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. 2024 Oct 11;476(12):1895–1911. doi: 10.1007/s00424-024-03027-7

Fig. 1.

Fig. 1

Ca2+ homeostasis in EA.hy926 cells with SphK1 knockdown, cell line 1 (SphK1-KD1). A Agonist-induced [Ca2+]i increases in the presence or absence of 1 mM extracellular Ca2+. Shown is a representative time course of [Ca2+]i after stimulation with histamine, and peak [Ca2+]i increases after stimulation with 100 µM ATP, 100 µM carbachol (Carb), 100 µM histamine (Hist), 1 µM LPA, or 1 µM S1P (means ± SEM from n = 3–5 independent experiments for each agonist). B Basal [Ca2+]i in the presence of 1 mM extracellular Ca2+ (data taken from the measurements shown in A; means ± SEM; n = 20). Data in A and B were analyzed by Student’s t-test (*p < 0.05; **p < 0.01; ****p < 0.0001). C Histamine-induced production of tritiated inositol phosphates ([3H]IPx) in cells labeled with [3H]inositol (means ± SEM; n = 4 independent experiments). Responses to histamine (100 µM) were analyzed for each cell line by one-sample t-test (*p < 0.05; ***p < 0.001) and compared between cell lines by Student’s t-test (n.s., not significant). D Representative time course of [Ca2+]i after addition of thapsigargin (selected from ~ 20 measurements per cell line)