Figure 4
Figure 4. INPP4B overexpression confers resistance to ara-C independent of its phosphoinositide phosphatase function. (A) Ectopic overexpression of wild-type (wt) INPP4B and phosphatase inactive INPP4B C842A in AML cell lines showing expression by western blot (bottom panels) and the concordant phosphatase activity (top panels). Overexpression of both INPP4B and the INPP4B C842A variant resulted in resistance to cytarabine in (B) MV4;11, (C) HEL, (D) HL60, and (E) U937 AML cells compared with vector control. Cells were subjected to drugs for 48 hours, and viability was measured by using flow cytometry. Results represent the mean ± SD of 3 independent experiments. P < .05 for survival curve comparisons between vector control and wild-type INPP4B (as indicated) and INPP4B C842A (not shown).

INPP4B overexpression confers resistance to ara-C independent of its phosphoinositide phosphatase function. (A) Ectopic overexpression of wild-type (wt) INPP4B and phosphatase inactive INPP4B C842A in AML cell lines showing expression by western blot (bottom panels) and the concordant phosphatase activity (top panels). Overexpression of both INPP4B and the INPP4B C842A variant resulted in resistance to cytarabine in (B) MV4;11, (C) HEL, (D) HL60, and (E) U937 AML cells compared with vector control. Cells were subjected to drugs for 48 hours, and viability was measured by using flow cytometry. Results represent the mean ± SD of 3 independent experiments. P < .05 for survival curve comparisons between vector control and wild-type INPP4B (as indicated) and INPP4B C842A (not shown).

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