Sodium Butyrate has been reported to cause hyperacetylation of histones due to its role as a histone deacetylase (HDAC) inhibitor (IC50 values are 0.3, 0.4, 0.3, mM for HDAC1, 2 and 7 respectively). This compound has been shown to cause induction of differentiation and gene expression and also prevent cell proliferation. Mechanistic studies suggest that the action of Sodium Butyrate is often mediated through Sp1/Sp3-associated HDAC activity which leads to transcriptional activation of the p21 gene. Additionally this agent demonstrates the ability to downregulate numerous genes associated with cytokine signaling, specifically, the IFN-γ (interferon γ) pathway.
1. Sealy, L., et al., 1978. The effect of sodium butyrate on histone modification. Cell. 14(1): 115-21. PMID: 667928 2. Davie, James R., et al., 2003. Inhibition of histone deacetylase activity by butyrate. The Journal of nutrition. 133(7 Suppl): 2485S-2493S. PMID: 12840228 3. Joseph, Jeena., et al., 2004. Expression profiling of sodium butyrate (NaB)-treated cells: identification of regulation of genes related to cytokine signaling and cancer metastasis by NaB. Oncogene. 23(37): 6304-15. PMID: 15318170 4. Sekhavat, Anoushe., et al., 2007. Competitive inhibition of histone deacetylase activity by trichostatin A and butyrate. Biochemistry and cell biology = Biochimie et biologie cellulaire. 85(6): 751-8. PMID: 18059533
Soluble in water (0.1 g/ml), DMSO (<1 mg/ml), ethanol (~5 mg/ml), and PBS pH7.2 (~10 mg/ml). Insoluble in ether.
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