Figure 2: FGF21 disruption does not rescue the neonatal growth defect of ksr2−/− mice. | Scientific Reports

Figure 2: FGF21 disruption does not rescue the neonatal growth defect of ksr2−/− mice.

From: Cell non-autonomous regulation of hepatic IGF-1 and neonatal growth by Kinase Suppressor of Ras 2 (KSR2)

Figure 2

(a) Serum FGF21 levels in PN6 and PN17 WT and ksr2−/− littermates (n = 6–9 per group). (b) Hepatic FGF21 mRNA in PN6 and PN17 WT and ksr2−/− littermates (n = 6, 6, 10, and 9 respectively). Levels of WT mice at PN6 were set to 1 and rps18 was used as an internal control. (c) Growth curves of PN6 to PN17 WT, ksr2−/−, fgf21−/−, and fgf21−/− ksr2−/− male and female mice (n = 10–15 per group, two- way ANOVA with repeated measures Bonferoni post hoc test was used). (d–f) Nose-to-anus length (d), bone mineral density (e), and bone mineral content (f) of male fgf21−/− and fgf21−/− ksr2−/− mice at 5 weeks of age (n = 8 per group). (g) Serum IGF-1 levels from male and female mice of the indicated genotypes at PN6 (n = 9, 7, 5, and 7 respectively) and PN17 (n = 12, 8, 9, and 12, respectively). (h) Hepatic IGF-1 mRNA levels from male and female mice of the indicated genotypes at PN6 (n = 4–6 per group) and PN17 (n = 7 per group). For comparison, IGF-1 levels of WT at PN6 were set to 1 and rps18 was used as an internal control. Data are shown as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001

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