Figure 6
Figure 6. Peptide aptamer containing RAD51(pY315) inhibits HomeoRR in BCR-ABL1-positive leukemia cells. BCR-ABL1–32Dcl3-pLB4 leukemia cells and CD34+ CML-CP primary cells were incubated with 2μM of rhodamine-labeled Y315F or pY315 aptamer, or left untreated (−). (A) Cellular uptake of the aptamers in BCR-ABL1–32Dcl3-pLB4 leukemia cells was visualized by fluorescence after 4-hour incubation (left boxes). DNA was counterstained with 4,6-diamidino-2-phenylindole (right boxes). (B) RAD51 nuclear foci were detected using anti-RAD51 antibody in BCR-ABL1–32Dcl3-pLB4 cells and CD34+ CML-CP cells as indicated. Data are number of RAD51 foci/cell ± SD. *P < .001 versus untreated cells (Mann-Whitney test). (C) HomeoRR activity in I-SceI transfected GFP+ cells. Data are percentage of G418-resistant clones ± SD. *P < .03 versus untreated cells (Student t test).

Peptide aptamer containing RAD51(pY315) inhibits HomeoRR in BCR-ABL1-positive leukemia cells. BCR-ABL1–32Dcl3-pLB4 leukemia cells and CD34+ CML-CP primary cells were incubated with 2μM of rhodamine-labeled Y315F or pY315 aptamer, or left untreated (−). (A) Cellular uptake of the aptamers in BCR-ABL1–32Dcl3-pLB4 leukemia cells was visualized by fluorescence after 4-hour incubation (left boxes). DNA was counterstained with 4,6-diamidino-2-phenylindole (right boxes). (B) RAD51 nuclear foci were detected using anti-RAD51 antibody in BCR-ABL1–32Dcl3-pLB4 cells and CD34+ CML-CP cells as indicated. Data are number of RAD51 foci/cell ± SD. *P < .001 versus untreated cells (Mann-Whitney test). (C) HomeoRR activity in I-SceI transfected GFP+ cells. Data are percentage of G418-resistant clones ± SD. *P < .03 versus untreated cells (Student t test).

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