The CARD11-BCL10-MALT1 (CBM) complex governs canonical NF-κB signaling and MALT1 protease activation downstream of TCR stimulation. Here, the authors evaluate the contribution of the E3 ligases LUBAC and TRAF6 in controlling CBM activity, using Jurkat and primary human T cells. Unlike TRAF6, LUBAC is largely dispensable for activating NF-κB, but it modifies BCL10 and regulates MALT1 protease activity by controlling substrate selectivity.
- Carina Graß
- Franziska Ober
- Daniel Krappmann
