2005年10月21日 · Here, we found that Pin1 binds c-Fos through specific pS/T-P sites within the c-Fos TAD, and that this interaction results in an enhanced transcriptional response of c-Fos to polypeptide growth factors that stimulate ERK. Our findings suggest that c-Fos represents a novel target for the isomerizing activity of Pin1 and support a role for Pin1 ...

2020年6月23日 · In this Review, we discuss the current understanding of this important class of kinases. We begin with a brief overview of the structure, regulation, substrate recognition and subcellular...

激活的ERK可以磷酸化c-Fos、c-Jun等转录因子，从而在细胞增殖和分化调节中起直接作用。 许多人类的肿瘤组织中都可发现MAPK-ERK信号通路处于异常高表达及高活性状态，促进肿瘤细胞增殖、分化、迁移和血管生成。

The activation of the activating protein-1 (AP-1) family of transcription factors, including c-Fos and c-Jun family members, is one of the earliest nuclear events induced by growth factors that stimulate extracellular signal-regulated kinases (ERKs). In the case of c-Fos, the activation of ERK leads to an increased expression of c-fos mRNA.

ras/raf/mek/erk便是与癌症相关的信号通路中最经典的一条。 一、细胞外、细胞膜上. 细胞膜外的是配体，与之相结的是位于细胞膜上的是受体，如egfr、her2、fgfr、vegfr等。 可关注公众号“基因app”，查看既往文章。 二、细胞质（信号传导链） 1、ras

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。

2024年1月17日 · We determined that phosphorylated c-Fos promoted colon cancer cells resistance to 5-FU by facilitating the cancer stemness. Mechanically, 5-FU treatment induced autolysosome-dependent degradation...

2012年8月1日 · The ERK1/2 catalyzed phosphorylation of nuclear transcription factors including those of Ets, Elk, and c-Fos represents an important function and requires the translocation of ERK1/2 into the nucleus by active and passive processes involving the nuclear pore.

2000年3月13日 · ATF1 and CREB can be phosphorylated by Rsk2 which is a protein kinase directly activated by Erk MAP kinases. These results suggest a signaling pathway in which Erk MAP kinase activates the c-...

星形细胞内富含的 PEA15（phosphoprotein enriched in astrocytes 15，磷酸蛋白 15）可与 ERK 紧密结合，并利用 ERK 的出核序列将其引导出核，因此通过过表达 PEA15 即能阻止 ERK 入核，降低 ERK 通路对细胞应答的调节活性。