Fig. 9

Model: Treatment with FGF19 or physiological activation of FGF15 in mice by feeding increases the interaction between endogenous SHP and SREBP-2 in the nucleus in the liver and inhibits expression of direct SREBP-2 targets in the sterol biosynthetic genes, in a SHP-dependent manner. FGF19-induced phosphorylation of SHP at Thr-55 appears to be important for functional interaction with SREBP-2 in the nucleus. Hepatic genes that have shared binding peaks of SHP and SREBP-2 identified by ChIP-seq, ChIP, or both are indicated in red