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. Author manuscript; available in PMC: 2015 Nov 30.
Published in final edited form as: Cell Rep. 2015 Nov 12;13(8):1658–1669. doi: 10.1016/j.celrep.2015.10.033

Figure 4. Baf60a regulates the bile acid metabolism gene program in a cell-autonomous manner.

Figure 4

(A) Heat map representation of gene regulation in response to Baf60a deficiency (BaLKO/flox/flox) and Baf60a overexpression (Baf60a/GFP) in primary hepatocytes.

(B-C) qPCR analysis of gene expression in primary hepatocytes isolated from flox/flox and BaLKO mice in the presence or absence of TCPOBOP treatment (TCP, 1 μM) for 24 h. In c, *P < 0.05 vs. vehicle treatment alone (the first bar); #P < 0.05 vs. TCP treatment alone (the second bar).

(D-E) qPCR analysis of gene expression in primary hepatocytes transduced with GFP or Baf60a adenoviruses and treated with or without TCP 1 μM for 24 h. *P < 0.05 vs. GFP expression alone; #P < 0.05 vs. TCP treatment or Baf60a expression alone.

(F) Plasma cholesterol levels in WD-fed WT mice transduced with adenovirusesexpressing GFP or Baf60a.

(G) qPCR analysis of hepatic gene expression in WT mice transduced withadenoviruses expressing GFP or Baf60a. Data in B-E represent mean ± s.d. andare representative of three independent experiments; Data in F and G representmean ± s.e.m. (n = 6); #P < 0.05, and *P < 0.05 by two-tailed Student's t-test.