Provenance

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charles.hoyt@scai.fraunhofer.de at 2018-04-03 15:17:47
Authors
Causal Biological Networks Database
Contact
CausalBiologicalNetworks.RD@pmi.com
Description
The Necroptosis network describes the causal mechanisms involved in the activation of the Fas receptor and TNFR1 receptor, leading to RIPK/ROS (reactive oxygen species) signaling and the subsequent induction of necroptosis as a result of exposure to environmental insults. The network includes the array of proinflammatory mediators released from necrotic cells that may contribute to COPD development. \Reviewed during Jamboree2015
License
Please cite: - www.causalbionet.com - https://bionet.sbvimprover.com as well as any relevant publications. The sbv IMPROVER project, the website and the Symposia are part of a collaborative project designed to enable scientists to learn about and contribute to the development of a new crowd sourcing method for verification of scientific data and results. The current challenges, website and biological network models were developed and are maintained as part of a collaboration among Selventa, OrangeBus and ADS. The project is led and funded by Philip Morris International. For more information on the focus of Philip Morris International’s research, please visit www.pmi.com.
Number Nodes
56
Number Edges
199
Number Components
2
Network Density
0.0646104
Average Degree
3.55357
Number Citations
108
Number BEL Errors
0

Content Statistics

Network Overlap

The node-based overlap between this network and other networks is calculated as the Szymkiewicz-Simpson coefficient of their respective nodes. Up to the top 10 are shown below.

Network Overlap
BEL Framework Large Corpus Document v20170611 43%
Apoptosis-2.0-Rn v2.0 34%
Necroptosis-2.0-Hs v2.0 31%
Necroptosis-2.0-Mm v2.0 31%
Selventa Protein Families Definitions v20150611 23%
BEL Framework Small Corpus Document v20150611 21%
Oxidative Stress-2.0-Rn v2.0 20%
Epithelial Innate Immune Activation-2.0-Rn v2.0 18%
Epithelial Mucus Hypersecretion-2.0-Rn v2.0 18%
Macrophage Signaling-2.0-Rn v2.0 16%

Sample Edges

a(CHEBI:"arachidonic acid") decreases a(CHEBI:ATP)

Arachidonic acid (AA) promoted BSO-induced cell death by accumulating reactive oxygen species (ROS) or hydroperoxides. AA inhibited caspase-3 activation and internucleosomal DNA fragmentation during the BSO-induced GSH depletion. Furthermore, AA reduced intracellular ATP content, induced dysfunction of mitochondrial membrane and enhanced 8-hydroxy-2'-deoxyguanosine (8-OH-dG) production. There was significant increase of 12-lipoxygenase activity in the presence of AA under the BSO-induced GSH depletion in C6 cells. These results suggest that AA promotes cell death by changing to necrosis from apoptosis through lipid peroxidation PubMed:11913980

a(CHEBI:"arachidonic acid") increases bp(GOBP:"necrotic cell death")

Arachidonic acid (AA) promoted BSO-induced cell death by accumulating reactive oxygen species (ROS) or hydroperoxides. AA inhibited caspase-3 activation and internucleosomal DNA fragmentation during the BSO-induced GSH depletion. Furthermore, AA reduced intracellular ATP content, induced dysfunction of mitochondrial membrane and enhanced 8-hydroxy-2'-deoxyguanosine (8-OH-dG) production. There was significant increase of 12-lipoxygenase activity in the presence of AA under the BSO-induced GSH depletion in C6 cells. These results suggest that AA promotes cell death by changing to necrosis from apoptosis through lipid peroxidation PubMed:11913980

a(CHEBI:"arachidonic acid") increases a(CHEBI:"reactive oxygen species")

Arachidonic acid (AA) promoted BSO-induced cell death by accumulating reactive oxygen species (ROS) or hydroperoxides. AA inhibited caspase-3 activation and internucleosomal DNA fragmentation during the BSO-induced GSH depletion. Furthermore, AA reduced intracellular ATP content, induced dysfunction of mitochondrial membrane and enhanced 8-hydroxy-2'-deoxyguanosine (8-OH-dG) production. There was significant increase of 12-lipoxygenase activity in the presence of AA under the BSO-induced GSH depletion in C6 cells. These results suggest that AA promotes cell death by changing to necrosis from apoptosis through lipid peroxidation PubMed:11913980

a(CHEBI:"reactive oxygen species") decreases bp(GOBP:"regulation of mitochondrial membrane potential")

Once ROS levels are induced, they appear to accelerate mitochondrial depolarization ​(Fig.55 and ​and7B). PubMed:10891504

a(CHEBI:"reactive oxygen species") decreases bp(GOBP:"regulation of mitochondrial membrane potential")

Silica was shown to induce elevated levels of intracellular ROS, resulting in a marked decrease in intracellular glutathione (GSH) and cysteine and a sustained presence of apoptotic AM in silica-exposed rats up to two weeks post-exposure. The apoptotic AM were characterized by decreased mitochondrial trans-membrane potential, increased mitochondrial release of cytochrome c, activated caspase 9 (but not caspase 8) and caspase 3 activities, PubMed:16754540

Sample Nodes

a(CHEBI:glutathione)

In-Edges: 132 | Out-Edges: 88 | Classes: 5 | Explore Neighborhood | Download JSON

a(CHEBI:"reactive oxygen species")

In-Edges: 1023 | Out-Edges: 827 | Classes: 1 | Children: 4 | Explore Neighborhood | Download JSON

p(RGD:Glul)

In-Edges: 4 | Out-Edges: 3 | Explore Neighborhood | Download JSON

p(RGD:Tnf)

In-Edges: 139 | Out-Edges: 306 | Explore Neighborhood | Download JSON

p(HGNC:MAP3K7)

In-Edges: 31 | Out-Edges: 67 | Explore Neighborhood | Download JSON

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 the open source project, PyBEL. Please feel free to contact us here to give us feedback or report any issues.