Figure 1.
Figure 1. IgE-induced survival in BMMCs or FLMCs lacking Lyn, Syk, Fyn, Gab2, and PI3K p85α. Mast cell survival assay. Mast cells were prepared from bone marrow cells of mice deficient in (A) Lyn, (C) Fyn, (D) Gab2, and (E) PI3K p85α and fetal liver cells from a (B) Syk-/- embryo (E13.5). Mast cell survival was compared with that of cells from littermate WT control mice that were prepared and cultured simultaneously as described in “Materials and methods.” (F-G) Effect of dominant–negative Akt on IgE-induced BMMC survival. BMMCs retrovirally expressing dominant–negative Akt (Akt.AA or KD) were blotted with anti-Akt and anti-Erk Abs as a control (F) and tested for survival (G). Relative intensity of AA and KD were 6.4- and 3.9-fold higher than that of pMX-puro vector (Mock), respectively. Data were means ± SD for triplicate assays. Similar results were obtained from at least 2 independent mice pairs. IgE concentration was 0 μg/mL (○), 1 μg/mL (⬡), and 10 μg/mL (▵).

IgE-induced survival in BMMCs or FLMCs lacking Lyn, Syk, Fyn, Gab2, and PI3K p85α. Mast cell survival assay. Mast cells were prepared from bone marrow cells of mice deficient in (A) Lyn, (C) Fyn, (D) Gab2, and (E) PI3K p85α and fetal liver cells from a (B) Syk-/- embryo (E13.5). Mast cell survival was compared with that of cells from littermate WT control mice that were prepared and cultured simultaneously as described in “Materials and methods.” (F-G) Effect of dominant–negative Akt on IgE-induced BMMC survival. BMMCs retrovirally expressing dominant–negative Akt (Akt.AA or KD) were blotted with anti-Akt and anti-Erk Abs as a control (F) and tested for survival (G). Relative intensity of AA and KD were 6.4- and 3.9-fold higher than that of pMX-puro vector (Mock), respectively. Data were means ± SD for triplicate assays. Similar results were obtained from at least 2 independent mice pairs. IgE concentration was 0 μg/mL (○), 1 μg/mL (⬡), and 10 μg/mL (▵).

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