由于ENL和CBX8结合，造成CBX8无法抑制转录延长

转录延长的发生是造成白血病的主要原因，而MLL是造成转录延长的关键。此项研究表明，MLL-ENL融合蛋白同样可以抑制调停基因表达的PRC1的活性，从而促进造血干细胞的分化。

生化研究表明，融合蛋白MLL-ENL的ENL会抑制PRC1的CBX8的活性。ENL和CBX8之间的关系是特异专一的。CBX8会抑制转录延长，但是由于ENL的作用，造成CBX8无法发挥作用。但是同时，无法结合CBX8的MLL-ENL融合蛋白无法有效地激活基因位点，而激活基因位点对于造血干细胞的分化是必须的。

此项研究表明，MLL-ENL融合蛋白可能会加强对于抑制基因表达的PRC1的抑制，同时促进造血干细胞的分化，并导致白血病的发生。

MLL-ENL Inhibits Polycomb Repressive Complex 1 to Achieve Efficient Transformation of Hematopoietic Cells

Emanuel Maethner,Maria-Paz Garcia-Cuellar,Constanze Breitinger,Sylvia Takacova,Vladimir Divoky,Jay L. Hess,Robert K. Slany

Stimulation of tranｓｃｒｉｐｔional elongation is a key activity of leukemogenic MLL fusion proteins. Here, we provide evidence that MLL-ENL also inhibits Polycomb-mediated silencing as a prerequisite for efficient transformation. Biochemical studies identified ENL as a scaffold that contacted the elongation machinery as well as the Polycomb repressive complex 1 （PRC1） component CBX8. These interactions were mutually exclusive in vitro, corresponding to an antagonistic behavior of MLL-ENL and CBX8 in vivo. CBX8 inhibited elongation in a specific reporter