Loss of Vav3 impairs leukemic proliferation and survival of p190-BCR-ABL⁺ B-cell progenitors. (A) Expansion (fold) of in vitro–cultured B-cell progenitors (CFU-proB) from WT (red lines), Vav1^−/−;Vav2^−/− (green lines), and Vav3^−/− (blue lines) cells transduced with either p190-BCR-ABL (solid lines) or mock vector (MIEG3, dotted lines). (B) S-phase fraction as assessed by bromodeoxyuridine incorporation of B-cell progenitors expressing either mock vector (hatched bars) or p190-BCR-ABL (solid bars) on day 6 of in vitro culture. (C) Apoptosis as assessed by annexin V binding of leukemic p190-BCR-ABL⁺ B-cell progenitors on day 16 of in vitro culture. (D) Representative example of immunoprecipitation and Western blot of pTyr-Vav and total Vav3 in p190-BCR-ABL⁺ B-cell progenitors from WT, Vav1^−/−;Vav2^−/−, and Vav3^−/− mice. Lysates from 5 × 10⁵ B-cell progenitors were immunoprecipitated, loaded, and blotted with Abs against phospho-tyrosine and Vav3. β-actin expression analysis from total lysate was used as a loading control (n = 3 independent experiments).