Fig 2: Protein extracts from liver from the indicated genotypes at day 5 from the protocol in Figure 4A were probed with NCOR1 or SMRT antibody. Beta-actin was used as a control.

Fig 3: Postnatal deletion of NCOR1 and SMRT is lethal. (A) Shown are the genotypes that were studied (control (n = 15), NCOR1 and SMRT single KO (n = 5), NCOR1/SMRT DKO, (n = 6). Tamoxifen was administered for five days between weeks 8 and 9 in male mice. (B) Protein extracts from the liver of the indicated genotypes were probed with NCOR1 or SMRT antibodies. Beta-actin was used as a control. (top panels). qPCR of liver, heart, kidneys, and small intestine (SI) for NCOR1 and SMRT were performed (bottom panels, n = 7–8 per genotype). (C) Percentage of mice from indicated genotypes that survived for 15 days and body weight, blood glucose, and temperature of the control and DKO mice (n = 15 control, 6 DKO and 5 NCOR1 KO and 5 SMRT KO). (D) Thyroid-stimulating hormone (TSH) levels were measured by ELISA and total thyroxine (TT4) levels were measured by radioimmunoassay (n = 15 control, 6 DKO). (E) qPCR of thyroid hormone–responsive genes (n = 6 per genotype). (F) Ejection fraction was measured by echocardiography before tamoxifen (pre) and one day after tamoxifen administration was completed (post) and percent change was determined (n = 3). (G) Blood for hematologic cell counts was assessed (n = 4–5 per genotype). Data are shown as mean +/− SEM ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, ∗∗∗∗P < 0.0001, post-hoc two-way ANOVA for survival analysis, otherwise unpaired student t-test.