Article
Loss of KMT2C reprograms the epigenomic landscape in hPSCs resulting in NODAL overexpression and a failure of hemogenic endothelium specification.
Epigenetics - 1 Jan 2000
Maurya Shailendra, Yang Wei, Tamai Minori, Zhang Qiang, Erdmann-Gilmore Petra, Bystry Amelia, Martins Rodrigues Fernanda, Valentine Mark C, Wong Wing H, Townsend Reid, Druley Todd E
Abstract excerpt
Germline or somatic variation in the family of KMT2 lysine methyltransferases have been associated with a variety of congenital disorders and cancers. Notably, KMT2A-fusions are prevalent in 70% of infant leukaemias but fail to phenocopy short latency leukaemogenesis in mammalian models, suggesting additional factors are necessary for transformation. Given the lack of additional somatic mutation, the role of...
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