| 货号 | 13461S |
| 反应种属 | Human |
| 来源宿主 | Rabbit |
| 应用 | W/IP |
| 目标/特异性 | Phospho-Akt1 (Ser129) (D4P7F) Rabbit mAb recognizes endogenous levels of Akt1 protein only when phosphorylated at Ser129. |
| 使用方法 | WB(1:1000) IP (1:50) |
| 供应商 | CST |
| 背景 | Akt, also referred to as PKB or Rac, plays a critical role in controlling survival and apoptosis (1-3). This protein kinase is activated by insulin and various growth and survival factors to function in a wortmannin-sensitive pathway involving PI3 kinase (2,3). Akt is activated by phospholipid binding and activation loop phosphorylation at Thr308 by PDK1 (4) and by phosphorylation within the carboxy terminus at Ser473. The previously elusive PDK2 responsible for phosphorylation of Akt at Ser473 has been identified as mammalian target of rapamycin (mTOR) in a rapamycin-insensitive complex with rictor and Sin1 (5,6). Akt promotes cell survival by inhibiting apoptosis through phosphorylation and inactivation of several targets, including Bad (7), forkhead transcription factors (8), c-Raf (9), and caspase-9. PTEN phosphatase is a major negative regulator of the PI3 kinase/Akt signaling pathway (10). LY294002 is a specific PI3 kinase inhibitor (11). Another essential Akt function is the regulation of glycogen synthesis through phosphorylation and inactivation of GSK-3α and β (12,13). Akt may also play a role in insulin stimulation of glucose transport (12). In addition to its role in survival and glycogen synthesis, Akt is involved in cell cycle regulation by preventing GSK-3β-mediated phosphorylation and degradation of cyclin D1 (14) and by negatively regulating the cyclin dependent kinase inhibitors p27 Kip1 (15) and p21 Waf1/Cip1 (16). Akt also plays a critical role in cell growth by directly phosphorylating mTOR in a rapamycin-sensitive complex containing raptor (17). More importantly, Akt phosphorylates and inactivates tuberin (TSC2), an inhibitor of mTOR within the mTOR-raptor complex (18,19). Research studies indicate that protein kinase CK2 phosphorylates Akt1 at Ser129 (20), which promotes association of Akt1 with the HSP90 chaperone and enhances Akt1 kinase activity by inhibiting dephosphorylation of Akt1 at Thr308 (21). CK2 phosphorylation of Akt1 at Ser129 can also enhance β-catenin transcriptional activity as well as cancer cell survival (22,23).Akt，又被称为PKB 或 Rac，在细胞的生长和凋亡中起到关键作用(1-3)。该蛋白激酶可以被胰岛素和多种生长和存活因子激活，在涉及PI3K激酶的wortmannin（渥曼青霉素）敏感信号通路中发挥作用（2,3）。Akt可由磷脂结合激活，该过程通过活化环中的Thr308 (4)位点以及羧基端Ser473位点的磷酸化完成，其中Thr308的磷酸化由PDK1完成。 之前推测PDK2在Ser473位点磷酸化Akt，后被证实为哺乳动物rapamycin（雷帕霉素）靶蛋白mTOR 的作用， 它存在在一个含有rictor和Sin1 的rapamycin（雷帕霉素）非敏感复合体中。 Akt促进细胞的生长通过抑制细胞的凋亡 ，例如Akt可以抑制下游靶蛋白Bad (7), forkhead 转录因子 (8), c-Raf (9), and caspase-9。PTEN是PI3K激酶/Akt信号通路的主要负调控因子(10)。 LY294002是特异性的 PI3K 激酶抑制剂(11)。Akt 的另外一个主要功能是通过磷酸化并进而抑制GSK-3α 和 β来调控糖原的合成(12,13)。 Akt 也可以调控胰岛素诱导的葡萄糖转运 (12)。除此之外，Akt还可以调控细胞周期，这个功能通过抑制GSK-3β，从而调控其下游的Cyclin D1 的磷酸化和降解 (14)，或者负向调控cyclin依赖的激酶抑制因子 p27 Kip (15) 和 p21 Waf1/CIP1 (16)来实现。 Akt 也可以通过直接磷酸化含有raptor的rapamycin（雷帕霉素）敏感复合体中的mTOR来调控细胞的生长(17)。 更重要的是， Akt磷酸化并失活TSC2， 而TCS2是mTOR-raptor复合物中mTOR的抑制因子(18,19)。研究表明蛋白激酶CK2可以磷酸化Akt1的Ser129（20），这会促进Akt1和HSP90伴侣蛋白的结合，并通过去磷酸化Akt1的Thr308增强Akt1激酶活性（21）。CK2磷酸化Akt1的Ser129可以增强β-catenin的转录活性同时促进癌细胞存活（22,23）。 |
| 存放说明 | -20C |
| 计算分子量 | 60 |
Western blot analysis of extracts from MCF7 cells, untreated (-) or λ phosphatase-treated (+), using Phospho-Akt1 (Ser129) (D4P7F) Rabbit mAb (upper) and Akt1 (C73H10) Rabbit mAb #2938 (lower). 使用Phospho-Akt1 (Ser129) (D4P7F) Rabbit mAb兔单抗 (上) 和Akt1 (C73H10) Rabbit mAb兔单抗 #2938 (下)对未处理(-)或λ phosphatase处理 (+)的MCF7细胞提取物进行western blot分析。 |
