Fig. 3: Phosphorylation signatures are independent of kinase activity by DKO, IR, K1030R, ∆CT, and JMO cells. | Nature Communications

Fig. 3: Phosphorylation signatures are independent of kinase activity by DKO, IR, K1030R, ∆CT, and JMO cells.

From: Unique ligand and kinase-independent roles of the insulin receptor in regulation of cell cycle, senescence and apoptosis

Fig. 3

a Quantitation of exemplary phosphosites in the enriched pathways (in Supplementary Fig. 3a) in the High-Phos in IR-ICD cluster. b REACTOME pathway enrichment analysis of phosphosites in the Low-Phos in IR-ICD cluster. The functional enrichment analysis was tested by the STRING database, where FDRs were calculated using the Benjamini–Hochberg procedure. c Quantification of exemplary phosphosites of Cell Cycle and Mitosis pathway in the Low-Phos in IR-ICD cluster. d, e Representation of the ATM signaling pathway (d) and quantification of some important phosphosites in the pathway (e). f, g Representation of the “SUMO E3 ligases SUMOylate target proteins” pathway (f) and quantification of some important phosphosites in the pathway (g). h Quantification of exemplary phosphosites associated with membrane trafficking in the Low-Phos in IR-ICD cluster. Data in (a, c, e, g, h) are means ± SEM of phosphosite intensity values (×104). P-values vs DKO (combined both basal and insulin for comparisons), one-way ANOVA followed by Dunnett’s multiple comparisons test (n = 3–6).

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