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. 2022 May 10;40(8):736–750. doi: 10.1093/stmcls/sxac033

Figure 6.

Figure 6.

KLF4 suppression of DDX58 in MLL-AF9 L-GMP cells. (A) qPCR of DDX58 transcripts in fl/fl and Δ/Δ MA9 L-GMP cells purified from 4 independent leukemic mice per group. (B) Binding of endogenous KLF4 to the DDX58 promoter by ChIP-PCR. (C) Immunoblot detection of DDX58 protein in whole bone marrow (WBM) and L-GMP cells from fl/fl and Δ/Δ mice (n = 4/group). (D) Immunoblot analysis of the AKT-mTOR pathway in fl/fl and Δ/Δ L-GMP cells (n = 4/group). (E) Immunoblot of DDX58 in Δ/Δ MA9 scrambled shRNA (scr sh) and DDX58 shRNA (DDX58 sh) Δ/Δ MA9 cells. (F) The colony-forming ability of Δ/Δ MA9 scrambled shRNA (scr.sh) and DDX58 shRNA (DDX58 sh) cells in methylcellulose (n = 3). (G) Expansion of MA9 (Neptune+) and DDX58-shRNA (GFP+) or scramble-shRNA (GFP+) in peripheral blood post-transplantation (n = 10/group). *P < .05, *P < .01, ***P < .001. Two-tailed Student’s t test was used in A, B, F, and G.