used a constitutively active MEK1 gene (CaMEK) transfection strategy to investigate whether CaMEK provides a protective effect against apoptosis and autophagy induced by hydrogen peroxide (H2O2) in neonatal rat cardiac ventricular cardiomyocytes (NCMs) and the underlying mechanisms
TSG-6 can inhibit the inflammatory response of transplanted vein grafts in rats and reduce vascular injury by downregulation of P38 and JNK signaling pathway.
Formalin injection with and without short-term (<10 min) general isoflurane anesthesia induced the same level of phosphorylated ERK expression in spinal cord.
OPG regulated the proliferation of chondrocytes via MEK/ERK signaling and directly affected chondrocytes by influencing the expression profile of ADAMTS-5 and TIMP-4.
Activation of MEK1 in intestinal epithelial cells is sufficient to induce an EMT (epithelial-to-mesenchymal transition) associated with tumor invasion and metastasis.
SGK1 expression during liver regeneration is a part of a signaling pathway that is necessary for enhancing ERK signaling activation through modulating the MEK/ERK complex formation.
Up-regulation of P-TEFb by the Mek1 signaling pathway contributes to stimulated transcription elongation of immediate early genes in neuroendocrine cells.
DYRK1A prolongs the kinetics of ERK activation by interacting with Ras B-Raf and MEK1 to facilitate the formation of a Ras/B-Raf/MEK1 multiprotein complex
The down-regulation of the MEK/Erk pathway by the proteasome plays roles in Wallerian degeneration of severed axons and axonal pruning in response to local NGF deprivation.
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