Figure 3.
CD19 regulates BCR signaling in a SOX11-dependent manner. (A) CRISPR/Cas9-mediated genetic depletion of CD19 decreased CD19 protein expression in JeKo-1 and Z-138 cells, along with (B) a reduction in the phosphorylation of BTK and AKT. Immunoblot experiments were performed to validate the results, whereas β-actin was assayed to ensure equivalent loading and transfer. (C) Immunoblot experiments were performed in PDX cells, with results indicating that high SOX11 expression leads to an increase in CD19 levels, leading to enhanced downstream BCR signaling. (D) Histograms depict the expression of B-cell and plasma cell surface markers (CD19, CD20, CD24, and CD138), as well as surface IgD and IgM, as measured by flow cytometry in SOX11 and CD19 knockout JeKo-1 cell lines, compared to that in the WT mice. CAR-T Res, CAR-T resistance; SCR, scramble control.

CD19 regulates BCR signaling in a SOX11-dependent manner. (A) CRISPR/Cas9-mediated genetic depletion of CD19 decreased CD19 protein expression in JeKo-1 and Z-138 cells, along with (B) a reduction in the phosphorylation of BTK and AKT. Immunoblot experiments were performed to validate the results, whereas β-actin was assayed to ensure equivalent loading and transfer. (C) Immunoblot experiments were performed in PDX cells, with results indicating that high SOX11 expression leads to an increase in CD19 levels, leading to enhanced downstream BCR signaling. (D) Histograms depict the expression of B-cell and plasma cell surface markers (CD19, CD20, CD24, and CD138), as well as surface IgD and IgM, as measured by flow cytometry in SOX11 and CD19 knockout JeKo-1 cell lines, compared to that in the WT mice. CAR-T Res, CAR-T resistance; SCR, scramble control.

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