[HTML][HTML] UPR, autophagy, and mitochondria crosstalk underlies the ER stress response
D Senft, AR Ze'ev - Trends in biochemical sciences, 2015 - cell.com
Cellular stress, induced by external or internal cues, activates several well-orchestrated
processes aimed at either restoring cellular homeostasis or committing to cell death. Those …
processes aimed at either restoring cellular homeostasis or committing to cell death. Those …
[HTML][HTML] The aftermath of the interplay between the endoplasmic reticulum stress response and redox signaling
KR Bhattarai, TA Riaz, HR Kim, HJ Chae - Experimental & molecular …, 2021 - nature.com
The endoplasmic reticulum (ER) is an essential organelle of eukaryotic cells. Its main
functions include protein synthesis, proper protein folding, protein modification, and the …
functions include protein synthesis, proper protein folding, protein modification, and the …
Endoplasmic reticulum: ER stress regulates mitochondrial bioenergetics
Endoplasmic reticulum (ER) stress activates an adaptive unfolded protein response (UPR)
that facilitates cellular repair, however, under prolonged ER stress, the UPR can ultimately …
that facilitates cellular repair, however, under prolonged ER stress, the UPR can ultimately …
Increased ER–mitochondrial coupling promotes mitochondrial respiration and bioenergetics during early phases of ER stress
Increasing evidence indicates that endoplasmic reticulum (ER) stress activates the adaptive
unfolded protein response (UPR), but that beyond a certain degree of ER damage, this …
unfolded protein response (UPR), but that beyond a certain degree of ER damage, this …
[HTML][HTML] Unfolding the interactions between endoplasmic reticulum stress and oxidative stress
G Ong, SE Logue - Antioxidants, 2023 - mdpi.com
Oxidative stress is caused by an imbalance in cellular redox state due to the accumulation of
reactive oxygen species (ROS). While homeostatic levels of ROS are important for cell …
reactive oxygen species (ROS). While homeostatic levels of ROS are important for cell …
Crosstalk between endoplasmic reticulum stress response and autophagy in human diseases
J Kwon, J Kim, KI Kim - Animal cells and systems, 2023 - Taylor & Francis
Cells activate protective mechanisms to overcome stressful conditions that threaten cellular
homeostasis, including imbalances in calcium, redox, and nutrient levels. Endoplasmic …
homeostasis, including imbalances in calcium, redox, and nutrient levels. Endoplasmic …
Endoplasmic reticulum stress and oxidative stress in cell fate decision and human disease
SS Cao, RJ Kaufman - Antioxidants & redox signaling, 2014 - liebertpub.com
Significance: The endoplasmic reticulum (ER) is a specialized organelle for the folding and
trafficking of proteins, which is highly sensitive to changes in intracellular homeostasis and …
trafficking of proteins, which is highly sensitive to changes in intracellular homeostasis and …
Stress-responsive regulation of mitochondria through the ER unfolded protein response
TK Rainbolt, JM Saunders, RL Wiseman - Trends in Endocrinology & …, 2014 - cell.com
The endoplasmic reticulum (ER) and mitochondria form physical interactions involved in the
regulation of biologic functions including mitochondrial bioenergetics and apoptotic …
regulation of biologic functions including mitochondrial bioenergetics and apoptotic …
Endoplasmic reticulum stress responses
M Schröder - Cellular and molecular life sciences, 2008 - Springer
In homeostasis, cellular processes are in a dynamic equilibrium. Perturbation of
homeostasis causes stress. In this review I summarize how perturbation of three major …
homeostasis causes stress. In this review I summarize how perturbation of three major …
Endoplasmic reticulum and the unfolded protein response: dynamics and metabolic integration
The endoplasmic reticulum (ER) is a dynamic intracellular organelle with multiple functions
essential for cellular homeostasis, development, and stress responsiveness. In response to …
essential for cellular homeostasis, development, and stress responsiveness. In response to …