Trichostatin A (TSA) is a potent and reversible inhibitor of histone deacetylases. In HeLa cells, TSA blocked cell cycle progression at G1 and induced a 12-fold increase in intracellular levels of gelsolin. In cells latently infected with HIV-1, TSA induced the transcriptional activation of the HIV-1 promoter, which resulted in a marked increase in virus production. In NIH 3T3 cells, TSA induced reversion of oncogenic ras-transformed cells to a normal morphology. In Jurkat cells, TSA inhibited IL-2 gene expression (IC50=73nM) and displayed immunosuppressive activity in a mouse model.
Induces increased acetylation of GATA4, a cardiac-specific transcription factor and increases cardiac muscle cell differentiation. Trichostatin A is a useful tool for induction of hyperacetylation of cellular histones and for further elucidation of their role in gene expression. Induces cell growth arrest at both G1 and G2/M phases. may induce apoptosis in some cases. It can induce accelerated dedifferentiation of primordial germ cells into embryonic germ cells.
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