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bp(GO:"response to endoplasmic reticulum stress")

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Entity

Name
response to endoplasmic reticulum stress
Namespace
go
Namespace Version
20180921
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/go-names.belns

Appears in Networks 5

The Ubiquitin Proteasome System in Neurodegenerative Diseases: Sometimes the Chicken, Sometimes the Egg v1.0.0

Promoting the clearance of neurotoxic proteins in neurodegenerative disorders of ageing v1.0.0

Interplay of pathogenic forms of human tau with different autophagic pathways v1.0.1

Activation and regulation of the inflammasomes v1.0.0

Molecular chaperones and proteostasis regulation during redox imbalance v1.0.0

In-Edges 3

bp(GO:"response to unfolded protein") increases bp(GO:"response to endoplasmic reticulum stress") View Subject | View Object

The UPR is a mechanism that involves a stress response in the ER, including increased biosynthesis of ER chaperones, in response to accumulation of misfolded/denatured/mutated proteins in this organelle (for a recent review on UPR, see Kaufman, 2002). PubMed:14556719

Appears in Networks:
Annotations
MeSH
Endoplasmic Reticulum

a(CHEBI:ambroxol) decreases bp(GO:"response to endoplasmic reticulum stress") View Subject | View Object

Ambroxol, which also decreased ER stress in D. mela- nogaster 201 , reduced α-synuclein levels in overexpress- ing, transgenic mice 202 . PubMed:30116051

Appears in Networks:

a(CHEBI:thapsigargin) increases bp(GO:"response to endoplasmic reticulum stress") View Subject | View Object

Cells expressing WT tau behave as control cells and display a dose-dependent increase in CMA activity upon exposure to paraquat (Fig. 3f) or thapsigargin (Fig. 3g) PubMed:29024336

Appears in Networks:
Annotations
MeSH
Intracellular Space
Confidence
High
MeSH
Brain

Out-Edges 6

bp(GO:"response to endoplasmic reticulum stress") increases act(complex(GO:"NLRP3 inflammasome complex")) View Subject | View Object

The authors proposed that another, not yet characterized, ER stress pathway activates the NLRP3 inflammasome90. PubMed:23702978

Appears in Networks:
Annotations
Confidence
High
MeSH
Extracellular Space
NeuroMMSigDB
Caspase subgraph

bp(GO:"response to endoplasmic reticulum stress") increases act(p(HGNC:HSPA5)) View Subject | View Object

Upon ER proteotoxic stress, GRP78 dissociates from its binding partners, which are then free to trigger the Unfolded Protein Response (UPR) by regulating specific gene responses aiming to restore ER proteome stability. PubMed:24563850

Appears in Networks:

bp(GO:"response to endoplasmic reticulum stress") decreases bp(HBP:misfolding) View Subject | View Object

The three sensors of ER proteotoxic stress facilitate contra- dictory responses since they either promote cell survival by decreasing the misfolded protein and/or oxidative load, or, if UPR fails, they promote the activation of apoptotic pathways that eventually result in cell death [57]. PubMed:24563850

Appears in Networks:

bp(GO:"response to endoplasmic reticulum stress") decreases bp(GO:"cell death") View Subject | View Object

The three sensors of ER proteotoxic stress facilitate contra- dictory responses since they either promote cell survival by decreasing the misfolded protein and/or oxidative load, or, if UPR fails, they promote the activation of apoptotic pathways that eventually result in cell death [57]. PubMed:24563850

Appears in Networks:

bp(GO:"response to endoplasmic reticulum stress") increases bp(GO:"cell death") View Subject | View Object

The three sensors of ER proteotoxic stress facilitate contra- dictory responses since they either promote cell survival by decreasing the misfolded protein and/or oxidative load, or, if UPR fails, they promote the activation of apoptotic pathways that eventually result in cell death [57]. PubMed:24563850

Appears in Networks:

bp(GO:"response to endoplasmic reticulum stress") increases bp(GO:"apoptotic process") View Subject | View Object

The three sensors of ER proteotoxic stress facilitate contra- dictory responses since they either promote cell survival by decreasing the misfolded protein and/or oxidative load, or, if UPR fails, they promote the activation of apoptotic pathways that eventually result in cell death [57]. PubMed:24563850

Appears in Networks:

About

BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.