Open image in new window Figure 1 Normal ER function and ER stress.
Therefore, ER stress that results from an imbalance between the cellular demand for ER function and ER capacity emerges as an important player in inflammatory responses and activation of cell death mechanisms in liver during I/R.
The increase in wolframin expression is attributable, at least in part, to enhanced WFS1 promoter activity stimulated by ER stress-inducing chemicals, thus indicating a direct link between wolframin function and ER stress responses [ 14].
According to our study of 2D electrophoresis, molecular chaperone proteins involved in mitochondrial function and ER stress, and cytoskeleton-related proteins were participated in photoactivated Lonicera japonica-induced CH27 cell death.
These processes are associated to a huge production of viral proteins into the ER, which disrupts its normal functions and induces ER stress [77].
Given the importance of ER/mitochondrial interactions to metabolic regulation, we have used mouse embryonic fibroblasts (MEFs) derived from Miner1 WT and KO mice to investigate the role of Miner1 in maintaining proper ER function and ER-mitochondrial communication.
This suggests that PBA and TUDCA may improve β cell functions and prevent ER stress-mediated β cell death and neurodegeneration in patients with Wolfram syndrome.
The mechanisms involved in the pathogenesis of COPD include inflammatory responses in the airway, loss of barrier function, oxidative, and ER stress responses.
This review article focuses on the activation of ER functions increasing ER membrane proteins and size and eliminating ER stress and major health problems including common cardiovascular, DM2, and other metabolic diseases.
However, a major limitation in alternative approaches to treating or preventing antiestrogen resistance is that we lack knowledge of the precise signaling mechanisms that underlie the regulation of ER function and development of ER-unresponsiveness in ER-positive breast cancer cells in vivo.
