Receptor Knockdown(受体敲低)研究综述
Receptor Knockdown 受体敲低 - Based on endocytosis inhibitors and receptor knockdown, the cellular uptake of P2Ns-GA is clathrin-mediated and dependent on TfR1 expression, but other trafficking mechanisms, particularly those involving caveo-lae/lipid rafts, can also play a role. [1]基于内吞作用抑制剂和受体敲低，P2Ns-GA 的细胞摄取是网格蛋白介导的，并且依赖于 TfR1 的表达，但其他运输机制，特别是那些涉及caveo-lae/脂质筏的运输机制，也可以发挥作用。 [1]
A2b Receptor Knockdown
A2B receptor knockdown prevented the effects of 2-chloroadenosine on cyclic AMP production and P-SMC proliferation and migration. [1] A2B receptor antagonist treatment or A2B receptor knockdown suppressed EGFR translocation, γH2AX/53BP1 focus formation, and colony formation of lung cancer cell lines A549, calu-6 and NCI-H446, compared with a normal cell line (beas-2b). [2]A2B 受体敲低阻止了 2-氯腺苷对环 AMP 产生和 P-SMC 增殖和迁移的影响。 [1] 与正常细胞系 (beas-2b) 相比，A2B 受体拮抗剂治疗或 A2B 受体敲低抑制了肺癌细胞系 A549、calu-6 和 NCI-H446 的 EGFR 易位、γH2AX/53BP1 病灶形成和集落形成。 [2]
Insulin Receptor Knockdown 胰岛素受体敲低
Hepatic Klf15 expression is significantly increased by the attenuation of the insulin signaling in STZ-induced insulin deficiency and insulin receptor knockdown models. [1] Insulin receptor knockdown inhibited proliferation and induced programmed cell death. [2]在 STZ 诱导的胰岛素缺乏和胰岛素受体敲低模型中，通过减弱胰岛素信号传导显着增加了肝 Klf15 的表达。 [1] 胰岛素受体敲低抑制增殖并诱导程序性细胞死亡。 [2]