Trichostatin A, Streptomyces sp. - CAS 58880-19-6 - Calbiochem

General description

A potent and reversible inhibitor of histone deacetylase. Blocks cell cycle progression at the G1 phase in HeLa cells and induces a 12-fold increase in intracellular levels of gelsolin. Induces reversion of oncogenic ras-tranformed NIH 3T3 cells to a normal morphology. Inhibits IL-2 gene expression (IC₅₀ = 73 nM) in Jurkat cells and shows immunosuppressive activity in a mouse model. IC₅₀ = 6 nM for HDAC1; 38 nM for HDAC4, and 8.6 nM for HDAC6A.

A potent and reversible, cell-permeable inhibitor of histone deacetylase. Blocks cell cycle progression at the G₁ phase in HeLa cells and induces a 12-fold increase in intracellular levels of gelsolin. Induces reversion of oncogenic ras-transformed NIH/3T3 cells to a normal morphology. Inhibits IL-2 gene expression (IC₅₀ = 73 nM) in Jurkat cells and shows immunosuppressive activity in a mouse model. Down-regulates p57^kip2 in Hep 3Bcells. IC₅₀ = 6 nM for HDAC1; 38 nM for HDAC4, and 8.6 nM for HDAC6A. 10 mM (500 µg/165 µl) solution of Trichostatin A, Streptomyces sp. (Cat. No. 647926) in DMSO is also available.

Biochem/physiol Actions

Cell permeable: yes

Primary Target
histone deactylase

Product does not compete with ATP.

Reversible: yes

Target IC₅₀: 73 nM inhibiting IL-2 gene expressionin Jurkat cells

Warning

Toxicity: Harmful (C)

Reconstitution

Following reconstitution in DMSO, aliquot and freeze (-20°C). Following reconstitution in ethanol, refrigerate (4°C). DMSO stock solutions are stable for up to 6 months at -20°C. Ethanol stock solutions are stable for up to 3 months at 4°C.

Other Notes

Furumai, R., et al. 2001. Proc. Natl. Acad. Sci. USA98, 87.
Gray, S.G. and Ekstrom, T.J. 1998. Biochem. Biophys. Res. Commun. 245, 423.
Takahashi, I., et al. 1996. J. Antibiot. 49, 453.
Taunton, J., et al. 1996. Science 272, 408.
Futamura, M., et al. 1995. Oncogene 10, 1119.
Hoshikawa, Y., et al. 1994. Exp. Cell Res. 214, 189.

Legal Information

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