HowToExplorePathways
ChiBE can act as the front-face software for Pathway Commons (PC) database. Even though there are several alternative ways to explore pathways in PC, here we provide an example of one method that we think is most useful. This method starts with sending a graph query to PC in SIF format (simplified binary view). The user then can select relations in this simple view and ask for details. Let's do it on BCL2L1 protein.
Step 1: Graph querying in SIF
From menu, do "Query --> Pathway Commons (in SIF) --> Neighborhood...".
This will show the parameters dialog for PC SIF neighborhood query.
Enter BCL2L1 in the gene symbols box, select "Both" as the stream direction, and push the "Select interaction type" button. Another dialog will open.
Select the SIF relation types "controls-state-change-of" for directed signaling, and "in-complex-with" for complex membership relations. Refer to this page for understanding SIF relation types. Press "OK".
The final query dialog should look like this:
Push "Execute". This should bring the below graph.
This is an overview simplified (SIF format) neighborhood of BCL2L1. Directed blue relations are "controls-state-change-of", and undirected relations are "in-complex-with".
Step 2: Navigating to details
To further navigate to the details in this simplified view, user can right click on any edge and select "Detailed View" on the popup menu. This is straightforward for the TP53 -> BCL2L1 relation, just right-click on that edge. But what if we want to go to the details of AKT1 -> BCL2L1 relation? AKT1 is in the box on the left top. If we right-click on its relation, we will see details for all the genes in that box, which is not very bad, but it can be too much. To limit the details to AKT1, users need to select both the AKT1 node and the relation (press CTRL for multiple select) and then right click on the relation when AKT1 is selected. This operation should bring the below detailed graph.
Here we understand that the nature of signaling from AKT1 to BCL2L1 is phosphorylation of the inhibitory binding partner of BCL2L1 by AKT1, which makes the complex dissociate and activate BCL2L1.