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. Author manuscript; available in PMC: 2018 Jun 22.
Published in final edited form as: Cell Chem Biol. 2017 May 4;24(6):673–684.e4. doi: 10.1016/j.chembiol.2017.04.009

Figure 3. Metabolic Alterations in ACSF3-Deficient Cells.

Figure 3

(A) Acetyl-CoA carboxylase (ACC) phosphorylation (Ser79) in ACSF3 KO and control cells in the presence or absence of 5 mM malonate for 24 hours (mean ± SEM, n=6 from two independent experiments, **p<0.01 for genotypic effect, with no effect of malonate treatment, determined by posttest after two-way ANOVA). See also Figure S2.

(B) [3H]acetate incorporation into total cellular lipids in the presence or absence of malonate (5mM) (mean ± SEM, n=6, representative of two independent experiments, **p<0.01 for genotypic effect, malonate treatment effect p=0.001 with significant interaction (p<0.05), determined by two-way ANOVA). (CPM = counts per minute).

(C) [U-14C]glucose and [U-14C]glutamine incorporation into the total lipid fraction (mean ± SEM, n=6, *p<0.05).

(D) [2-14C]malonate into total cellular lipids (n=12, pooled from two independent experiments).

(E) Immunoblotting for lipoic acid-modified proteins, DLAT (E2 of pyruvate dehydrogenase) and DLST (E2 of α-ketoglutarate dehydrogenase), with HSC70 as loading control.

(F) Select metabolite levels in the presence or absence of 5 mM malonate for 24 hours (mean ± SEM, n=10, **p<0.01 by posttest after two-way ANOVA). More metabolites and two-way ANOVA results in Table S1.