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. Author manuscript; available in PMC: 2014 Jul 14.
Published in final edited form as: Nat Med. 2008 Jul 27;14(8):828–836. doi: 10.1038/nm.1853

Figure 2.

Figure 2

FOXA2 expression is reduced in human cholestatic livers

(a) Western blot analysis of protein nuclear extracts (30 μg) from three pediatric controls (corresponding to Control 3, 5, and 4 in Supplementary Table 3) and two patients with primary sclerosing cholangitis (corresponding to Cholestatic 5 and 6 in Supplementary Table 3) with antibodies against FOXA2 and TFIID (TBP) (loading control). FOXA2 protein levels were virtually undetectable in patients with primary sclerosing cholangitis.

(b) Western blot analysis of protein nuclear extracts (30 μg) from four pediatric controls (corresponding to Control 1 through 4 in Supplementary Table 3) and four patients with biliary atresia (corresponding to Cholestatic 1 through 4) with antibodies against FOXA2 and TFIID (TBP) (loading control). FOXA2 protein levels were virtually undetectable in patients with biliary atresia.

Immunohistochemical detection of FOXA2 protein in liver sections of adult (c) and pediatric (f) control and cholestatic patients (d–e, g–h). Labels in each panel correspond to patient numbers listed in Supplementary Table 3. While FOXA2 staining is clearly present in hepatocyte nuclei of the controls, FOXA2 presence is virtually absent in hepatocytes of the adult patients with primary sclerosing cholangitis (c, d) and pediatric patients with biliary atresia (g, h).