Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

QRICH1 Dictates the Outcome of ER Stress through Transcriptional Control of Proteostasis

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE146842 | GEO | 2021/02/17

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

QRICH1 dictates the outcome of ER stress through transcriptional control of proteostasis.

Project description:Tissue homeostasis is perturbed in a diversity of inflammatory pathologies. These changes can elicit endoplasmic reticulum (ER) stress, protein misfolding, and cell death. ER stress triggers the unfolded protein response (UPR), which can promote recovery of ER proteostasis and cell survival or trigger programmed cell death. Here, we leveraged single-cell RNA sequencing to define dynamic transcriptional states associated with the adaptive versus terminal UPR in the mouse intestinal epithelium. We integrated these transcriptional programs with genome-scale CRISPR screening to dissect the UPR pathway functionally. We identified QRICH1 as a key effector of the PERK-eIF2α axis of the UPR. QRICH1 controlled a transcriptional program associated with translation and secretory networks that were specifically up-regulated in inflammatory pathologies. Thus, QRICH1 dictates cell fate in response to pathological ER stress.

| S-EPMC8315080 | biostudies-literature

QRICH1 Dictates the Outcome of ER Stress through Transcriptional Control of Proteostasis [RNA-seq]

Project description:Perturbation of tissue homeostasis accompanies a diversity of inflammatory pathologies and imposes metabolic constraints at the cellular level that elicit ER stress, protein misfolding, and cell death. In response to ER stress, cells initiate the unfolded protein response (UPR), which determines divergent cell fate decisions, either promoting recovery of ER proteostasis and cell survival or triggering programmed cell death. However, the mechanisms by which the UPR transitions from the adaptive to terminal state are not fully understood. Here, we identify QRICH1 as a previously uncharacterized transcriptional regulator of a gene modulethat differentially engages the terminal versus adaptive UPR.

2021-02-17 | GSE146840 | GEO

QRICH1 Dictates the Outcome of ER Stress through Transcriptional Control of Proteostasis [ChIP-seq]

2021-02-17 | GSE146839 | GEO

QRICH1 Dictates the Outcome of ER Stress through Transcriptional Control of Proteostasis

Project description:QRICH1 Dictates the Outcome of ER Stress through Transcriptional Control of Proteostasis

| PRJNA612072 | ENA

QRICH1 Dictates the Outcome of ER Stress through Transcriptional Control of Proteostasis [ChIP-seq]

Project description:QRICH1 Dictates the Outcome of ER Stress through Transcriptional Control of Proteostasis [ChIP-seq]

| PRJNA612076 | ENA

QRICH1 Dictates the Outcome of ER Stress through Transcriptional Control of Proteostasis [RNA-seq]

Project description:QRICH1 Dictates the Outcome of ER Stress through Transcriptional Control of Proteostasis [RNA-seq]

| PRJNA612075 | ENA

Stress-Independent Activation of XBP1s and/or ATF6 Reveals Three Functionally Distinct ER Proteostasis Environments

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-04-23 | E-GEOD-44951 | biostudies-arrayexpress

Stress-Independent Activation of XBP1s and/or ATF6 Reveals Three Functionally Distinct ER Proteostasis Environments

Project description:This SuperSeries is composed of the SubSeries listed below.

2013-04-23 | GSE44951 | GEO

BOK controls ER proteostasis and physiological ER stress responses in neurons.

Project description:The Bcl-2 family proteins BAK and BAX control the crucial step of pore formation in the mitochondrial outer membrane during intrinsic apoptosis. Bcl-2-related ovarian killer (BOK) is a Bcl-2 family protein with a high sequence similarity to BAK and BAX. However, intrinsic apoptosis can proceed in the absence of BOK. Unlike BAK and BAX, BOK is primarily located on the endoplasmic reticulum (ER) and Golgi membranes, suggesting a role for BOK in regulating ER homeostasis. In this study, we report that BOK is required for a full ER stress response. Employing previously characterized fluorescent protein-based ER stress reporter cell systems, we show that BOK-deficient cells have an attenuated response to ER stress in all three signaling branches of the unfolded protein response. Fluo-4-based confocal Ca2+ imaging revealed that disruption of ER proteostasis in BOK-deficient cells was not linked to altered ER Ca2+ levels. Fluorescence recovery after photobleaching (FRAP) experiments using GRP78/BiP-eGFP demonstrated that GRP78 motility was significantly lower in BOK-deficient cells. This implied that less intraluminal GRP78 was freely available and more of the ER chaperone bound to unfolded proteins. Collectively, these experiments suggest a new role for BOK in the protection of ER proteostasis and cellular responses to ER stress.

| S-EPMC9434404 | biostudies-literature

G9a dictates neuronal vulnerability to inflammatory stress via transcriptional control of ferroptosis.

Project description:Neuroinflammation leads to neuronal stress responses that contribute to neuronal dysfunction and loss. However, treatments that stabilize neurons and prevent their destruction are still lacking. Here, we identify the histone methyltransferase G9a as a druggable epigenetic regulator of neuronal vulnerability to inflammation. In murine experimental autoimmune encephalomyelitis (EAE) and human multiple sclerosis (MS), we found that the G9a-catalyzed repressive epigenetic mark H3K9me2 was robustly induced by neuroinflammation. G9a activity repressed anti-ferroptotic genes, diminished intracellular glutathione levels, and triggered the iron-dependent programmed cell death pathway ferroptosis. Conversely, pharmacological treatment of EAE mice with a G9a inhibitor restored anti-ferroptotic gene expression, reduced inflammation-induced neuronal loss, and improved clinical outcome. Similarly, neuronal anti-ferroptotic gene expression was reduced in MS brain tissue and was boosted by G9a inhibition in human neuronal cultures. This study identifies G9a as a critical transcriptional enhancer of neuronal ferroptosis and potential therapeutic target to counteract inflammation-induced neurodegeneration.

| S-EPMC9355351 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data