Fig. 5: MIST1 is a putative transcription factor of TRIB3. | Cell Death & Disease

Fig. 5: MIST1 is a putative transcription factor of TRIB3.

From: MIST1 regulates endoplasmic reticulum stress-induced hepatic apoptosis as a candidate marker of fatty liver disease progression

Fig. 5

A Distribution of MIST1 binding frequency around transcription start sites. B MIST1 target candidate genes were identified as an intersection of the MIST1-bound genes, MIST1-positive correlated genes, and genes with reduced expression in Mist1KO mice. C ChIP-seq binding peaks of MIST1 around target genes. D Scatterplot of normalized expression of candidate MIST1 target genes of CCl4-treated and wild-type (WT) mice. E Western blot for TRIB3 and ATF4 in liver specimens from CCl4-treated control (WT) and Mist1KO mice. F Relative luciferase activity of the TRIB3 promoter with tunicamycin-induced ER stress in HepG2 cells with MIST1 knockdown and control cells; n = 3 per each group. G, H Relative mRNA and protein expression of ER stress-related molecules in HepG2 cells cultured with (+) or without (−) tunicamycin, MIST1 siRNA, and/or control siRNA; n = 3 per each group. I Immunocytochemistry of TRIB3 in control and siRNA-treated HepG2 cells. J TRIB3-positive cells in tunicamycin-treated HepG2 cells over time; n = 3 per each group. All data are presented as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001 (unpaired Student’s t-test or one-way ANOVA with Dunnett’s multiple comparisons).

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