Figure 4.
Expression of CD79B determines α-BCR–induced signaling strength. The MCL cell line Granta 519 was left unstimulated or was activated with different concentrations of F(ab′2) anti-IgM (α-IgM) for 4 minutes. (A) Cells were stained with anti-CD79B antibody (Ab), together with phosphospecific Abs. This strategy allowed gating on distinct levels of CD79B and mapping of α-BCR–induced signaling specifically to the distinct CD79B expression levels, from low to high. α-BCR–induced signaling is shown as heatmaps, where phosphorylation levels are relative to unstimulated cells within the same level of CD79B expression. (B) Overexpression of full length CD79B by retroviral transduction further enhances α-BCR–induced signaling. α-BCR–induced signaling assay was performed as in panel A. One representative experiment is shown, and in panel C, mean ± standard error of the mean (SEM) (n = 3). SSC, side scatter.

Expression of CD79B determines α-BCR–induced signaling strength. The MCL cell line Granta 519 was left unstimulated or was activated with different concentrations of F(ab′2) anti-IgM (α-IgM) for 4 minutes. (A) Cells were stained with anti-CD79B antibody (Ab), together with phosphospecific Abs. This strategy allowed gating on distinct levels of CD79B and mapping of α-BCR–induced signaling specifically to the distinct CD79B expression levels, from low to high. α-BCR–induced signaling is shown as heatmaps, where phosphorylation levels are relative to unstimulated cells within the same level of CD79B expression. (B) Overexpression of full length CD79B by retroviral transduction further enhances α-BCR–induced signaling. α-BCR–induced signaling assay was performed as in panel A. One representative experiment is shown, and in panel C, mean ± standard error of the mean (SEM) (n = 3). SSC, side scatter.

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