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. 2019 Apr 11;104(12):2418–2428. doi: 10.3324/haematol.2018.208843

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Figure 6. — Proposed mechanism through which Rac1/DOCK2 and FLT3-ITD cooperate to regulate the DNA damage response in FLT3-ITD leukemic cells. FLT3-ITD activates STAT5, directly or through activation of Rac1. Activated STAT5 leads to activation of CHK1, WEE1, PIM-1 and RAD51, which in turn increases DNA repair activity in the cell. FLT3-ITD also activates mismatch repair activity via activation of ERK1/2. DOCK2 activates Rac1 activity through its function as a guanine nucleotide exchange factor (GEF), and also modulates FLT3-ITD expression via regulation of Meis1 and Myb.