Fig. 5: Differential signaling by JM-a- and JM-b-like RTKs.
From: An extracellular receptor tyrosine kinase motif orchestrating intracellular STAT activation
a, b Phosphorylation of STAT5a and STAT5b (on Y694/699) in HC11 cells after stimulating endogenous ErbB4 JM-a, FGFR1/FGFR2, PDGFRA, INSR or EGFR/ErbB2 with their respective ligands NRG-1, FGF-3, PDGF-AA, insulin or EGF. Panel b depicts densitometric quantification of independent experiments (n = 3-6). Two-tailed Mann–Whiney U (EGF, STAT5b) or T-test (rest). c Cell death of serum-starved HC11 cells cultured in the presence of the indicated siRNAs and either NRG-1 or insulin. Cell death was measured by analyzing cellular morphology with IncuCyte live cell imaging. Pooled results from n = 17 wells (mean ± SEM) from 3 independent experiments. Two-tailed Mann–Whitney U-test (from the 24 h time point). d Clusterization of JM-a-like and JM-b-like RTKs based on their mass spectrometry-derived interactomes. AP-MS, affinity purification coupled to mass spectrometry; BioID, proximity-dependent biotin identification. The P-values were estimated from the simulated cumulative distribution function of random categorization. In the boxplots the line represents the median, the box the interquartile range and whiskers the whole range of values. Source data are provided as a Source Data file.
