Figure 4
Figure 4. Skp2 deficiency rescues the BM defect in long-term reconstitution on PTEN inactivation. (A) The breeding strategy for WT, PTEN+/−, PTEN+/−Skp2−/−, and Skp2−/− mice. (B) Kaplan-Meier plot analysis of cumulative survival of the recipient mice after the fourth round of transplantation with WT, PTEN+/−, PTEN+/−Skp2−/−, and Skp2−/− BM cells (log-rank value = 0.018; n = 5). (C-E) The CBC test was performed to determine the number of WBCs (C), platelets (D), and RBCs (E) from the recipient mice after the fourth round of BM transplantation (*P < .05; n = 5).

Skp2 deficiency rescues the BM defect in long-term reconstitution on PTEN inactivation. (A) The breeding strategy for WT, PTEN+/−, PTEN+/−Skp2−/−, and Skp2−/− mice. (B) Kaplan-Meier plot analysis of cumulative survival of the recipient mice after the fourth round of transplantation with WT, PTEN+/−, PTEN+/−Skp2−/−, and Skp2−/− BM cells (log-rank value = 0.018; n = 5). (C-E) The CBC test was performed to determine the number of WBCs (C), platelets (D), and RBCs (E) from the recipient mice after the fourth round of BM transplantation (*P < .05; n = 5).

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