Provenance

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miguel.angel.ibarra.arellano@scai-extern.fraunhofer.de at 2018-09-11 15:35:39
Authors
Miguel A. Ibarra-Arellano
Contact
miguel.angel.ibarra.arellano@scai-extern.fraunhofer.de
Description
colorectal cancer Knowledge Assembly with drug associations.
License
Fraunhofer SCAI copyright
Copyright
Copyright (c) 2018, SCAI. All Rights Reserved.
Number Nodes
122
Number Edges
254
Number Components
3
Network Density
0.0172063
Average Degree
2.08197
Number Citations
39
Number BEL Errors
192

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
CRC_combined.bel v1.0 99%
CRC_combined v1.1 99%
Colorectal Cancer Model v2.0.6 99%
BEL Framework Large Corpus Document v20170611 54%
BEL Framework Small Corpus Document v20150611 34%
fc34ba14-6a91-4142-811b-cacad7ad64ce_3150.txt v1.0 33%
Selventa Protein Families Definitions v20150611 18%
BEL Framework Example 3 Document v2015611 14%
Notch-2.0-Hs v2.0 12%
Test1 v1.1.1 12%

Sample Edges

deg(p(HGNC:PLAU)) decreases path(MESHD:"Neoplasm Invasiveness")

The enhanced invasiveness of gelsolin-overexpressing cells was attenuated by treatment with function-blocking antibodies to either uPA or its receptor uPAR, indicating that uPA/uPAR activity is crucial for gelsolin-dependent invasion. PubMed:22927998

Annotations
NCBI Taxonomy Ids
9606
Experimental Factor Ontology (EFO)
Caco-2
Disease Ontology (DO)
colorectal cancer
MeSH
Neoplasms

path(MESHD:Melanoma) association p(HGNC:BRAF)

Signatures for BRAF oncogene have been revealed in melanoma. PubMed:22515520

Annotations
NCBI Taxonomy Ids
9606
Experimental Factor Ontology (EFO)
SW480
Disease Ontology (DO)
colorectal cancer
MeSH
Neoplasms

p(HGNC:HEXA) directlyDecreases act(p(HGNC:HEXA), ma(cat))

The unglycosylated alpha-subunit, resulting from genetic alteration of all three glycosylation sites or synthesis of the wild-type protein in the presence of tunicamycin, was catalytically inactive. It was found to be improperly folded into an insoluble aggregate, linked through inappropriate disulfide bonds. The unglycosylated protein was trapped in the lumen of the endoplasmic reticulum and was found in a complex with the Ig heavy chain-binding protein, BiP. The properties of the nonglycosylated, misfolded alpha-subunit were similar to some mutant alpha-subunits in Tay-Sachs disease patients. PubMed:1533633

Annotations
NCBI Taxonomy Ids
9606
Experimental Factor Ontology (EFO)
COS-1 cell
Disease Ontology (DO)
colorectal cancer
MeSH
Tay-Sachs Disease

Sample Nodes

p(HGNC:AKT1)

In-Edges: 267 | Out-Edges: 239 | Explore Neighborhood | Download JSON

p(HGNC:IL4)

In-Edges: 77 | Out-Edges: 196 | Explore Neighborhood | Download JSON

a(CHEBI:"reactive oxygen species")

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

bp(GOBP:"apoptotic process")

In-Edges: 916 | Out-Edges: 234 | Classes: 1 | Children: 2 | Explore Neighborhood | Download JSON

bp(GOBP:"Wnt signaling pathway")

In-Edges: 156 | Out-Edges: 113 | Children: 5 | 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.