Provenance

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charles.hoyt@scai.fraunhofer.de at 2018-04-03 15:18:54
Authors
Causal Biological Networks Database
Contact
CausalBiologicalNetworks.RD@pmi.com
Description
The Mechanisms of Cellular Senescence network depicts the causal mechanisms that are involved in induction of senescence in non-transformed cells in response to a variety of external stimuli (including replicative senescence, stress-induced senescence, and oncogene-induced senescence). The network includes components that participate in intercellular signaling such as growth factors, chemokines, cytokines and proteases, which ultimately lead to manifestation of the senescence-associated secretory phenotype (SASP). \nReviewed 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
200
Number Edges
349
Number Components
52
Network Density
0.00876884
Average Degree
1.745
Number Citations
195
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 51%
Mapk-2.0-Rn v2.0 29%
Epigenetics-2.0-Rn v2.0 29%
Selventa Protein Families Definitions v20150611 29%
Epithelial Innate Immune Activation-2.0-Rn v2.0 27%
Senescence-2.0-Hs v2.0 26%
Senescence-2.0-Mm v2.0 25%
Immune Regulation of Tissue Repair-2.0-Rn v2.0 24%
Osmotic Stress-2.0-Rn v2.0 24%
Endothelial Innate Immune Activation-2.0-Rn v2.0 23%

Sample Edges

act(p(SFAM:"MAPK p38 Family"), ma(kin)) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))

These demonstrate that Ang II is capable of inducing CRP generation in macrophages via AT(1)-ROS-ERK1/2/p38MAPK-NF-kB signal pathway, which contributes to better understanding of the proinflammatory and proatherosclerotic actions of Ang II. PubMed:21325823

act(p(SFAM:"MAPK p38 Family"), ma(kin)) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))

p38 activity was required to enhance the accessibility of the cryptic NF-kappa B binding sites contained in H3 phosphorylated promoters, which indicated that p38-dependent H3 phosphorylation may mark promoters for increased NF-kappa B recruitment. PubMed:11743587

act(p(SFAM:"MAPK p38 Family"), ma(kin)) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))

Thus, suppression of p38 activity using SB203580 and siRNA transfection resulted in the significant reduction of IKK activity, DC maturation, and CXCL2 upregulation by toxin A. These results suggest that p38 MAPK may lead to the activation of IKK and NF-kappaB signaling, resulting in enhanced DC maturation and CXCL2 expression in response to C. difficile toxin A stimulation. PubMed:18985311

Sample Nodes

p(SFAM:"MAPK p38 Family")

In-Edges: 300 | Out-Edges: 234 | Explore Neighborhood | Download JSON

p(RGD:Il1a)

In-Edges: 8 | Out-Edges: 14 | Explore Neighborhood | Download JSON

p(RGD:Ccl3)

In-Edges: 11 | Out-Edges: 19 | 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:Mapk3)

In-Edges: 173 | Out-Edges: 60 | 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.