Figure 3
Figure 3. VEGF stimulates PKCβII activity in CLL cells. (A) Western blot analysis of Btk in whole-cell lysates and in anti–pS180-Btk immunoprecipitates from CLL cells treated with 100 ng/mL VEGF in the presence and absence of 100nM LY379196. This experiment is representative of 3 using different CLL cases. (B) Effect of 100 ng/mL VEGF on BCR-induced intracellular Ca2+ release in CLL cells. Fura-2-loaded CLL cells were stimulated with 20 μg/mL anti-IgM antibody (BCR-XL) in the presence and absence of VEGF. LY379196 (100nM) was used to reverse the effects of VEGF. (C) Data presented in panel B, highlighting that the incubation of CLL cells with VEGF induced significant inhibition of intracellular Ca2+ release (P = .05, n = 6).

VEGF stimulates PKCβII activity in CLL cells. (A) Western blot analysis of Btk in whole-cell lysates and in anti–pS180-Btk immunoprecipitates from CLL cells treated with 100 ng/mL VEGF in the presence and absence of 100nM LY379196. This experiment is representative of 3 using different CLL cases. (B) Effect of 100 ng/mL VEGF on BCR-induced intracellular Ca2+ release in CLL cells. Fura-2-loaded CLL cells were stimulated with 20 μg/mL anti-IgM antibody (BCR-XL) in the presence and absence of VEGF. LY379196 (100nM) was used to reverse the effects of VEGF. (C) Data presented in panel B, highlighting that the incubation of CLL cells with VEGF induced significant inhibition of intracellular Ca2+ release (P = .05, n = 6).

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