https://www.selleckchem.com/pr....oducts/chaetocin.htm
05). Interference of ESR2 caused significant reduction in the expressions of ER stress-related proteins and apoptosis-related proteins, up-regulated the genes related to cell proliferation, and increased intracellular pERK/ERK ratio in C28I2 cells. The effect of E2 binding to ERβ, which promoted the expressions of ER stress associated proteins and apoptosis related proteins, was obviously antagonized by treatment of the cells with U0126. The binding of E2 to ERβ promotes ER stress and apoptosis in human chondrocytes by activating ERK
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