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. 2021 Jun 10;12:689472. doi: 10.3389/fimmu.2021.689472

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Copyright © 2021 Smith and Burger

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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The B cell receptor (BCR) signaling pathway and the effect of kinase inhibitors. The BCR pathway trifurcates into, from left, NF-κB, NFAT and AP-1 signaling. The AP-1 pathway is believed to be connected to the BCR through LYN, SYK and ZAP70 (not depicted). Filled protein symbols correspond to Gain-of-Function (GoF) drug resistance mutations. BTK inhibitors (BTKi) and p110δ inhibitors (p110δi) are marked with yellow background. The MYD88 L265P GoF mutation found in 95% of WM patients, and also in ABC-type DLBCL, and in some CLL patients induces an activated endolysosome containing TLR9 and the BCR. proteins affected by BTKi, proteins affected by p110δi.

Inline graphic — The B cell receptor (BCR) signaling pathway and the effect of kinase inhibitors. The BCR pathway trifurcates into, from left, NF-κB, NFAT and AP-1 signaling. The AP-1 pathway is believed to be connected to the BCR through LYN, SYK and ZAP70 (not depicted). Filled protein symbols correspond to Gain-of-Function (GoF) drug resistance mutations. BTK inhibitors (BTKi) and p110δ inhibitors (p110δi) are marked with yellow background. The MYD88 L265P GoF mutation found in 95% of WM patients, and also in ABC-type DLBCL, and in some CLL patients induces an activated endolysosome containing TLR9 and the BCR. proteins affected by BTKi, proteins affected by p110δi.