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T8375-05 Trichostatin A (TSA) (Histone Deacetylase Inhibitor)89/1/20 CAS: 58880-19-6

Specifications
References
CAS Number
58880-19-6
Grade
Highly Purified
Molecular Formula
C17H22N2O3
Molecular Weight
302.4
EU Commodity Code
38220090
Shipping Temp
Blue Ice
Storage Temp
-20°C
4,6-Dimethyl-7-[p-dimethylaminophenyl]- 7-oxohepta-2, 4-dienohydroxamic acid)

Trichostatin A is an antifungal antibiotic that is a reversible, potent and specific inhibitor of mammalian histone deacetylase (HDAC) both in vivo and in vitro. Histone deacetylase inhibition causes chromatin relaxation and gene expression modulation. May induce apoptosis. TSA inhibits the eukaryotic cell cycle and induces morphological reversion of transformed cells. It blocks cell cycle progression at G1 phase in Hela Cells. TSA causes accumulation of highly acetylated histones in vivo, while inhibiting the activity of partially purified histone deacetylase in vitro.

Applications
Suitable for use in Inhibition of Histone Deacetylation. Other applications not tested.
Recommended Dilution
Inhibition of Histone Deacetylation: Incubation of A431 cells with 50-100ng/ml Trichostatin A for 24 hours inhibited deacetylation of histones in vivo, as detected using anti-acetylated Histone H4. The optimal concentration of Trichostatin A should be empirically determined for the type of cells and assay used.
Storage and Stability
May be stored at 4°C for short-term only. Aliquot to avoid repeated freezing and thawing. Store at -20°C. Aliquots are stable for 3-4 months at -20°C. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap.
Source
Streptomyces hygroscopicus
Purity
Highly Purified (≥ 99% by HPLC).
Concentration
~5mg/ml
Form
Supplied as a liquid in methanol.
Important Note
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications without the expressed written authorization of United States Biological.
References
1. Taunton, et al., Science 272: 408 (1996) 2. Yoshida, Beppu, Exper. Cell Res. 177: 122 (1988). 3. Yoshida, M., et al., Trichostatin A and trapoxin: novel chemical probes for the role of histone acetylation in chromatin structure and function. Bioessays 17: 423-430 (1995). 4. Minucci, S., et al., A histone deacetylase inhibitor potentiates retinoid receptor action in embryonal carcinoma cells. PNAS USA 94: 11,295-11,300 (1997). 5. Brehm, A., et al., Retinoblastoma protein recruits histone deacetylase to repress transcription. Nature 391: 597-601 (1998). 6. Sowa, R., et al., Histone deacetylase inhibitor activates the WAF1/Cip1 gene promoter through the Sp1 sites Biochem. Biophys. Res. Comm. 241: 142-150 (1997). 7. Medina, V., et al., Induction of caspase-3 protease activity and apoptosis by butyrate and trichostatin A (inhibitors of histone deacetylase): dependence on protein synthesis and synergy with a mitochondrial/cytochrome c-dependent pathway. Cancer Res. 57: 3697-3707 (1997). 8. Kim, M.S., et al., Inhibition of histone deacetylase increases cytotoxicity to anticancer drugs targeting DNA. Cancer Res. 63: 7291-7300 (2003).
USBio References
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