Browse
Submit Data
Databases
API
Help

Dataset Information

11 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Inositol Requiring Enzyme (IRE), a multiplayer in sensing endoplasmic reticulum stress.

ABSTRACT: The endoplasmic reticulum (ER) can sense a wide variety of external and internal perturbations and responds by mounting stress coping responses, such as the unfolded protein response (UPR). The UPR is composed of three stress sensors, namely IRE1α, PERK, and ATF6 that are activated to re-establish ER homeostasis. IRE1α represents the most ancient branch of the UPR affecting many cellular processes in plant and animal cells. IRE1α is a type I transmembrane protein with kinase/nuclease activities in response to ER stress. Both the ER luminal and cytosolic IRE1α interactomes have been identified revealing a multifunctional role of the ER stress sensor. IRE1α is also associated with organellar membrane contacts to promote rapid communication between intracellular organelles under stress conditions.

SUBMITTER: Zhou Z

PROVIDER: S-EPMC8765250 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Similar Datasets

The Endoplasmic Reticulum Stress Sensor Inositol-Requiring Enzyme 1? Augments Bacterial Killing through Sustained Oxidant Production.

Project description: Not available

| S-EPMC4502229 | biostudies-literature

Mechanism of inositol-requiring enzyme 1-alpha inhibition in endoplasmic reticulum stress and apoptosis in ovarian cancer cells.

Project description: Not available

| S-EPMC7642155 | biostudies-literature

Ginkgolide K protects the heart against endoplasmic reticulum stress injury by activating the inositol-requiring enzyme 1α/X box-binding protein-1 pathway.

Project description: Not available

| S-EPMC4945765 | biostudies-literature

Lipid bilayer stress-activated IRE-1 modulates autophagy during endoplasmic reticulum stress

Project description:Metabolic disorders such as obesity and nonalcoholic fatty liver disease (NAFLD) are emerging disorders that affect the global population. One facet of the disorders is attributed to the disturbance of membrane lipid homeostasis. Perturbation of endoplasmic reticulum (ER) homeostasis through changes in membrane phospholipid composition results in activation of the unfolded protein response (UPR) and causes dramatic translational and transcriptional changes in cell. To restore cellular homeostasis, the three highly conserved UPR transducers ATF6, IRE1, and PERK mediate cellular processes upon ER stress. The roles of the UPR in proteostatic stress caused by the accumulation of misfolded protein is well understood but lipid perturbation-induced UPR remains elusive. We found that genetically attenuated PC synthesis in C. elegans causes lipid droplets accumulation if not for the intervention of the UPR program. Transcriptional profiling of lipid perturbation-induced ER stress animals shows a unique subset of genes modulated in an UPR-dependent manner that are unaffected by proteostatic stress. Among these, we identified IRE1-modulated autophagy genes that trigger liberation of free fatty acids from excess lipid droplets suggesting a stress release mechanism by which free fatty acids are rechannelling to restore lipid homeostasis. Considering the important role of lipid homeostasis and how its impairment contributes to the pathologies in metabolic diseases, our data uncovers the indispensable role of a fully functional UPR program in regulating lipid homeostais in the face of chronic ER stress.

2018-10-31 | GSE99763 | GEO

Inositol requiring enzyme 1? augments angiogenesis for diabetic wound healing

Project description:The microarray analysis is to investigate the different expression profile of microRNAs in bone marrow-derived progenitor cells from type 2 diabetic mice and healthy control mice. microRNA expression profiles were compared between bone marrow-derived progenitor cells from either type 2 diabetic db/db mice or their in-colony control litter db/+ mice. Total RNA was extracted from bone marrow-derived progenitor cells from either type 2 diabetic db/db mice (Jackson lab, # 000642) or their in-colony control litter db/+ mice. N=3 per group.

2015-09-02 | E-GEOD-72616 | biostudies-arrayexpress