We recently reported that there is a crosstalk between p38 and Akt pathways in non-small-cell lung carcinoma cells, and this crosstalk is associated with E-cadherin and special AT-rich sequence-binding protein 2 expressions.

MAPKKK 磷酸化并激活 MKK3/6，后者即是 p38 MAPK 激酶。 MKK3/6 也可在凋亡因素的刺激下直接由 ASK1 激活。 p38 MAPK 参与调节 HSP27、MAPKAPK-2 (MK2)、MAPKAPK-3 (MK3) 和其他几种转录因子，包括 ATF-2、Stat1、Max/Myc 复合体、MEF-2 和 Elk-1，而 CREB 通过激活 MSK1 间接调控。 Coulthard LR, White DE, Jones DL, McDermott MF, Burchill SA (2009) p38 (MAPK): stress responses from molecular mechanisms to therapeutics.

MAPKKK 磷酸化并激活 MKK3/6，后者即是 p38 MAPK 激酶。 MKK3/6 也可在凋亡因素的刺激下直接由 ASK1 激活。 p38 MAPK 参与调节 HSP27、 MAPKAPK-2 (MK2)、 MAPKAPK-3 (MK3) 和其他几种转录因子，包括 ATF-2 、 Stat1 、 Max/Myc 复合体 、 MEF-2 和 Elk-1，而 CREB 通过激活 MSK1 间接调控。 P38参与着许多的细胞生理和病理的过程，包括细胞的凋亡、细胞应激、细胞周期和机体的炎症反应. p38 MAPK与肿瘤. 当细胞受到炎症、细胞因子和化疗药物等细胞外 …

2004年12月1日 · Recent work has demonstrated that both the phosphatidylinositol 3-kinase (PI3K)/Akt and p38 pathways play important roles in myogenesis. Here, we describe the interactions between these pathways in C2C12 cells. Overall, our results suggest that Akt acts downstream of p38 in myogenic cell differentiation.

我们的研究结果表明，白藜芦醇抑制增殖，但通过抑制 Akt/mTOR 和激活 p38-MAPK 通路诱导细胞凋亡和自噬。 白藜芦醇诱导的自噬可能作为促进 NSCLC 细胞存活的保护机制。

Activation of the mitogen-activated protein kinase (MAPK) signaling pathway is associated with a variety of cellular functions, including cell proliferation, differentiation, cell survival, and cell migration, through the activation of ERK, p38 MAPK, and JNK; in turn, they activate the transcription factors of kinases [15, 16, 17].

2004年4月30日 · To evaluate the roles of 4 putative downstream molecules (ERK, p38 MAPK, JNK and AKT) of the RET signal pathway in the tumorigenesis of papillary carcinomas, the expression patterns of RET and phosphorylated forms of ERK, p38 MAPK, JNK and AKT were evaluated in 115 cases of papillary thyroid carcino …

To determine whether Akt and MAPK pathways were required for IL-8 increase induced by VP-16 and doxorubicin, A375 cells were pretreated for 30 minutes with SH-5, an Akt inhibitor, with SB...

此外，PRN联合As 2 O 3 下调phosphorylated Akt，增强phosphorylated p38-MAPK和Cleaved Caspase-3的表达，进而促进肿瘤细胞凋亡。PRN可能成为临床上辅助As 2 O 3 治疗肿瘤中的潜在的辅助治疗药物。

As shown in Fig. 3A, B, TC activated ERK, Akt, p38 MAPK signaling, indicated by the increased phosphorylation of ERK, Akt, and p38 MAPK, whereas JNK signaling was not activated by TC in...