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Inhibitor of Sir2p (IC50 = 60 μM), an NAD+-dependent Sir2 family deacetylase required for chromatin-dependent silencing in yeast.
|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.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 198.22. 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|
|1 mM||5.04 mL||25.22 mL||50.45 mL|
|5 mM||1.01 mL||5.04 mL||10.09 mL|
|10 mM||0.5 mL||2.52 mL||5.04 mL|
|50 mM||0.1 mL||0.5 mL||1.01 mL|
References are publications that support the biological activity of the product.
Bedalov et al (2001) Identification of a small molecule inhibitor of Sir2p. Proc.Natl.Acad.Sci.U.S.A. 98 15113 PMID: 11752457
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Keywords: Splitomicin, Splitomicin supplier, Sir2p, inhibitors, inhibits, Sirtuin, Sir2-like, Family, Deacetylases, Class, III, HDACs, (Sirtuins), 1542, Tocris Bioscience
2 Citations for Splitomicin
Citations are publications that use Tocris products. Selected citations for Splitomicin include:
Kumari and Usdin (2014) Polycomb group complexes are recruited to reactivated FMR1 alleles in Fragile X syndrome in response to FMR1 transcription. Hum Mol Genet 23 6575 PMID: 25055869
Stavrou et al (2015) Reduced thrombosis in Klkb1-/- mice is mediated by increased Mas receptor, prostacyclin, Sirt1, and KLF4 and decreased tissue factor. J Neurosci 125 710 PMID: 25339356
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Literature in this Area
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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.