Figure 4. Zcchc11 stabilizes the IGF-1 3′ UTR.

(A) Northern blotting was used to identify the predominant IGF-1 isoform expressed in the livers of wild type and Zcchc11-deficient mice at 8 days old. (B) The 3′ UTR from this isoform, cloned onto the end of a firefly luciferase reporter and co-transfected, along with a Renilla Luciferase containing a minimal promoter for normalization, decreased reporter expression in H1299 cells. (C) These same constructs were transfected in H1299 cells along with plasmids encoding EGFP, Zcchc11, catalytically inactive Zcchc11 (DADA), or the N-terminal half of Zcchc11. The full-length Zcchc11 increased expression of the IGF-1 3′ UTR reporter, which was significantly inhibited by selective mutation of the catalytic domain or complete deletion of the C terminal half. *p<0.05 vs. EGFP †p<0.05 vs Zcchc11 by one-way ANOVA.