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. Author manuscript; available in PMC: 2023 Nov 16.
Published in final edited form as: Science. 2023 Mar 16;380(6640):93–101. doi: 10.1126/science.ade3925

Fig. 5. DecryptM analysis of rituximab reveals antibody-based killing of B-cells via activation of the BCR-MAPK signalling axis.

Fig. 5

(A) Viability assays of rituximab (RTX) sensitive and resistant cell lines. (B) Protein expression of B-cell receptor and lipid raft components in the same cell lines. (C) Number of dose-response regulated phosphopeptides at different times of RTX treatment for the same cell lines (left axis, bars) and the kinetics of RTX binding to these cells (right axis, lines). (D) Temporal dynamics of apoptosis induction upon addition of RTX to SUDHL-4 cells with and without prior siRNA-mediated knock-down of B-cell receptor and lipid raft components. Induction of apoptosis was monitored by annexin V-labeling using live cell imaging. Shaded areas indicate the standard deviation of replicate experiments (n=3). (E) Summary representation of the major five pathways involved in BCR-signaling and working model based on time- and dose-resolved decryptM profiles as well as pharmacological inhibition of certain proteins (yellow) of how engagement of these pathways (or lack thereof) leads to RTX-mediated cell death. Figures in red indicate the fold change of RTX-induced phosphorylation regulation.