Here we characterize the differential mechanisms of ERK 1/2 pathway activation by three human EP 3 receptor isoforms stably expressed in human embryonic kidney cells (HEK). We also show that these differences in ERK 1/2 signaling mechanisms result in differences in the activation of both ELK1 and AP-1 transcription.

Using immunoblot analysis we found that nM concentrations of PGE(2) strongly stimulated the phosphorylation of ERK 1/2 by the EP(3-II) and EP(3-III) isoforms; whereas, ERK 1/2 phosphorylation by the EP(3-Ia) isoform was minimal and …

2020年6月1日 · As a specific G-protein coupled PGE2 receptor, EP3 is demonstrated as a negative prognosticator of cervical malignancy. Now, we aimed to investigate the pathological mechanism of EP3 in modulating cervical cancer carcinogenesis.

In this study we provide evidence that expressing murine EP3 α, β, and γ receptor variants in tumor cells reduces to the same degree their tumorigenic potential in vivo. In addition, activation of each of the three mEP3 variants induces enhanced cell-cell contact and reduces cell proliferation in vitro in a Rho-dependent manner.

活化的erk的靶点包括p90核糖体s6激酶(rsk)和细胞质磷脂酶a2（cpla2）。 ERK也会入核，磷酸化转录因子 Elk-1 (383位和389位的丝氨酸)。 通常只有一种高度活化的ERK1或ERK2存在于细胞内，相比非磷酸化的形式其活性高出1000倍。

2019年7月29日 · In SK-BR-3, EP3 antagonism showed a significant decrease in Gi-protein levels, an increase in cAMP levels, and no significant change in p-ERK1/2 expression. Conclusion: Antagonism of the EP3 receptor results in a reduced proliferation and migration of SK-BR-3 breast cancer cells, potentially mediated via a Gi-protein-cAMP pathway.

前列腺素E2 (Prostaglandin E2，PGE2)是一种炎性介质，对肿瘤细胞的生长与侵袭能力有显著的促进作用。 在肝细胞癌细胞中，PGE2与细胞膜上的四种EPR (E prostanoid … 展开v. 万方数据知识服务平台-中外学术论文、中外标准、中外专利、科技成果、政策法规等科技文献的在线服务平台。

cj-42794 (cj-042794) 是一种口服有效的选择性前列腺素e受体 4 (ep4) 拮抗剂，其 ic 50 值为 10 nm，其选择性是 ep1、ep2 和 ep3 的 200 倍。cj-42794 可用于胃溃疡的研究。

2025年2月14日 · ERK（Extracellular Regulated Protein Kinases）即细胞外调节蛋白激酶，包括ERK1和ERK2，是将信号从细胞表面受体传导至细胞核的关键激酶。 ERK1和ERK2的分子量分别为44kDa和42kDa。

The most significant increases in PGE 2-induced Erk phosphorylation were observed in EP1- and EP3-transfected cells, while PGE 2 treatment slightly increased Erk phosphorylation in EP2-transfected cells, suggesting that EP2 overexpression specifically promotes the phosphorylation of p38. Then we focused on the EP2-p38 pathway.