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Several studies evaluate the topology of disease genes in global interaction networks and have found that related disease genes are more likely to interact, and that cancer genes are associated with high network centrality [ 10- 12].
The availability of robust datasets derived from the primary literature and HTP studies has enabled graphical representation and interrogation of global interaction networks, and the prediction of gene and network function [ 11].
Our goal is to mine for cancer-associated subgraphs from the global interaction networks; however, PPI data that are specific to a cancer tumor do not exist in the public domain.
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We identify 5 transcription factors in the global interaction network: FOS, FOXO1, NFAT5, NFKB1 and TP53.
TP53 has a degree of 10 in both Module 10 and the global interaction network.
Using degree distribution to find hubs, this network has five protein hubs (AKT2, RAC1,2, TP53, GNAI3 and CROP) with out-degree greater than 3. AKT2, RAC1,2 and TP53 are also hubs in the global interaction network (see above).
NFAT5 links Modules 1 and 9. Despite the fact that Module 1 is relatively large (92 nodes), in the global interaction network NFAT5 has a degree of only 3, so it is not a highly connected node.
The heterodimer_association of NFKBIA and NFKB1 is included in a large cycle in Module 2. In the global interaction network, genes that are directly connected to NFKB1 (inclusive) have small degree (<4) and therefore are not hubs.
The resulting network is the global interaction network (GLIN).
Additional file 6: Topological parameters of the global interaction network (GLIN) and other three viruses networks.
The resulting global interaction network consisted of 10,882 nodes and 70,385 interactions.
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