 |
| 参考文献 | 1 . Lukas, J. et al. (1996) Mol Cell Biol 16, 6917-25. 2 . Bai, F. et al. (2003) Mol. Cell. Biol. 23, 1269-1277. 3 . Noh, S.J. et al. (1999) Cancer Res 59, 558-64. 4 . Guan, K.L. et al. (1994) Genes Dev 8, 2939-52. 5 . Hirai, H. et al. (1995) Mol Cell Biol 15, 2672-81. |
Western blot analysis of extracts from HeLa, 293 and Ramos cells, using p18 INK4C (DCS118) Mouse mAb.western blot方法检测HeLa, 293 和Ramos细胞提取物，使用的抗体为p18 INK4C (DCS118) Mouse mAb。 |
