Trichostatin A is a potent and non-competitive reversible inhibitor of histone deacetylases （HDAC） with a Ki of 3.4 nM. 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 and displayed immunosuppressive activity in a mouse model. Induces increased acetylation of GATA4， a cardiac-specific transcription factor and increases cardiac muscle cell differentiation. In normal rat fibroblasts， induced Friend cell differentiation and inhibited the G1 and G2 phases of the cell cycle. Trichostatin A is a useful tool for induction of hyperacetylation of cellular histones and for further elucidation of their role in gene expression.
