Journal: Scientific reports

Article Title: Inhibiting histone deacetylases suppresses glucose metabolism and hepatocellular carcinoma growth by restoring FBP1 expression.

doi: 10.1038/srep43864

Figure Lengend Snippet: Figure 2. Effects of HDAC inhibitors on FBP1 mRNA expression in HCC cells. HepG2 and SK-Hep1 cells were treated with different dosages of HDAC inhibitors including NaBu (A), SAHA (B) and LBH589 (C) for 24 hours. Cells were harvested and FBP1 mRNA expression was analyzed by real-time RT-PCR and GAPDH was used as an internal control. *P < 0.05, **P < 0.01, ***P < 0.001.

Article Snippet: For chemical treatment experiments, cells were treated with various concentrations of sodium butyrate (NaBu), SAHA (Sigma-Aldrich, St. Louis, MO) or LBH589 (Selleckchem, Houston, TX).

Techniques: Expressing, Quantitative RT-PCR, Control

Journal: Scientific reports

Article Title: Inhibiting histone deacetylases suppresses glucose metabolism and hepatocellular carcinoma growth by restoring FBP1 expression.

doi: 10.1038/srep43864

Figure Lengend Snippet: Figure 3. Effects of HDAC inhibitors on FBP1 protein expression in HCC cells. HepG2 and SK-Hep1 cells were treated with different dosage of HDAC inhibitors including NaBu (A), SAHA (B) and LBH589 (C) for 24 hours. Cells were harvested and FBP1 protein was analyzed by western blotting. ERK2 protein was used as a loading control. Cropped gels were displayed and full-length gels and blot were included in the Supplementary Information file.

Article Snippet: For chemical treatment experiments, cells were treated with various concentrations of sodium butyrate (NaBu), SAHA (Sigma-Aldrich, St. Louis, MO) or LBH589 (Selleckchem, Houston, TX).

Techniques: Expressing, Western Blot, Control

Journal: iScience

Article Title: BRD3 PROTAC degrader targets H3K18ac to alleviate retinal microglia-driven uveitis

doi: 10.1016/j.isci.2025.114526

Figure Lengend Snippet: The regulation of H3K18ac by BRD3 degradation is mediated by HDACs, and CCL5 is its target (A) The expression of several deacetylase enzymes (HDAC1, HDAC2, Sirt1, and Sirt3) in control group, LPS group, and D072 treatment group experiments in vitro . (B) The expression levels of SIRT1 under various treatments (LPS stimulation, D072 treatment, or siBRD3 knockdown), Sirt1 changes in proteins and mRNA. (C) The mRNA levels of cxcl10, ccl5, HK3, and nos2 in control group, LPS group, D072 treatment group, D072 + SIRT1 inhibitor (EX-527 treated) group in vitro . (D) The expression levels of CCL5, CXCL10, HK3, and NO2 under the intervention of each group of HDAC inhibitors. (Inhibitor terminology and function: SB: sodium butanoate [HDACs inhibitor], EX-527 [SIRT1 inhibitor], SIRT-IN-2 [SIRT1, 2, 3 inhibitors], SIRT6-IN-5 [SIRT6 inhibitor], and 97491 [SIRT7 inhibitor]). (E) The expression changes of H3K18ac under the intervention of each group of HDAC inhibitors. (Inhibitor terminology and function: SB: sodium butanoate [HDACs inhibitor], EX-527 [SIRT1 inhibitor], SIRT-IN-2 [SIRT1, 2, 3 inhibitors], SIRT6-IN-5 [SIRT6 inhibitor], and 97491 [SIRT7 inhibitor]). (A) Upper: representative western blot images of HDAC1, HDAC2, SIRT1, and SIRT3 in each group. Lower: quantification of the relative changes of the left ( n = 3/group; mean ± SD; ns, p > 0.05, ∗p < 0.05, ∗∗∗p < 0.001; one-way ANOVA). (B) Left: representative western blot images and the corresponding quantification of the relative protein levels of SIRT1 in each group. Right: quantification of the relative mRNA changes of the SIRT1 in different groups. ( n = 3/group; mean ± SD; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001; one-way ANOVA). (C) Quantification of the mRNA level of Cxcl10 , Ccl5 , Hk3 , and inos after SIRT1 inhibitor EX-527 treatment. ( n = 3/group; mean ± SD; ∗∗p < 0.01, ∗∗∗p < 0.001; one-way ANOVA). (D) Quantification of the mRNA level of Cxcl10 , Ccl5 , Hk3 , and inos under different HDAC inhibitor treatment. ( n = 3/group; mean ± SD; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001; one-way ANOVA). Inhibitor terminology and function: SB: sodium butanoate (HDACs inhibitor), EX-527 (SIRT1 inhibitor), SIRT-IN-2 (SIRT1, 2, 3 inhibitors), SIRT6-IN-5 (SIRT6 inhibitor), and 97491 (SIRT7 inhibitor). (E) Quantification of the relative H3K18ac protein level under each treatment. ( n = 3/group; mean ± SD; ∗∗∗p < 0.001; one-way ANOVA). (F) Left: transwell images of different groups; scale bars: 100 μm. Right: quantification of migration cells under each treatment. ( n = 3/group; mean ± SD; ∗∗∗p < 0.001; one-way ANOVA). (G) Quantification statistics concentration of CCL5 in each group. ( n = 3/group; mean ± SD; ∗∗∗p < 0.001; one-way ANOVA).

Article Snippet: Sodium butanoate , Targetmol , T1393.

Techniques: Expressing, Histone Deacetylase Assay, Control, In Vitro, Knockdown, Western Blot, Migration, Concentration Assay

Journal: Environmental science. Nano

Article Title: Surface-controlled dissolution rates: a case study of nanoceria in carboxylic acid solutions

doi: 10.1039/C9EN00222G

Figure Lengend Snippet: Dissolution rate coefficients: controls and carboxylic acids.

Article Snippet: Materials The chemicals, their sources, purity, and CAS numbers were adipic acid, TCI, ≥ 99%, 124-04-9; ammonium nitrate, Fisher, ACS grade, 6484-52-2; citric acid monohydrate, Fisher, ACS grade, 5949-29-1; DL-3-hydroxybutyric acid sodium salt, Chem Impex Int’l Inc., 100.30%, 150-83-4 & 306-31-0; DL-malic acid, Alfa Aesar, 98%, 6915-15-7; glutaric acid, Acros organics, 99%,110-94-1; hydrogen peroxide 3% W/W, BDH chemicals, 7722-84-1; horseradish peroxide type II, Sigma, 150-250 U/mg, 9003-99-0; lactic acid, TCI, ≥ 85%, 50-21-5; pimelic acid, Alfa Aesar, 98+%, 111-16-0; sodium acetate, VWR, ACS grade, 127-09-3; sodium azide, Sigma, 99.8%, 26628-22-8; sodium nitrate, BDH chemicals, ACS grade, 7631-99-4; succinic acid, TCI America, ≥ 99%,110-15-6; and tricarballylic acid, Alfa Aesar, 98%, 99-14-9.

Techniques: Dissolution