Figure 2
Figure 2. Deficiency of Rac1 or Rac2 impairs MA9 leukemia maintenance in vitro. Western blot analysis demonstrated efficiency of lentiviral knockdown of Rac1 (A) and Rac2 (B) in murine LDBM. Band densitometry is normalized to β-actin and NT control. Knockdown of Rac1 (C) or Rac2 (F) in the fully transformed murine MA9 leukemia inhibits in vitro growth as shown by loss of Venus+ cells over time. Venus+ percentage was normalized to analysis day 0 (= day 4 after transduction). Rac1 (D) or Rac2 (G) knockdown induces apoptosis in MA9 cells as shown by annexin V/7-AAD staining. Rac1 (E) or Rac2 (H) knockdown causes loss of colony-forming MA9 cells. All figures are representative of 3-5 independent experiments.

Deficiency of Rac1 or Rac2 impairs MA9 leukemia maintenance in vitro. Western blot analysis demonstrated efficiency of lentiviral knockdown of Rac1 (A) and Rac2 (B) in murine LDBM. Band densitometry is normalized to β-actin and NT control. Knockdown of Rac1 (C) or Rac2 (F) in the fully transformed murine MA9 leukemia inhibits in vitro growth as shown by loss of Venus+ cells over time. Venus+ percentage was normalized to analysis day 0 (= day 4 after transduction). Rac1 (D) or Rac2 (G) knockdown induces apoptosis in MA9 cells as shown by annexin V/7-AAD staining. Rac1 (E) or Rac2 (H) knockdown causes loss of colony-forming MA9 cells. All figures are representative of 3-5 independent experiments.

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