Trichostatin A (TSA) is a potent histone deacetylase (HDAC) inhibitor. It inhibits HDAC 1, 2, 3, 6, 10, 11 at IC50s of less than 10 nM, with over 300-fold selectivity against class IIa HDACs. TSA affects DNA replication and gene expression by inhibiting HDAC activity and therefore altering the histone modifications and access of DNA inside chromatin.
Trichostatin A induces apoptosis and cell growth arrest at both G and G/M phases. As HDACs are overexpressed in many cancer types, TSA is widely used to probe the tumorigenesis mechanism targeting HDAC. Trichostatin A was found to prevent the differentiation of embryonic stem cell, while TSA treatment increased functional characteristics of human ESC/iPSC-derived cardiomyocytes.
|Solubility:||Up to 50 mM in DMSO|
|Synonyms:||Trichostatin A, TSA|
Shipping Condition: The product is shipped in a glass vial at ambient temperature.
Storage condition: For longer shelf life, store solid powder or DMSO solution at -20oC desiccated.
|1.||Lobera M, et al. Selective class IIa histone deacetylase inhibition via a nonchelating zinc-binding group. Nat Chem Biol. 2013; 9(5):319-25. Pubmed ID: 23524983|
|2.||Timmermann S, et al. Histone acetylation and disease. Cell Mol Life Sci. 2001; 58(5-6):728-36. Review Pubmed ID: 11437234|
|3.||Lee JH, et al. Histone deacetylase activity is required for embryonic stem cell differentiation. Genesis. 2004; 38(1):32-8. Pubmed ID: 14755802|
|4.||Otsuji TG, et al. Dynamic link between histone H3 acetylation and an increase in the functional characteristics of human ESC/iPSC-derived cardiomyocytes. PLoS One. 2012; 7(9):e45010 Pubmed ID: 11437234|