Fig. 2: KSTAR applied to diverse cell models of kinase activation and inhibition.
From: KSTAR: An algorithm to predict patient-specific kinase activities from phosphoproteomic data
Full KSTAR results for data in this figure available in Supplementary Note 3). Panel titles give the reference for the publication study of the phosphoproteomic data. All KSTAR predictions use the same legend for score size and significance as given above panel A. a Predicted activation patterns of HMEC cell lines (P for parental 184A1 and 24H for HER2 overexpressing 184A1) in response to EGF and HRG stimulation. b Predicted activation patterns of TCR stimulation in Jurkat cells shows early and robust activation of TCR-specific kinases (this figure is in seconds). c Predicted kinase patterns in response to inhibition of BCR-ABL inhibition by dasatinib in K562 cells with a detailed plot of significance changes for the ABL family kinases demonstrating a decrease, but continued activity of the oncogene. Kinase activity decreases in receptor tyrosine kinases (RTKs) correspond with findings of the original publication34 as do changes in the off-target interactions with Src family kinases (SFKs). d AKT inhibition by five inhibitors, all competitive ATP inhibitors, except MK-2206 an allosteric inhibitor of AKT, demonstrate robust inhibition of all AKT homologs and interesting increases in CSNK2A1. e Vemurafenib treatment, targeting the BRAFV600E mutation found in Colo205 colorectal cancer cells, but not the HCT116 cell line, demonstrates a decrease in MAPK activity specific to BRAF mutation, although still statistically significant MAPK activity. Source data are provided with this paper.
