Trichostatin A
CAS: 58880-19-6
Name:
Trichostatin A
Other names:
TSA; Trichostatin A (TSA); TSA, Trichostatin A
Trichostatin A (TSA) 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 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. A glucoside analog of Trichostatin A is also offered as Trichostatin C (sc-202369). Trichostatin A is an inhibitor of TERT, HDAC1, HDAC4 and HDAC6.
Interactions
Description
UniProt ID
Toxicity
- oral LD50 [mouse] mg/kg
- Unavailable
- oral LD50 [rat] mg/kg
- Unavailable
- oral LD50 [rabbit] mg/kg
- Unavailable
Effects on organism
No
No
No
Longevity mechanisms activation
Suppression of aging mechanisms
No dataRelation to biomarkers of Aging
Can significantly improve hUC-MSCs proliferation and delay hUC-MSCs aging
Relation to aging associated genes
No data available
Model organism
Experimental conditions
29oCLife Extension
- Mean LS (%)
- 27.3
- Median LS (%)
- —
- Mortality rate derease (%)
- —
- Max LS (%)
- 37.9
- Cell CLS
- —
- Cell RLS
- —
Concentration wth maximum effect
10 mkM