Provenance

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charles.hoyt@scai.fraunhofer.de at 2018-04-03 15:17:20
Authors
Causal Biological Networks Database
Contact
CausalBiologicalNetworks.RD@pmi.com
Description
The Mast Cell Activation network depicts the causal mechanisms that occur in mast cells following exposure to antigen and IgE/Fc receptor ligation and stimulation with IL4 and KITLG. The network also includes elements involved in the resulting downstream signal transduction (e.g. Lyn, MEK and MAPK1, and LTC4) that lead to mast cell activation and subsequent release of several cytokines and other factors such as histamine and prostaglandin D2.
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
46
Number Edges
93
Number Components
4
Network Density
0.0449275
Average Degree
2.02174
Number Citations
67
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 54%
Mast cell activation-2.0-Hs v2.0 41%
Mast cell activation-2.0-Mm v2.0 41%
Epithelial Innate Immune Activation-2.0-Rn v2.0 33%
Selventa Protein Families Definitions v20150611 28%
B-cell Signaling-2.0-Rn v2.0 26%
Epithelial Mucus Hypersecretion-2.0-Rn v2.0 20%
Immune Regulation of Tissue Repair-2.0-Rn v2.0 20%
Neutrophil Signaling-2.0-Rn v2.0 20%
Th1-Th2 Signaling-2.0-Rn v2.0 20%

Sample Edges

a(SCHEM:Calcium) directlyIncreases act(p(SFAM:"PRKC Family"), ma(kin))

Here we demonstrate that functional uncoupling between CD38 and Cx43 in CD38-transfected 3T3 murine fibroblasts is paralleled by decreased [Ca(2+)](i) levels as a result of reduced intracellular conversion of NAD(+) to cADPR PubMed:11602597

a(SCHEM:"Smoke, cigarette") increases p(HGNC:CXCL8)

In results, read the section "cAMP signalling attenuates CSE-induced IL-8 release from human ASM cells": "The CSE-induced IL-8 release was almost fully inhibited by co-treatment with the β2-agonist fenoterol (0.1 and 1 µM; P<0.001 both; Fig. 1A)..." Other:22363678

act(p(SFAM:"PLA2 Family"), ma(cat)) increases a(CHEBI:"arachidonic acid")

As shown in Table I⇓, endogenous sPLA2 induced an increase in cPLA2 activity in BMMC. Furthermore, endogenous sPLA2 released AA from BMMC (Table I⇓). In contrast, levels of other unsaturated fatty acids (LA and OA) were not influenced when BMMC were incubated with partially purified endogenous sPLA2 (Table I⇓). Other:10946309

act(p(SFAM:"PLA2 Family"), ma(cat)) increases a(CHEBI:"arachidonic acid")

ANG II has been shown to phosphorylate and activate PLA2, which leads to production of arachidonic acid (AA) and its metabolites. The derivatives of AA function in maintaining vascular tone and in VSMC NAD(P)H oxidation (63). The cyclooxygenase-derived prostaglandins, such as PGI2 and PGE2 are vasodilatory, and are counteracted by PGH2 and thromboxane A2, which promote vasoconstriction. PubMed:16870827

act(p(SFAM:"PLA2 Family"), ma(cat)) increases a(CHEBI:"arachidonic acid")

Moreover, coupling of heterotrimeric G proteins containing G alpha i3 C S to the m2 mAChR resulted in pertussis toxin-resistant inhibition of adenylyl cyclase, stimulation of phospholipase C-induced intracellular Ca2+ release, and phospholipase A2-mediated arachidonic acid release. Therefore, these studies provide conclusive evidence that heterotrimeric G proteins containing just G alpha i3 can regulate multiple effector enzymes within the same cell type. PubMed:7961942

Sample Nodes

p(HGNC:CXCL8)

In-Edges: 334 | Out-Edges: 142 | Explore Neighborhood | Download JSON

p(RGD:Mapk1)

In-Edges: 233 | Out-Edges: 67 | Explore Neighborhood | Download JSON

p(RGD:Il10)

In-Edges: 26 | Out-Edges: 10 | Explore Neighborhood | Download JSON

p(RGD:Syk)

In-Edges: 14 | Out-Edges: 6 | 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.