hat inhibitor anacardic acid  (MedChemExpress)

Journal: Cell Death & Disease

Article Title: Effects of short-chain fatty acids in inhibiting HDAC and activating p38 MAPK are critical for promoting B10 cell generation and function

doi: 10.1038/s41419-021-03880-9

Figure Lengend Snippet: A Purified splenic B cells were polarized to Bregs after a 2-day coculture with indicated SCFAs or Trichostatin A (TSA, an HDAC inhibitor with high efficiency) in the presence of LPS; the nuclear protein was prepared and tested for HDAC inhibition by ELISA. B – D B10 cell frequency in purified splenic B cells cultured with or without sodium acetate ( B ), HDAC inhibitors TSA or vorinostat ( C ), or HAT inhibitor (HATi) anacardic acid ( D ) under the existence of CD40 mAb or LPS for 2 days. Results were shown as representative FACS plots or bar graphs. The data are presented as mean ± SD from three independent experiments. * P < 0.05, ** p < 0.01, and *** p < 0.001 compared to Ctrl or as indicated.

Article Snippet: In some experiments, cells were treated with inhibitors or metabolites, including HDACis TSA (1–10 nM; Beyotime) and vorinostat (100–500 nM; MCE), GPR41 agonist AR420626 (1–10 μM; APExBIO), GPR43 agonist (1–10 μM; Sigma-Aldrich) or antagonist GLPG0974 (500 nM; Sigma-Aldrich), GPR109A agonist niacin (1 mM; Sigma-Aldrich), HAT inhibitor anacardic acid (1–10 μM; MCE), ERK1/2 inhibitor U0126 (5 μM; MCE), p38 inhibitor SB 203580 (5 μM; MCE), or JNK inhibitor SP600125 (1 μM; MCE).

Techniques: Purification, Inhibition, Enzyme-linked Immunosorbent Assay, Cell Culture

Journal: The Journal of Biological Chemistry

Article Title: Heparanase and Syndecan-1 Interplay Orchestrates Fibroblast Growth Factor-2-induced Epithelial-Mesenchymal Transition in Renal Tubular Cells

doi: 10.1074/jbc.M111.279836

Figure Lengend Snippet: HAT involvement. A, HAT activity in nuclear extract isolated from WT and HPSE-silenced cells with and without FGF-2 treatment. B, α-SMA, MMP-9, VIM, FN, HPSE, and SDC1 mRNA expression levels in WT HK2 cells cultured with and without FGF-2 and anacardic acid (HAT inhibitor) determined by real-time PCR. The results were normalized using GAPDH as an internal control and represent the mean ± S.D. (error bars) of two separate experiments performed in triplicate. ##, p < 0.001 versus WT control cells; **, p < 0.001 versus WT cells treated with FGF-2.

Article Snippet: Cells were grown to subconfluence and starved for 24 h in serum-free medium and then cultured in serum-free medium with 10 ng/ml FGF-2 (BD Biosciences) treatments for a further 6 or 24 h. Experiments were performed with and without adding the PI3K pathway inhibitor wortmannin (1 μ m ) (Calbiochem), the HAT inhibitor anacardic acid (20 μ m ) (Santa Cruz Biotechnology), and the HPSE inhibitor low molecular weight heparin (50 μg/ml) (Alfa Wassermann) 30 min before the FGF-2 treatment.

Techniques: Activity Assay, Isolation, Expressing, Cell Culture, Real-time Polymerase Chain Reaction, Control