Fig. 8: Schematic model depicting the role of RBM17 in primitive AML cells. | Nature Communications

Fig. 8: Schematic model depicting the role of RBM17 in primitive AML cells.

From: The splicing factor RBM17 drives leukemic stem cell maintenance by evading nonsense-mediated decay of pro-leukemic factors

Fig. 8

RBM17 is abnormally higher expressed in the most primitive cell fractions of AML compared to AML blasts, which contributes to efficient splicing of many pro-leukemic factors EZH2, RBM39 and HNRNPDL, along with EIF4A2 that functions in translation control, to sustain LSC functions. Knockdown of RBM17 promotes inclusions of cryptic exons or introns into mRNAs of these pro-leukemic factors, leading to their mRNA degradations due to NMD and consequently resulting in translation blockade, cell apoptosis, limited colony-forming and engraftment capacities, and promoted differentiation in primitive AML cells.

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