Upload at 2018-04-03 15:19:43
Causal Biological Networks Database
The Xenobiotic Metabolism Response depicts the causal mechanisms that are involved in xenobiotic metabolism response, including the various environmental stressors and signaling components that regulate AHR and cytochrome p450 enzymes.\u003c/p\u003e\n\u003ch2\u003eJamboree Review Focus\u003c/h2\u003e\n\u003cp\u003eIdentify additional lung-relevant phase II (GST) and phase III (SLC) mechanisms that study protein/activity relationships as opposed to gene expression. Expand phase I regulation beyond AHR to include other transcription factors relevant for airway epithelia such as CAR, LXR and PXR. Reviewed during Jamboree2014
Please cite: - - 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
Number Nodes
Number Edges
Number Components
Network Density
Average Degree
Number Citations
Number BEL Errors

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
Xenobiotic Metabolism Response-2.0-Hs v2.0 44%
Xenobiotic Metabolism Response-2.0-Mm v2.0 44%
BEL Framework Large Corpus Document v20170611 29%
Oxidative Stress-2.0-Rn v2.0 23%
Selventa Protein Families Definitions v20150611 13%
Oxidative Stress-2.0-Hs v2.0 12%
Oxidative Stress-2.0-Mm v2.0 12%
BEL Framework Small Corpus Document v20150611 10%
NFE2L2 Signaling-2.0-Rn v2.0 10%
Exported from Bel-c 15.bel v2.0.4 7%

Sample Edges

a(CHEBI:phenobarbital) decreases act(p(SFAM:"GST Family"), ma(cat))

Subcellular levels of different isoenzymes of glutathione S-transferases (GSTs) and their catalytic activities in rat liver, lung and brain tissues were compared following treatment with phenobarbital (PB), -naphthoflavone (BNF) ............4 days of PB and 10 days of BNF treatments, respectively. The longer duration of treatments had a suppressive effect on the GST activity, particularly in the mitochondrial and microsomal fractions. PubMed:9664123

a(CHEBI:phenobarbital) increases p(SFAM:"GST Family")

Subcellular levels of different isoenzymes of glutathione S-transferases (GSTs) and their catalytic activities in rat liver, lung and brain tissues were compared following treatment with phenobarbital (PB), -naphthoflavone (BNF) and dexamethasone (DEX)........PB and BNF treatments markedly induced the amount of GST proteins in all the tissues studied with the maximum induction in the cytosol after 4 days of PB and 10 days of BNF treatments, respectively PubMed:9664123

a(CHEBI:"reactive oxygen species") increases a(CHEBI:"4-hydroxynon-2-enal")

Reactive oxygen species (ROS), either directly or via the formation of lipid peroxidation products, such as 4-hydroxy-2-nonenal, acrolein PubMed:15313424

a(SCHEM:"Diesel exhaust particles") increases a(CHEBI:"reactive oxygen species")

Using fluorescent probes, we detected ROS production in bronchial and nasal epithelial cells exposed to native DEP PubMed:12730081

Sample Nodes


In-Edges: 8 | Out-Edges: 91 | Classes: 4 | Explore Neighborhood | Download JSON


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:Akt1, pmod(Ph))

In-Edges: 33 | Out-Edges: 10 | Explore Neighborhood | Download JSON


In-Edges: 45 | Out-Edges: 398 | Explore Neighborhood | Download JSON


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