Figure 5. Proteomic and transcriptomic analyses of GPR52-null breast cell lines and resected breast tumors.

(A-B) Differentially expressed proteins in the GPR52 KO cell lines with P-value <0.05, FDR<0.05, and fold-change greater than two were imported into IPA for each of the three cell lines. The common predicted upstream regulators (A) and top diseases and functions (B) with a P-value <0.05 are depicted. Pathways are marked N/A (not-applicable) if the z-score is not determined. (C) Normalized expression of GPR52 in TCGA-BRCA cohort resected breast tumors D) Graphical representation of proportion of patients with undetected (black) and detected (grey) GPR52 mRNA in resected breast tumors. E) DEGs in GPR52 KO MDA-MB-468 cells and the GPR52-null TCGA-BRCA cohort with P-value <0.05, FDR<0.05, and fold-change greater than two were imported into IPA for pathway analysis. Upstream regulators predicted to be responsible for the DEGs observed in both datasets with a P-value <0.05 are depicted. (F-H) Phosphoproteomic analysis was conducted on the groups outlined in Fig 5A. KEA3 software was used to rank kinases that were predicted to be active in the vector control (F) and GPR52 KO (G) cell lines. H) The difference in rank of kinases which were reported for both the GPR52 KO and vector control groups.