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- PI3K/AKTPI3K/AKT
- PI3K-Akt通路PI3K - Akt signal pathway
- PI3K/Akt/mTORPI3K/Akt/mTOR signal pathway
- PI3k/Akt抑制剂PI3k/Akt inhibitor
- PI3K-AKT信号通路PI3K-AKT signal pathway
- PI3KPI3 K
- p-AKTp-AKT
- 基因Aktgenes Akt
- Wortmannin抑制PI3K途径对K562细胞增殖和Ara-C诱导的细胞凋亡的影响Effects of PI3K on K562 Cell Proliferation and Apoptosis Induced by Ara-C
- AKT蛋白AKT protein
- Akt通路Akt signal pathway
- 利用信号通路特异性抑制剂抑制实验，提示PI3K在ADAS细胞向内皮细胞分化中And PI3 kinase inhibitor LY294002 blocked the differentiation of ADAS cells into endothelial cells in vitro.
- PI3K-AktPI3K-Akt
- PI3K／AktPI3K/Akt
- 原癌基因产物c CBL对BCR/ABL酪氨酸激酶活性无反向调节作用 ,它是连接BCR/ABL与PI3K之间的重要桥梁分子。c CBL Has no regulatory effects on BCR/ABL tyrosine kinase. c CBL is assumed to be the linkage between BCR/ABL and PI3K and subsequently activates PI3K. [
- PKB／AktPKB/Akt
- Akt／PKBAkt kinase/protein kinase B
- Akt／mTORAkt/mTOR
- 作用 2 4h后细胞实验组细胞BCL -2蛋白表达较对照组降低 ,说明Wortmannin可促进K5 62细胞的凋亡。 结论 Wortmannin可以通过抑制PI3K通路抑制K5 62细胞的增殖。Conclusion Wortmannin could inhibitedtheproliferationofK5 6 2cells ,andwascellcyclespecificagent (CCSA) .
- P13K／AktPI3 K/Akt
