Novel Pkc(新颖的PKC)研究综述
Novel Pkc 新颖的PKC - We recently identified the leucine-rich repeat adhesion protein, trophoblast glycoprotein (TPBG), as a novel PKCα-dependent phosphoprotein in retinal rod bipolar cells (RBCs). [1] Crucially, TCR dependent upregulation of the important T cell signaling lipid diacylglycerol (DAG), which is fundamental for activation of conventional and novel PKCs, was abolished in ΔNSM cells. [2] We recently identified the leucine‐rich repeat (LRR) adhesion protein, trophoblast glycoprotein (TPBG), as a novel PKCα‐dependent phosphoprotein in retinal rod bipolar cells (RBCs). [3] ERK activation by the eicosanoid was reduced by the "pan" PKC inhibitor GF109203X but not by the classical PKC inhibitor Gö6976, suggesting the involvement of novel PKCs in this effect. [4] The allergen induced decrease of CBF was abolished by GF 109203X, a novel PKC (n PKC) isoform inhibitor, whereas the decrease was not attenuated by Go-6976, a specific inhibitor of conventional PKC (Cpkc) isoform. [5]我们最近将富含亮氨酸的重复粘附蛋白、滋养层糖蛋白 (TPBG) 鉴定为视网膜杆状双极细胞 (RBC) 中一种新型的 PKCα 依赖性磷蛋白。 [1] 至关重要的是，重要的 T 细胞信号转导脂质二酰基甘油 (DAG) 的 TCR 依赖性上调是激活传统和新型 PKC 的基础，但在 ΔNSM 细胞中已被消除。 [2] 我们最近将富含亮氨酸重复 (LRR) 的粘附蛋白、滋养层糖蛋白 (TPBG) 鉴定为视网膜杆状双极细胞 (RBC) 中一种新型的 PKCα 依赖性磷蛋白。 [3] “泛” PKC 抑制剂 GF109203X 减少了类花生酸对 ERK 的激活，但经典 PKC 抑制剂 Gö6976 没有减少，这表明新的 PKC 参与了这种作用。 [4] 新型 PKC (n PKC) 同种型抑制剂 GF 109203X 消除了过敏原引起的 CBF 减少，而传统 PKC (Cpkc) 同种型的特异性抑制剂 Go-6976 并未减弱这种减少。 [5]
novel pkc isoform 新型 Pkc 异构体
Currently, modes of AC9 regulation include stimulation by Gαs, protein kinase C (PKC) βII, or calcium-calmodulin kinase II (CaMKII) and inhibition by Gαi/o, novel PKC isoforms, or calcium-calcineurin. [1] The novel PKC isoform, PKC-theta, is particularly enriched in T lymphocyte populations, serving a critical role in signal transduction after CD3/CD28 T cell receptor stimulation. [2] Classical and/or Novel PKC isoform inhibition changes the shape of the PC3 cells, they show a more rounded morphology, whereas PKD inhibition causes prostate cancer cell to elongate. [3]目前，AC9 的调节模式包括 Gαs、蛋白激酶 C (PKC) βII 或钙钙调蛋白激酶 II (CaMKII) 的刺激和 Gαi/o、新型 PKC 同种型或钙调神经磷酸酶的抑制。 [1] 新型 PKC 异构体 PKC-theta 在 T 淋巴细胞群中特别丰富，在 CD3/CD28 T 细胞受体刺激后的信号转导中起关键作用。 [2] 经典和/或新型 PKC 同种型抑制改变了 PC3 细胞的形状，它们显示出更圆的形态，而 PKD 抑制导致前列腺癌细胞伸长。 [3]