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. Author manuscript; available in PMC: 2018 Nov 2.
Published in final edited form as: Cell. 2017 Oct 19;171(4):824–835.e18. doi: 10.1016/j.cell.2017.09.045

Figure 3. FOXO1 interacts with SIN3A through its NH2-terminus.

Figure 3

A, Gck expression in L-Foxo1 primary hepatocytes transfected with WT-FOXO1 and Δ256-FOXO1 (AA1-256) adenoviruses in the presence or absence of insulin (n=4 from 1 mouse). B, Gck expression in WT primary hepatocytes transfected with FOXO1 and Δ19-FOXO1 (without AA126-144) plasmids in the presence or absence of insulin (n=8 from 2 mice). C, Schematic representation of SIN3A interacting domain (SID) locations and mutations of the FOXO1 N-terminal domain. D, Gck expression in WT primary hepatocytes transfected with FOXO1 and SID mutant FOXO1 plasmids (n=8 from 3 mice). E, Co-immunoprecipitation of SIN3A and FOXO1 in primary hepatocytes. F, SIN3A ChIP-qPCR on P5 (−1187 to −1040), P20 (−219 to −77), P21 (−154 to −9) and P22 (−93 to +52) in primary hepatocytes treated with cAMP/dex or cAMP/dex/insulin (n=6). Data are means ± s.e.m. *P<0.05, **P<0.01, ***P<0.001 compared to control conditions. See also Figure S4.