Product Overview

Stemolecule™ RG108 is the highest purity preparation available, only from Stemgent. RG108 is a cell-permeable, specific DNA methyltransferase inhibitor. The DNA methylation level markedly fluctuates during early embryonic development. Unlike somatic cells that undergo massive apoptosis on loss of the DNA methyltransferase Dnmt1, tolerance of genomic demethylation is a unique property of ES cells. In mouse, three DNA methyltransferases, Dnmt1, Dnmt3a and Dnmt3b, coordinately regulate global methylation in the genome. Embryos exhibit an early-lethal phenotype upon loss of Dnmt1 or Dnmt3a/b^1,2. However, both Dnmt1^-/- and Dnmt3a^-/-/b^-/- ES cells are viable when maintained in the undifferentiated status. As the Dnm1^-/- ES cells differentiate massive apoptosis occurs, whereas the Dnm3a^-/-/b^-/- cells are unable to initiate differentiation upon leukemia inhibitory factor (LIF) withdrawal, remaining viable and retaining markers characteristic of undifferentiated ES cells. These cells could not form teratoma in vivo ^3,4. RG108 is a potent small molecule DNA methyltransferase inhibitor, which provides a great tool to study methlytransferase in vivo and in vitro biological functions ⁵. It is particularly useful due to its non-covalent binding into the enzyme activation domain, which makes the inhibition reversible. RG108 can be used to examine tolerance of global genomic demethylation of induced pluripotent stem (iPS) cells that is one of the unique properties of ES cells.

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RG108 is a potent small molecule DNA methyltransferase inhibitor, which provides a great tool to study methlytransferase in vivo and in vitro biological functions ⁵. It is particularly useful due to its non-covalent binding into the enzyme activation domain, which makes the inhibition reversible. RG108 can be used to examine tolerance of global genomic demethylation of induced pluripotent stem (iPS) cells that is one of the unique properties of ES cells.

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References

1. Li, E., et al., Cell (1992) 69: 915-926.
2. Okano, MDW, et al, Cell (1999) 99: 247-257.
3. Jackson, M., et al., Mol Cell Biol (2004) 24: 8862-8871.
4. Tsumura, A., et al., Genes to Cells (2006)11: 805-814.
5. Brueckner, B., et al, Cancer Res. 65, 6305-6311 (2005)