Histone Deacetylases (HDACs)

Eukaryotic transcriptional regulation is strongly influenced by the post-translational modification of histones. The balance of histone acetylation and deacetylation plays a critical role in this regulation. Histone acetylation induced by histone acetyl transferases (HATs) is associated with gene transcription, while histone hypoacetylation induced by histone deacetylase (HDAC) activity is associated with gene silencing. Each cell type requires a specific gene expression pattern, thus prescribing a certain requirement of HDAC expression. Altered expression and mutations of genes that encode HDACs have been linked to tumor development since they induce the aberrant transcription of key genes regulating important cellular functions such as cell proliferation, cell-cycle regulation and apoptosis. Histone deacetylase (HDAC) inhibitors are emerging as an exciting new class of potential anticancer agents for the treatment of solid and hematological malignancies. In recent years, an increasing number of structurally diverse HDAC inhibitors have been identified that inhibit proliferation and induce differentiation and/or apoptosis of tumor cells in culture and in animal models. HDAC inhibition causes acetylated nuclear histones to accumulate in both tumor and normal tissues, providing a surrogate marker for the biological activity of HDAC inhibitors in vivo. Thus, HDACs are among the most promising therapeutic targets for cancer treatment, and they have inspired researchers to study them extensively. BioVision's HDACs portfolio includes HDAC activity, inhibitor screening and immunoprecipitation assays, specific inhibitors, recombinant proteins and antibodies.

Histone Deacetylases (HDACs) Subcategories