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Class I (Rpd3-like) proteins comprise HDAC1, HDAC2, HDAC3, and HDAC8 and are predominantly expressed in the nucleus.
|Cat. No.||Product Name / Activity|
|Dual histone deacetylase (HDAC) 6/8 inhibitor|
|Class I histone deacetylase inhibitor; orally active|
|Potent and selective class I histone deacetylase inhibitor; antitumor|
|Potent class I and IIb HDAC inhibitor|
|HDAC (Class I) inhibitor|
|Histone deacetylase inhibitor|
|Potent and selective HDAC8 inhibitor|
|Potent and selective HDAC3 inhibitor|
|Highly potent and selective HDAC2 inhibitor|
|Arginase/deacetylase superfamily||Histone deacetylase family||Class I||HDAC1, HDAC2, HDAC3, HDAC8|
|Class II||Class IIa||HDAC4, HDAC5, HDAC7, HDAC9|
|Deoxyhypusine synthase like NAD/FAD-binding domain superfamily||Sir2 regulator family||Class III||I||SIRT1, SIRT2, SIRT3|
Tocris offers the following scientific literature for Class I HDACs to showcase our products. We invite you to request* your copy today!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
Written by Susanne Müller-Knapp and Peter J. Brown, this review gives an overview of the development of chemical probes for epigenetic targets, as well as the impact of these tool compounds being made available to the scientific community. In addition, their biological effects are also discussed. Epigenetic compounds available from Tocris are listed.
In normal cells, each stage of the cell cycle is tightly regulated, however in cancer cells many genes and proteins that are involved in the regulation of the cell cycle are mutated or over expressed. Adapted from the 2015 Cancer Product Guide, Edition 3, this poster summarizes the stages of the cell cycle and DNA repair. It also highlights strategies for enhancing replicative stress in cancer cells to force mitotic catastrophe and cell death.
Adapted from the 2015 Cancer Product Guide Edition 3, this poster summarizes the main epigenetic targets in cancer. The dysregulation of epigenetic modifications has been shown to result in oncogenesis and cancer progression. Unlike genetic mutations, epigenetic alterations are considered to be reversible and thus make promising therapeutic targets.
Rheumatoid arthritis (RA) is a chronic destructive inflammatory autoimmune disease that results from a breakdown in immune tolerance, for reasons that are as yet unknown. This poster summarizes the pathology of RA and the inflammatory processes involved, as well as describing some of the epigenetic modifications associated with the disease and the potential for targeting these changes in the discovery of new treatments.
|Gene||Species||Gene Symbol||Gene Accession No.||Protein Accession No.|