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Biological Activity for Tubacin
Tubacin is a selective inhibitor of HDAC6; inhibits the second deacetylase domain (DD2). Does not inhibit HDAC6 histone deacetylase activity; reversibly inhibits α-tubulin deacetylation. Increases α-tubulin acetylation levels with no effect on histone acetylation or cell cycle progression.
External Portal Information for Tubacin
Chemicalprobes.org is a portal that offers independent guidance on the selection and/or application of small molecules for research. The use of Tubacin is reviewed on the Chemical Probes website.
Technical Data for Tubacin
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
Solubility Data for Tubacin
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions for Tubacin
The following data is based on the product molecular weight 721.86. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|0.1 mM||13.85 mL||69.27 mL||138.53 mL|
|0.5 mM||2.77 mL||13.85 mL||27.71 mL|
|1 mM||1.39 mL||6.93 mL||13.85 mL|
|5 mM||0.28 mL||1.39 mL||2.77 mL|
References for Tubacin
References are publications that support the biological activity of the product.
Haggarty et al (2003) Multidimensional chemical genetic analysis of diversity-orientated synthesis-derived deacetylase inhibitors using cell-based assays. Chem.Biol. 10 383 PMID: 12770821
Haggarty et al (2003) Domain-selective small-molecule inhibitor of histone deacetylase 6 (HDAC6)-mediated tubulin deacetylation. Proc.Natl.Acad.Sci.USA 100 4389 PMID: 12677000
Jiang et al (2008) Direct binding with histone deacetylase 6 mediates the reversible recruitment of parkin to the centrosome. J.Neurosci. 28 12993 PMID: 19036992
If you know of a relevant reference for Tubacin, please let us know.
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Keywords: Tubacin, Tubacin supplier, Tubacin, HDAC, inhibitors, class, II, histone, deacetylase, inhibits, deacetylases, alpha-tubulin, α-tubulin, a-tubulin, acetylation, HDAC6, epigenetics, [537049-40-4], Class, HDACs, 3402, Tocris Bioscience
Citations for Tubacin
Citations are publications that use Tocris products.
Currently there are no citations for Tubacin. Do you know of a great paper that uses Tubacin from Tocris? Please let us know.
Reviews for Tubacin
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Literature in this Area
Tocris offers the following scientific literature in this area 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.
Epigenetics Scientific Review
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.
Cell Cycle & DNA Damage Repair Poster
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.
Epigenetics in Cancer Poster
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 Poster
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.