Trichostatin A

Epigenetic modifier; Inhibits histone deacetylase (HDAC)1 and HDAC6

Trichostatin A

Epigenetic modifier; Inhibits histone deacetylase (HDAC)1 and HDAC6

From: 250 USD
Catalog #
72282_C
Epigenetic modifier; Inhibits histone deacetylase (HDAC)1 and HDAC6

Overview

Trichostatin A is a potent and reversible inhibitor of Histone Deacetylase (HDAC), therefore acting as an epigenetic modifier by preventing the removal of acetyl groups from lysine residues on histone tails. Trichostatin A inhibits both class I and class II HDACs, including HDAC1 (IC₅₀ = 6 nM), HDAC4 (IC₅₀ = 38 nM), and HDAC6 (IC₅₀ = 8.6 nM). (Furumai et al.; Yoshida et al.)

REPROGRAMMING
· Increases the reprogramming efficiency of mouse embryonic fibroblasts to induced pluripotent stem (iPS) cells (Huangfu et al.).
· Resets epigenetic memory in mouse iPS cells, in combination with 5-Azacytidine (Kim et al.).
·Increases the efficiency of cloned mouse embryo development by somatic cell nuclear transfer (Kishigami et al.).

MAINTENANCE AND SELF-RENEWAL
· Prevents dedifferentiation of primary rat hepatocytes in culture, maintaining liver-specific cellular functions (Henkens et al.).

DIFFERENTIATION
· Promotes differentiation of hepatocytes from human mesenchymal stem cells (Snykers et al.).
Alternative Names
TSA
Cell Type
Hepatic Cells, Mesenchymal Stem and Progenitor Cells, Pluripotent Stem Cells
Species
Human, Mouse, Rat, Non-Human Primate, Other
Application
Differentiation, Maintenance, Reprogramming
Area of Interest
Epithelial Cell Biology, Stem Cell Biology
CAS Number
58880-19-6
Chemical Formula
C₁₇H₂₂N₂O₃
Molecular Weight
302.4 g/mol
Purity
≥ 98%
Pathway
Epigenetic
Target
HDAC

Protocols and Documentation

Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.

Document Type
Product Name
Catalog #
Lot #
Language
Product Name
Trichostatin A
Catalog #
72282, 72284
Lot #
All
Language
English
Document Type
Safety Data Sheet
Product Name
Trichostatin A
Catalog #
72282, 72284
Lot #
All
Language
English

Applications

This product is designed for use in the following research area(s) as part of the highlighted workflow stage(s). Explore these workflows to learn more about the other products we offer to support each research area.

Resources and Publications

Publications (7)

Epigenetic memory in induced pluripotent stem cells. Kim K et al. Nature 2010 SEP

Abstract

Somatic cell nuclear transfer and transcription-factor-based reprogramming revert adult cells to an embryonic state, and yield pluripotent stem cells that can generate all tissues. Through different mechanisms and kinetics, these two reprogramming methods reset genomic methylation, an epigenetic modification of DNA that influences gene expression, leading us to hypothesize that the resulting pluripotent stem cells might have different properties. Here we observe that low-passage induced pluripotent stem cells (iPSCs) derived by factor-based reprogramming of adult murine tissues harbour residual DNA methylation signatures characteristic of their somatic tissue of origin, which favours their differentiation along lineages related to the donor cell, while restricting alternative cell fates. Such an 'epigenetic memory' of the donor tissue could be reset by differentiation and serial reprogramming, or by treatment of iPSCs with chromatin-modifying drugs. In contrast, the differentiation and methylation of nuclear-transfer-derived pluripotent stem cells were more similar to classical embryonic stem cells than were iPSCs. Our data indicate that nuclear transfer is more effective at establishing the ground state of pluripotency than factor-based reprogramming, which can leave an epigenetic memory of the tissue of origin that may influence efforts at directed differentiation for applications in disease modelling or treatment.
Induction of pluripotent stem cells by defined factors is greatly improved by small-molecule compounds Huangfu D et al. Nat Biotechnol 2008

Abstract

Reprogramming of mouse and human somatic cells can be achieved by ectopic expression of transcription factors, but with low efficiencies. We report that DNA methyltransferase and histone deacetylase (HDAC) inhibitors improve reprogramming efficiency. In particular, valproic acid (VPA), an HDAC inhibitor, improves reprogramming efficiency by more than 100-fold, using Oct4-GFP as a reporter. VPA also enables efficient induction of pluripotent stem cells without introduction of the oncogene c-Myc.
Trichostatin A, a critical factor in maintaining the functional differentiation of primary cultured rat hepatocytes. Henkens T et al. Toxicology and applied pharmacology 2007 JAN

Abstract

Histone deacetylase inhibitors (HDI) have been shown to increase differentiation-related gene expression in several tumor-derived cell lines by hyperacetylating core histones. Effects of HDI on primary cultured cells, however, have hardly been investigated. In the present study, the ability of trichostatin A (TSA), a prototype hydroxamate HDI, to counteract the loss of liver-specific functions in primary rat hepatocyte cultures has been investigated. Upon exposure to TSA, it was found that the cell viability of the cultured hepatocytes and their albumin secretion as a function of culture time were increased. TSA-treated hepatocytes also better maintained cytochrome P450 (CYP)-mediated phase I biotransformation capacity, whereas the activity of phase II glutathione S-transferases (GST) was not affected. Western blot and qRT-PCR analysis of CYP1A1, CYP2B1 and CYP3A11 protein and mRNA levels, respectively, further revealed that TSA acts at the transcriptional level. In addition, protein expression levels of the liver-enriched transcription factors (LETFs) hepatic nuclear factor 4 alpha (HNF4alpha) and CCAAT/enhancer binding protein alpha (C/EBPalpha) were accordingly increased by TSA throughout culture time. In conclusion, these findings indicate that TSA plays a major role in the preservation of the differentiated hepatic phenotype in culture. It is suggested that the effects of TSA on CYP gene expression are mediated via controlling the expression of LETFs.

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