Acetyl-FOXO1A (Lys294) Antibody - #AF2305

Fig. 5: ACLY regulated MYC expression via promoting the acetylation of FoxO1 and H3. A KEGG analysis of DEGs from transcriptomic sequencing showing the top 20 enriched pathways involved in ACLY regulation in LPS-induced HUVEC. B, C Levels of acetyl-CoA in HUVEC treated with BMS-303141 before LPS stimulation were measured (n = 6). D Western blot analysis showing the global acetylation of lysine in HUVEC treated with or without BMS-303141 before LPS stimulation. (E–H) HUVEC were pretreated with BMS-303141 or transfected with siRNA specific to ACLY before stimulatedn with LPS for 1 h. Levels of phosphorylated and total ACLY, acetylated and total FoxO1, as well as MYC were tested using Western blot assays. I Immunofluorescence staining showing FoxO1 localization in HUVEC stimulated with LPS in the presence of BMS-303141 (10 µM) or C646 (5 µM). J, K Western blot analysis showing the levels of acetylated FoxO1 and acetylated H3, and the expression of MYC in HUVEC with ACLY-WT (WT) or ACLY-S455D (S455D) overexpression, respectively. L Immunofluorescence staining representing FoxO1 nuclear export in ACLY-WT- and ACLY-S455D-overexpressing HUVEC (white arrow). M, N ACLY-WT-overexpressing (WT) or ACLY-S455D-overexpressing (S455D) HUVEC were treated with p300 inhibitor C646 (5 µM) and the levels of

Figure 16. |(See previous page). Inhibition of FOXO1 and autophagy decreased lipid content and the level of proteins related to the autophagy process in the S100A11 overexpression Hepa 1–6 cells.(F) Quantification of the results from panel E by ImageJ. Western blot detection and quantification of related proteins in the S100A11 overexpression Hepa 1–6 cells treated with (G and H) 10 nmol/L BAF, (I and J) 2 mmol/L 3-MA, and (K and L) RNA interference of Atg7, respectively.