Provenance

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charles.hoyt@scai.fraunhofer.de at 2018-04-03 15:17:57
Authors
Causal Biological Networks Database
Contact
CausalBiologicalNetworks.RD@pmi.com
Description
The Neutrophil Signaling network depicts the causal mechanisms that lead to various cellular functions in neutrophils, such as polarization, extravasation, respiratory burst, response to stimuli, and chemotaxis, in response to upstream signals such as CSF3, TNF, IL8, CXCL12, F2, and FPR1. \nReviewed during Jamboree2014\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
186
Number Edges
629
Number Components
17
Network Density
0.0182796
Average Degree
3.38172
Number Citations
357
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 59%
Epithelial Innate Immune Activation-2.0-Rn v2.0 45%
Dendritic Cell Signaling-2.0-Rn v2.0 44%
Tissue Damage-2.0-Rn v2.0 44%
Immune Regulation of Tissue Repair-2.0-Rn v2.0 42%
Macrophage Signaling-2.0-Rn v2.0 40%
Neutrophil Signaling-2.0-Hs v2.0 37%
Epithelial Mucus Hypersecretion-2.0-Rn v2.0 36%
Neutrophil Signaling-2.0-Mm v2.0 35%
NK Signaling-2.0-Rn v2.0 35%

Sample Edges

act(complex(SCOMP:"IkappaB Kinase Complex"), ma(kin)) directlyIncreases p(HGNC:NFKBIA, pmod(Ph, Ser, 36))

In the classical NF-{kappa}B signaling pathway, IKK{beta} is both necessary and sufficient for phosphorylation of I{kappa}B{alpha} on Ser 32 and Ser 36, and I{kappa}B{beta} on Ser 19 and Ser 23. PubMed:15371334

act(complex(SCOMP:"IkappaB Kinase Complex"), ma(kin)) directlyIncreases p(HGNC:NFKBIA, pmod(Ph, Ser, 36))

The IKK immunoprecipitates from thrombin-treated cells showed increased phosphorylation of GST-IkBalpha compared with the immunoprecipitates from control cells (Fig. 6), indicating the activation of IKK by thrombin. PubMed:15843586

Sample Nodes

p(SFAM:"MAPK p38 Family")

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

a(CHEBI:lipopolysaccharide)

In-Edges: 277 | Out-Edges: 1541 | Explore Neighborhood | Download JSON

p(RGD:Ccl3)

In-Edges: 11 | Out-Edges: 19 | Explore Neighborhood | Download JSON

a(CHEBI:acetylcholine)

In-Edges: 81 | Out-Edges: 91 | Explore Neighborhood | Download JSON

a(CHEBI:"reactive oxygen species")

In-Edges: 1023 | Out-Edges: 827 | Classes: 1 | Children: 4 | 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.