p38 and ERK1/2-dependent activation of c-Jun is required for the downregulation of oxidative stress-induced ER α in hypothalamic astrocytes

Conclusions: The current data demonstrate that oxidative stress leads to loss of ERα involving the activation of the p38 and ERK1/2 pathways a nd the induction of the c-Jun protein in hypothalamic astrocytes. C-Jun protein regulates ERα gene expression via direct transcriptional repression or involving histone acetylation modifications at ERα gene promoter sites.

Source: Neuroendocrinology - January 3, 2023 Category: Endocrinology Source Type: research