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p(HGNC:CYCS)

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Entity

Name
CYCS
Namespace
HGNC
Namespace Version
20180215
Namespace URL
https://arty.scai.fraunhofer.de/artifactory/bel/namespace/hgnc/hgnc-20180215.belns

Appears in Networks 3

Tau oligomers-Cytotoxicity, propagation, and mitochondrial damage v1.0.0

Tau oligomers-Cytotoxicity, propagation, and mitochondrial damage from Shafiei et al., 2017

Activation and regulation of the inflammasomes v1.0.0

Extracellular low-n oligomers of tau cause selective synaptotoxicity without affecting cell viability v1.0.0

In-Edges 3

a(HBP:"Tau oligomers") increases sec(p(HGNC:CYCS)) View Subject | View Object

Suggestively, as tau oligomers concentrate at the mitochondrial membrane, cytochrome C is released, leading to caspase-9 activation via a complex with apoptotic-peptidase activating- factor-1 (Apaf-1; Li et al., 1997) PubMed:28420982

Appears in Networks:
Annotations
MeSH
Mitochondrial Membranes
Confidence
Medium
MeSH
Neurons
MeSH
Alzheimer Disease

complex(p(HGNC:APAF1), p(HGNC:CYCS)) hasComponent p(HGNC:CYCS) View Subject | View Object

Appears in Networks:

p(HBP:"Tau oligomers", var("p.Lys280del")) increases sec(p(HGNC:CYCS)) View Subject | View Object

To address this question, we first applied the oligomers directly after the purification of the protein eluting from the Butyl FF 16/ 10 column (without buffer exchange; 1, 5, and 10 mM) to SHSY5Y cells and observed a variety of toxic effects, including pronounced reduction in the cell viability (by MTT assay, Fig. 3A), increase in apoptotic cells (by Hoechst staining, Supplementary Fig. 4A), loss of mitochondrial membrane potential (by JC1 assay, Supplementary Fig. 4B), caspase 3/7 activation (Supplementary Fig. 4C-D), and cytochrome-c release (Supplementary Fig. 4), within 5 hours of incubation. PubMed:28528849

Appears in Networks:
Annotations
Experimental Factor Ontology (EFO)
SK-N-SH

Out-Edges 2

tloc(p(HGNC:CYCS), fromLoc(MESH:Mitochondria), toLoc(MESH:Cytosol)) increases act(complex(GO:apoptosome)) View Subject | View Object

Indeed, inflammasomes (which induce pyroptosis through caspase 1 or caspase 11 activation) and apoptosomes (which activate caspase 9 in response to cytochrome c release from mitochondria) are two mechanisms by which compromised cells are eliminated. PubMed:23702978

Appears in Networks:
Annotations
Confidence
Medium
NeuroMMSigDB
Apoptosis signaling subgraph
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
XIAP subgraph

tloc(p(HGNC:CYCS), fromLoc(MESH:Mitochondria), toLoc(MESH:Cytosol)) increases complex(p(HGNC:APAF1), p(HGNC:CYCS)) View Subject | View Object

Indeed, the binding of cytochrome c that has been released from mitochondria to apoptotic protease-activating factor 1 (APAF1) and the subsequent assembly of the apoptosome only occurs when subphysiological K+ concentrations are reached in compromised cells77,78. PubMed:23702978

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
XIAP subgraph

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.