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Fig. 4 | Cancer & Metabolism

Fig. 4

From: Normalization of hepatic ChREBP activity does not protect against liver disease progression in a mouse model for Glycogen Storage Disease type Ia

Fig. 4

Prolonged ChREBP knockdown in L-G6pc−/− mice induces DNA damage, cellular senescence, and hepatocyte dedifferentiation. Data after 21–26 days of shChREBP/L-G6pc−/− and n = 8/group, unless stated otherwise. (A) CIN marker genes, spontaneous chromosome bridge incidence (with representative image), (B) Hepatocyte ploidy, (C) γH2Ax positivity (n = 4–8/group) and PARP protein expression, (D) Cgas and senescence-associated genes and p21 protein, and (E) HNF4A-related genes. (F) Reporter transcription factors analysis (after 10 days of shChREBP/L-G6pc−/−). (G-H) Hepatocyte differentiation marker genes (n = 7–8). Blots/Ponceau S: Fig. S4B-C. A/C-E/G-H: median ± interquartile range. B: box-and-whisker plots. A-E/G-H: Kruskal Wallis H-test, post-hoc Conover pairwise comparisons, *p < 0.05, **p < 0.01, ***p < 0.001 vs shSCR/L-G6pc+/+; ^ vs shChREBP/L-G6pc+/+; # vs shSCR/L-G6pc−/−

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