Abstract:Somatic mutations in protein lysine methyltransferases are frequently observed in cancer cells. We show here that the NSD1 mutations Y1971C, R2017Q and R2017L observed mostly in solid cancers are catalytically inactive suggesting that NSD1 acts as tumor suppressor gene in these tumors. In contrast, the frequent T1150A in NSD2 and its T2029A counterpart in NSD1, both observed in leukemia, are hyperactive and introduce up to H3K36me3 in biochemical and cellular assays, while wildtype NSD2 and NSD1 only generate … Show more
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