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charles.hoyt@scai.fraunhofer.de at 2018-04-03 15:17:34
Authors
Causal Biological Networks Database
Contact
CausalBiologicalNetworks.RD@pmi.com
Description
The NFE2L2 Signaling network depicts the causal mechanisms that are involved in transcriptional activation of NFE2L2 (central mediator of the cellular oxidative stress response), its interaction with MAF proteins, and its downstream target genes such as ATF4, GCLC, NQO1, and PRDX1.\u003c/p\u003e\n\u003ch2\u003eJamboree Review Focus\u003c/h2\u003e\n\u003cp\u003eInteraction of NFE2L2 with MAF proteins. Reviewed during Jamboree2014
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
84
Number Edges
149
Number Components
14
Network Density
0.0213712
Average Degree
1.77381
Number Citations
59
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 43%
Oxidative Stress-2.0-Rn v2.0 40%
Selventa Protein Families Definitions v20150611 31%
NFE2L2 Signaling-2.0-Hs v2.0 24%
NFE2L2 Signaling-2.0-Mm v2.0 24%
BEL Framework Small Corpus Document v20150611 14%
Fibrosis-2.0-Rn v2.0 14%
Apoptosis-2.0-Rn v2.0 13%
Dendritic Cell Signaling-2.0-Rn v2.0 13%
Epithelial Mucus Hypersecretion-2.0-Rn v2.0 13%

Sample Edges

p(HGNC:NFE2L2, pmod(Ph, Ser, 40)) directlyIncreases tloc(p(HGNC:NFE2L2), fromLoc(GOCC:cytoplasm), toLoc(GOCC:nucleus))

In related experiments, the majority of the Nrf2S40-phosphorylated protein was found localized in the nucleus (Fig. 5D, lower panel). PubMed:19920073

p(HGNC:NFE2L2, pmod(Ph, Ser, 40)) directlyIncreases tloc(p(HGNC:NFE2L2), fromLoc(GOCC:cytoplasm), toLoc(GOCC:nucleus))

## from full text ## coexpression of the GFP fusion protein with Keap1 and the Nrf2(S40E) mutant, in which Ser40 was replaced with Glu to mimic constitutive phosphorylation, showed nuclear accumulation in the absence of stimulus (Fig. 4, B and C), PubMed:12700136

bp(GOBP:"response to oxidative stress") increases tloc(p(MGI:Keap1), fromLoc(GOCC:cytoplasm), toLoc(GOCC:nucleus))

However, after oxidative stress induced by a variety of agents, Keap1 redistributed and accumulated in the nucleus (Fig. 1A and D). This redistribution was not unique to NIH 3T3 fibroblasts. In the human hepatoblastoma cell line HepG2 (Fig. 1B), as well as in Cos7 fibroblasts (Fig. 1C), endogenous Keap1 also accumulated in the nucleus after DEM treatment. PubMed:15899855

a(CHEBI:curcumin) increases tloc(p(HGNC:NFE2L2), fromLoc(GOCC:cytoplasm), toLoc(GOCC:nucleus))

Dietary curcumin led to increase in NF-E2-related factor-2 (Nrf2) protein levels and enhanced its nuclear translocation in liver and lungs of mice as compared with controls. PubMed:18321868

Sample Nodes

p(SFAM:"MAPK p38 Family")

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

a(CHEBI:curcumin)

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

p(RGD:Mapk3)

In-Edges: 173 | Out-Edges: 60 | Explore Neighborhood | Download JSON

p(RGD:Mapk1)

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

p(RGD:Akt1)

In-Edges: 67 | Out-Edges: 59 | 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.