Figure 1: ksr2^−/− mice exhibit low serum IGF-1 and neonatal growth defects.

(a) PN17 WT and ksr2^−/− mice littermates. (b) Growth curves of WT and ksr2^−/− mice from PN6 to PN17 (n = 11 WT group, n = 15 ksr2^−/− group, two-way ANOVA with repeated measures Bonferoni post hoc test). (c–e) Nose-to-anus length (c), bone mineral density (BMD) (d), and bone mineral content (BMC) (e) of WT and ksr2^−/− male and female mice at 5 weeks of age (n = 16, 15, 16, and 8, respectively). (f) Serum GH of WT and ksr2^−/− mice at PN6 (n = 7 per group) and PN17 (n = 9 per group). (g) Serum IGF-1 of WT and ksr2^−/− mice at PN6 and PN17. (n = 9, 7, 12, and 8, respectively). (h) Hepatic IGF-1 mRNA levels in WT and ksr2^−/− mice at PN6 and PN17 (n = 6–7 per group). For comparison, IGF-1 levels of WT mice at PN6 were set to 1 and rps18 was used as an internal control. (i) Analysis of serum IGFBPs from WT and ksr2^−/− mice. Aliquots (0.5 μl) of serum prepared from animals at the indicated postnatal times were subjected to ligand blot analysis probed with ¹²⁵I-IGF2. The data shown are representative of duplicate runs for each of 3 distinct sets of serum samples. (j) IGFBP2 and IGFBP3 mRNA levels were measured by qPCR in PN17 liver tissue (n = 4–6 per group). Levels of WT mice were set to 1. 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.