Figure 3.
Leukemic transformation is dependent on UBTF-TD expression. (A) Schematic of FKBP12F36V-HA-UBTF-TD lentiviral construct and generation of cbCD34+ UBTF-TD degradation model. (B) Time-course degradation of FKBP12F36V-HA-UBTF-TD after treatment with dTAG-13 (1 μM) in cbCD34+ cells. Immunoblot with HA- and β-actin–specific antibodies. (C) Growth rate after dTAG-13 treatment. cbCD34+ cells expressing FKBP12F36V-HA-UBTF-TD or HA-UBTF-TD were counted over time while treated with DMSO or 1μM dTAG-13. Log of fold change was calculated from starting cell number of 200K cells. (∗∗∗ indicates P value < .001; ∗∗ indicates P value < .01, after adjustment by 2-stage step-up method (Benjamini, Krieger, and Yekutieli). (D) Immunophenotyping of cells from panel C after 10 days of treatment. (E) Wright-Giemsa staining to assess cellular morphology of cells from panels A and B after 10 days of treatment. DMSO, dimethyl sulfoxide.

Leukemic transformation is dependent on UBTF-TD expression. (A) Schematic of FKBP12F36V-HA-UBTF-TD lentiviral construct and generation of cbCD34+ UBTF-TD degradation model. (B) Time-course degradation of FKBP12F36V-HA-UBTF-TD after treatment with dTAG-13 (1 μM) in cbCD34+ cells. Immunoblot with HA- and β-actin–specific antibodies. (C) Growth rate after dTAG-13 treatment. cbCD34+ cells expressing FKBP12F36V-HA-UBTF-TD or HA-UBTF-TD were counted over time while treated with DMSO or 1μM dTAG-13. Log of fold change was calculated from starting cell number of 200K cells. (∗∗∗ indicates P value < .001; ∗∗ indicates P value < .01, after adjustment by 2-stage step-up method (Benjamini, Krieger, and Yekutieli). (D) Immunophenotyping of cells from panel C after 10 days of treatment. (E) Wright-Giemsa staining to assess cellular morphology of cells from panels A and B after 10 days of treatment. DMSO, dimethyl sulfoxide.

Close Modal

or Create an Account

Close Modal
Close Modal