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Biological Activity for BRD 4770
BRD 4770 is a G9a inhibitor and S-adenosyl methionine (SAM) mimetic. Inhibits methylation of H3K9 (EC50 ~ 5 μM) and induces senescence in PANC-1 cells. Induces ATM activation without DNA damage. Cell permeable.
Technical Data for BRD 4770
|Storage||Store at +4°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.
References for BRD 4770
References are publications that support the biological activity of the product.
Yuan et al (2012) A small-molecule probe of the histone methyltransferase G9a induces cellular senescence in pancreatic adenocarcinoma. ACS Chem.Biol. 7 1152 PMID: 22536950
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Citations for BRD 4770
Citations are publications that use Tocris products.
Currently there are no citations for BRD 4770.
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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.
Epigenetics Research Bulletin
Produced by Tocris and updated in 2014, the epigenetics research bulletin gives an introduction into mechanisms of epigenetic regulation, and highlights key Tocris products for epigenetics targets including:
- DNA Methyltransferases
- Histone Deacetylases
- Histone Demethylases
- Histone Methyltransferases
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.