IndraLab

"KRAS also activates ERK2 protein by upregulating ERK1."

"Another one is that mutant Kras-activated ERK2 directly phosphorylates SNAIL [ xref ]."

"In vitro phosphorylation assays revealed that EGFP-K-Ras (V12) enhanced the activity of HA-ERK-2 by a factor of 3.3 +/- 0.37 (+/- SD, n = 5) compared to mock transfected controls."

"By the nanoimmunoassay (NIA), KRAS is found to activate the protein ERK2, whereas ERK1 activation is found in non-KRAS-associated human lung tumors."

"KRAS proto-oncogene, GTPase (KRAS) mutations activate mitogen activated protein kinase 1 (ERK) and then promote the degradation of FBW7 through the ubiquitin-proteasomes pathway in a phosphorylation dependent manner, sequentially abrogating the function of FBW7 as a tumor suppressor."

"KRAS also activates ERK2 protein by upregulating ERK1."

"Indeed, both K-RAS mutant PC cell lines and resected tumor patients showed high levels of p-DRP1 on Ser616, mediated at least in part by K-RAS-dependent activation of ERK2 kinase."

"Here, HLD contributed to fibro-inflammatory responses in the pancreas.Oncogenic activated Kras promotes downstream stimulation of COX2, phosphor-ERK, and macrophage infiltration in the area surrounded by the pancreas’ neoplastic lesion leading to the motivation of the formation of pancreatic intraepithelial neoplasia [227]."

"Further molecular studies elicited that Kras G12D activated ERK2 and enhanced the invasion of pancreatic cancer cells via MMP-1 [XREF_BIBR]."

"Constitutive K-Ras G12D Activation of ERK2 Specifically Regulates 3D Invasion of Human Pancreatic Cancer Cells via MMP-1."

"Specifically, the constitutive activation of ERK2 by K-Ras G12D is necessary for the upregulation of MMP-1 RNA, its secreted protein, and its proteolytic activity."

"This evidence suggests that constitutive activation of MAPK1 synergistically induced by frequent mutation of KRAS2 and the loss of function of DUSP6 plays key roles in pancreatic carcinogenesis and progression."

"In our study, we demonstrated that up-regulation of E-cadherin by AKR1B10 knocked down or inhibition in CD18 pancreatic carcinoma cells appeared via down-regulation of mutant Kras activated ERK2, Akt and Ikk-alpha and NF-kappaB signaling, which was parallel with the effect of siRNA-knockdown K-Ras in CD18 pancreatic carcinoma cells."

"XREF_BIBR, XREF_BIBR) The present study clearly showed that KRAS G12V as well G12A induced ERK1 and ERK2 activation and anchorage independent growth in NIH3T3 cells and the growth advantage of mutated KRAS transfected MOTN-1 cells in IL-2 depleted medium."

"ERK phosphorylation that was constitutive in mutant ras MM cells was completely abolished by the MEK inhibitor PD98059 (Figure 2C, left panels), as was the ERK phosphorylation reinduced in wild-type cells by readdition of IL-6 (Figure 2C, right panel).......In addition, re-exposure to IL-6 could reinduce AKT phosphorylation in wild-type cells in a wortmannin-sensitive fashion. Moreover, the constitutively maintained AKT phosphorylation in the mutation-containing cells was also sensitive to wortmannin. These data indicate the PI3-K/AKT cascade is a ras effector in these mutant ras–containing MM cells."