Skip to main content
Fig. 3 | Cell Communication and Signaling

Fig. 3

From: Large-scale phosphoproteomics reveals activation of the MAPK/GADD45β/P38 axis and cell cycle inhibition in response to BMP9 and BMP10 stimulation in endothelial cells

Fig. 3

Bioinformatic analyses of the phosphoproteomic changes in response to BMP9 and BMP10 in HUVECs. A Gene ontology on biological processes (≥ 1.5-fold enrichment, P ≤ 0.05) was conducted using Metascape, based on DPS gene list for BMP9 and BMP10. Only the common clusters between BMP9 and BMP10 are shown, with the top 5 terms for each cluster. The full list of clusters and their corresponding terms are outlined in Table S5. B Scatter Plot of KinSwing scores of kinases whose activities were predicted to be significantly changed in response to BMP9 and/or BMP10. Positive swing scores indicate predicted activation of a kinases, while negative scores indicate predicted under-activation of a kinase. C Post translational modification signature enrichment analysis (PTM-SEA) performed using PTMsigDB. Bar plot represents the top signatures enriched in BMP9 and/or BMP10 stimulated HUVECs compared to NS cells, ordered in terms of average FDR from both comparisons. Each bar represents a signature (kinase or perturbation). PERT, Perturbation; PSP, Phosphositeplus. D Hypothetical signaling framework in response to BMP9 and BMP10 based on phosphoproteomic analysis and literature-based data. Phosphorylated residues with increased abundance in response to BMP9 and BMP10 are marked in red, while those displaying decreased abundance are marked in blue. Bold numbers represents phosphosites with low-throughput papers derived from PhosphositePlus. Grey curved rectangles represent BMP9 and BMP10-derived differentially phosphorylated proteins, white ones are from literature. Orange curved rectangles: bioinformatic-predicted kinases (KinSwing or PTM-SEA). Solid orange rectangles: GO-BP analysis-identified processes, white from literature. Dashed lines signify uncharacterized mechanisms

Back to article page