Bak1 is a target of miR-26a for its myeloprotection from chemotherapeutic agent. (A) Putative miR-26a target site in the 3′UTR of mouse Bak1. Red characters denote the sites with highly probable preferential conservation between mammals. (B) Relative luciferase activity of reporter constructs containing the wild-type or mutant (mut) 3′UTR of mouse Bak1 in HEK293 cells cotransfected with either miR-26a precursor transducing lentivirus (miR-26a OE), miR-26a tough-decoy inhibitor transducing virus (miR-26a TuD) inhibitor, or negative control (ctrl). Data (mean ± SD) were pooled from 2 experiments. (C) Relative expression level of Bak1 messenger RNA in LSK population 5 days after 5-FU treatment. Data (mean ± SD) were pooled from 2 experiments involving a total of 6 mice per group. (D) Targeted mutation of the Bak1 gene increased survival of LSK in BM at day 5 after 5-FU 150 mg/kg treatments. Data (mean ± SD) shown are percentages of LSK in BM (n = 3 for Bak1^+/+ mice and n = 4 for Bak1^−/− mice). (E) Percent survival of Bak1^+/+ and Bak1^−/− LSK in BM. Data (mean ± SD) shown are percentages of LSK, after normalization using means of LSK percentages from BM of 2 untreated Bak1^+/+ and Bak1^−/− mice as 100%. (F) The numbers of WBCs, red blood cells (RBCs), and platelets (PLTs) 10 days after 5-FU 150 mg/kg treatments between Bak1^−/− mice and wild-type mice. Data (mean ± SD) were pooled from 2 experiments involving a total of 7 mice per group. *P < .05, **P < .01. Error bars indicate SD.