Extended Data Fig. 2: FBP1 is transcriptionally activated by TP53.
From: FBP1 controls liver cancer evolution from senescent MASH hepatocytes
a, Schematic of the FBP1 gene 5′ and 3′ regions, showing putative TP53 binding sites and amplicons used for ChIP-qPCR. b, Relative amounts of Fbp1, p21 and Tp53 mRNAs in primary hepatocytes from Tp53F/F and Tp53ΔHep mice. c, IB demonstrating shRNA mediated TP53 knockdown and FBP1 downregulation in human hepatocytes. d, Relative FBP1, p21CIP1 and TP53 mRNA amounts in human primary hepatocytes stably transfected with shCtrl, shTP53#1 and shTP53#2. e, f, Relative FBP1, p21CIP1 and TP53 mRNAs in HepG2 (e) and SK-HEP-1 (f) cells stably transfected with shCtrl, shTP53#1 and shTP53#2. IB showing TP53 knockdown in SK-HEP-1 cells is on the right. g-j, ChIP-qPCR probing TP53 recruitment to the Fbp1 gene in Tp53F/F and Tp53ΔHep livers (g), SK-HEP-1 (h), HepG2 (i) and Huh7 (j) cells (n = 3 BR each). k, Relative FBP1, p21CIP1and TP53 mRNAs (left, middle) and proteins (right) in NCD and HFD and CSD and HFrD fed Tp53F/F and Tp53ΔHep mice (16 weeks; n = 5 biological replicates/BR). Quantification of relative normalized protein amounts is shown below each strip. Data in b, d, e, f, g, h, i, j and k are mean ± SEM. Statistical significance determined by two-sided unpaired t-test or Mann–Whitney U test (b, g, h, i and j) and one-way ANOVA with Tukey post-hoc tests or Kruskal–Wallis test with Dunn post-hoc tests (d, e, f and k) based on data normality distribution. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, ns, not significant.
