Provenance

Upload
charles.hoyt@scai.fraunhofer.de at 2018-04-03 15:18:15
Authors
Causal Biological Networks Database
Contact
CausalBiologicalNetworks.RD@pmi.com
Description
The Osmotic Stress network depicts the causal mechanisms that regulate osmotic stress including NFAT5, aquaporins, and CFTR pathways downstream of the hyperosmotic response.
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
60
Number Edges
107
Number Components
23
Network Density
0.030226
Average Degree
1.78333
Number Citations
77
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 63%
Osmotic Stress-2.0-Hs v2.0 42%
Osmotic Stress-2.0-Mm v2.0 41%
Oxidative Stress-2.0-Rn v2.0 37%
Epithelial Mucus Hypersecretion-2.0-Rn v2.0 36%
Growth Factor-2.0-Rn v2.0 29%
Epithelial Innate Immune Activation-2.0-Rn v2.0 27%
Hypoxic Stress-2.0-Rn v2.0 25%
Senescence-2.0-Rn v2.0 24%
Neutrophil Signaling-2.0-Rn v2.0 22%

Sample Edges

act(complex(SCOMP:"AMP Activated Protein Kinase Complex"), ma(kin)) directlyIncreases p(HGNC:CFTR, pmod(Ph, Ser, 768))

AMPK phosphorylates CFTR in vitro at two essential serines (Ser(737) and Ser(768)) in the R domain, PubMed:19095655

act(complex(SCOMP:"AMP Activated Protein Kinase Complex"), ma(kin)) directlyIncreases p(HGNC:CFTR, pmod(Ph, Ser, 768))

AMPK-dependent CFTR phosphorylation renders the channel resistant to activation by PKA and PKC without preventing phosphorylation by these kinases. We found that Ser768, a CFTR R domain residue considered to be an inhibitory PKA site, is the dominant site of AMPK phosphorylation in vitro. Ser-to-Ala mutation at this site enhanced baseline CFTR activity and rendered CFTR resistant to inhibition by AMPK PubMed:19419994

bp(GOBP:"response to osmotic stress") association bp(GOBP:"nucleotide-excision repair, DNA damage recognition")

Acute elevation of NaCl causes DNA double-strand breaks in cell culture, and the DNA breaks persist even after the cells are adapted to high NaCl. Other:14983007

a(CHEBI:aldosterone) increases act(complex(SCOMP:"NADPH Oxidase Complex"), ma(cat))

Addition of aldosterone to neonatal rat cardiac myocytes caused the activation of NADPH oxidase and intracellular ROS production in a dose-dependent manner (10-(9)-10(-7) mol/L). NADPH oxidase activation was evident as soon as 5 min after aldosterone treatment. PubMed:18360057

Sample Nodes

a(CHEBI:"reactive oxygen species")

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

p(RGD:Nfkbia)

In-Edges: 129 | Out-Edges: 96 | Explore Neighborhood | Download JSON

a(CHEBI:aldosterone)

In-Edges: 14 | Out-Edges: 120 | Explore Neighborhood | Download JSON

p(RGD:Mapk14)

In-Edges: 44 | Out-Edges: 26 | Explore Neighborhood | Download JSON

p(RGD:Erbb3)

In-Edges: 9 | Out-Edges: 1 | 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.