Figure 1
Figure 1. RSK2 is activated in diverse human leukemia cells transformed by different leukemogenic tyrosine kinases including BCR-ABL and FLT3-ITD. (A) Immunoblotting detects S386 phosphorylation of RSK2 in diverse hematopoietic cancer cell lines expressing diverse leukemogenic tyrosine kinases, including EOL-1 (HIP1L1-PDGFRA), HEL (JAK2 V617F), KARPAS (NPM-ALK), K562 (BCR-ABL), Molm14 (FLT3-ITD), Mo91 (TEL-TrkC), OPM1 (FGFR3). ANBL6 is a human myeloma cell line without dysregulated expression of tyrosine kinase and included as a negative control. (B-C) Immunoblotting shows that targeting BCR-ABL by imatinib in K562 cells (B) and FLT3 by TKI258 in Mv(4;11) and Molm14 cells (C) decreases phosphorylation of RSK2 S386.

RSK2 is activated in diverse human leukemia cells transformed by different leukemogenic tyrosine kinases including BCR-ABL and FLT3-ITD. (A) Immunoblotting detects S386 phosphorylation of RSK2 in diverse hematopoietic cancer cell lines expressing diverse leukemogenic tyrosine kinases, including EOL-1 (HIP1L1-PDGFRA), HEL (JAK2 V617F), KARPAS (NPM-ALK), K562 (BCR-ABL), Molm14 (FLT3-ITD), Mo91 (TEL-TrkC), OPM1 (FGFR3). ANBL6 is a human myeloma cell line without dysregulated expression of tyrosine kinase and included as a negative control. (B-C) Immunoblotting shows that targeting BCR-ABL by imatinib in K562 cells (B) and FLT3 by TKI258 in Mv(4;11) and Molm14 cells (C) decreases phosphorylation of RSK2 S386.

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