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. 2020 May 8;11:2319. doi: 10.1038/s41467-020-16128-5

Fig. 7. Targeting the Btk SH2-KD interface decreases the viability of B-cell lymphoma cells and inhibits BCR signaling.

Fig. 7

a Cumulative cell number of HBL-1 cells lentivirally transduced with a doxycycline-inducible system for expression of rF10 or rNB control repebodies (n = 4). Parental cells are non-transduced cells. b Apoptosis analysis of transduced HBL-1 expressing the repebodies for 7 days. A representative gating of FACS staining is shown on top. The quantification of early (7AAD-/Annexin V+) and late (7AAD+/Annexin V+) apoptotic cells was obtained from two independent experiments (n = 2). Parental HBL-1 cells treated with 10 µM of ibrutinib for 48 h were used as positive control. c Immunoblot analysis from transduced HBL-1 cells expressing the repebodies (Flag-tagged) for 48 h. BCR signaling was stimulated with anti-human IgM or mock-treated for 2 min before cell lysis. Ibrutinib treatment (100 nM) was performed for 15 min prior to anti-IgM stimulation. Tubulin was used as loading control. d Quantification of Btk pY551 shown in c and normalized to total Btk expression. Data are mean ± SD from two biological replicates (n = 3) and P-values were calculated using an unpaired t-test. *P ≤ 0.05. e Immunoblotting from transduced DOHH2 cells expressing the repebodies as performed in c. Source data are provided as a Source Data file.