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. 2023 Sep 30;14:6119. doi: 10.1038/s41467-023-41860-z

Fig. 2. PAX4 knockdown and knockout impair glucose-stimulated insulin-secretion and reduce insulin content in human EndoC-βH1 cells.

Fig. 2

a Experimental design for PAX4 knockdown approaches using siRNA and shRNA in EndoC-βH1 cells. b PAX4 gene expression following transient transfection of siPAX4 and non-targeting (siNT) control in EndoC-βH1 cells. c Glucose-stimulated insulin secretion of 2.8 mM and 16.7 mM glucose in siNT and siPAX4 EndoC-βH1 cells, normalized to total protein then to 2.8 mM glucose. d PAX4 gene expression in PAX4-knockdown (shPAX4) and control (shScramble) EndoC-βH1 cells following six passages of antibiotic selection (n = 6). e Glucose-stimulated insulin secretion assay comparing shPAX4 and shScramble EndoC-βH1 cells, normalized to total DNA and then to 2.8 mM glucose (n = 3). f Relative fold change of total insulin content in shPAX4 and shScramble EndoC-βH1 cells, normalized to total DNA content (n = 3). g INS transcript expression in shScramble and shPAX4 EndoC-βH1 cells (n = 8). h GCG transcript expression in shScramble and shPAX4 EndoC-βH1 cells (n = 6). i ARX transcript expression in shScramble and shPAX4 EndoC-βH1 cells (n = 6). Data are presented as mean ± SEM. Each data point represents one independent experiment. Statistical analysis of two samples was performed by paired t test or a two-way ANOVA for comparison of multiple groups. *p < 0.05, ***p < 0.001, ****p < 0.0001. Source data is provided in the Source Data File.