Here we show that the K-Ras – JNK axis plays a pivotal role in the maintenance of pancreatic CSCs/CSLCs. In vitro inhibition of JNK, either pharmacological or genetic, caused loss of the self-renewal and tumor-initiating capacity of pancreatic CSLCs.

K-Ras可以激活PI3K / AKT通路，但其主要靶点是MAPK信号级联反应，包括c-Jun N端激酶（JNK）和p38丝裂原活化蛋白激酶（p38 MAPK）。 在该团队以前的研究中，发现机械应力通过激活胰腺癌和脑癌细胞系中的P13K / AKT和MEK1 / ERK1信号级联来促进生长分化因子15（GDF15）诱导的 ...

The purpose of the present study was to examine the role of JNK in cell transformation by investigating the effect of targeted disruptions of the murine Jnk genes on Ras-stimulated transformation. We show that JNK deficiency causes profound increases in the number and growth of Ras-induced tumor nodules in vivo.

2017年6月27日 · We identified fiery mountain (fmt), a regulatory subunit of the protein phosphatase 6 (PP6) complex, as a tumor suppressor that synergizes with RasV12 to drive c-Jun N-terminal kinase (JNK)-dependent tumor growth and invasiveness. We show that Fmt negatively regulates JNK upstream of dTAK1.

The data suggest that HMGB1 is required for erastin-induced ferroptosis, the regulation of transferrin receptor protein 1 (TfR1) mRNA levels, and c-Jun N-terminal kinase (JNK) and p38 phosphorylation in the rat sarcoma (RAS)-JNK/p38 pathway.

2024年9月28日 · We found that knockdown of Crk, the Drosophila ortholog of human CRK (CT10 regulatory kinase) and CRKL (Crk-like) adapter proteins, significantly suppresses growth of RasV12/scrib−/− tumors by...

Rho 亚家族是小分子G蛋白Ras超家族（Ras见帖： Ras-Raf-MEK-ERK1/2信号通路 ）的成员之一。应激刺激（如紫外线、热休克、高渗刺激、蛋白合成抑制剂等)、细胞因子（TNF-α、IL-1)、生长因子（EGF）、某些G蛋白偶联的受体激活，均可激活 Rho 亚家族（Rac、Rho、cdc42）[1,2,5]。

2016年12月1日 · Here, we identify a route for the phospho-inhibition of Ras/Raf/MEK/ERK pathway signaling that is mediated by the stress-activated JNK cascade. We find that key Ras pathway components, the RasGEF Sos1 and the Rafs, are phosphorylated on multiple S/TP sites in response to JNK activation and that the hyperphosphorylation of these sites renders ...

2006年11月2日 · In cooperation with two oncogenic events, activated Ras and disrupted epithelial integrity, JNK enhances tumor malignancy via Fos‐dependent activation of the gene encoding Mmp1.

2014年7月15日 · Here we show that the K-Ras - JNK axis plays a pivotal role in the maintenance of pancreatic CSCs/CSLCs. In vitro inhibition of JNK, either pharmacological or genetic, caused loss of the self-renewal and tumor-initiating capacity of pancreatic CSLCs.