Figure 5
Figure 5. Lack of GILZ enhances B-cell survival. (A) Percentage of live cells of BM CD19+ cells from WT and gilz KO mice after 24 or 48 hours in vitro (n = 4/5). (B-D) Frequency of B220+Ki67+ cells (B), B220+AnnexinV+ cells (C), and B220+Caspase+ (D) isolated from the BM of WT and gilz KO mice after 48 hours in vitro (n = 4/5). (E) WB analysis of cleaved caspase 3 expression in BM CD19+ cells isolated from WT and gilz KO mice. The same number of cells was loaded; WB with laminin B antibodies served as loading control. (F) Frequency of Caspase+ cells and Ki67+ on PreProB cells, ProB cells, PreB cells, immature B cells, and mature B cells isolated from the BM of WT and KO mice (n = 10/12). (G) Frequency of Caspase+ on B cells (B220+) and non–B cells (B220–) from BM isolated from WT and gilz KO mice (n = 10/12). *P < .05, *P < .05, **P < .005, ***P < .0005.

Lack of GILZ enhances B-cell survival. (A) Percentage of live cells of BM CD19+ cells from WT and gilz KO mice after 24 or 48 hours in vitro (n = 4/5). (B-D) Frequency of B220+Ki67+ cells (B), B220+AnnexinV+ cells (C), and B220+Caspase+ (D) isolated from the BM of WT and gilz KO mice after 48 hours in vitro (n = 4/5). (E) WB analysis of cleaved caspase 3 expression in BM CD19+ cells isolated from WT and gilz KO mice. The same number of cells was loaded; WB with laminin B antibodies served as loading control. (F) Frequency of Caspase+ cells and Ki67+ on PreProB cells, ProB cells, PreB cells, immature B cells, and mature B cells isolated from the BM of WT and KO mice (n = 10/12). (G) Frequency of Caspase+ on B cells (B220+) and non–B cells (B220) from BM isolated from WT and gilz KO mice (n = 10/12). *P < .05, *P < .05, **P < .005, ***P < .0005.

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