AI Article Synopsis
- NF-kappaB (Rel) transcription factors are important for regulating both normal and abnormal immune cell functions, especially in the context of lymphomas.
- The proteins Bcl-10 and MALT1 play key roles in connecting antigen-receptor signals to the NF-kappaB pathway, but they affect this process differently in B cells.
- Bcl-10 is crucial for activating RelA and c-Rel by recruiting IKK, facilitating cell survival and division, while MALT1 mainly activates c-Rel for specific responses, without playing a role in IKK recruitment or overall proliferation.
Article Abstract
NF-kappaB (Rel) transcription factors control physiological and pathological immune cell function. The scaffold proteins Bcl-10 and MALT1 couple antigen-receptor signals to the canonical NF-kappaB pathway and are pivotal in lymphomagenesis. Here we found that Bcl-10 and MALT1 differentially regulated B cell receptor-induced activation of RelA and c-Rel. Bcl-10 was essential for recruitment of the kinase IKK into lipid rafts for the activation of RelA and c-Rel, for blocking apoptosis and for inducing division after B cell receptor ligation. In contrast, MALT1 participated in survival signaling but was not involved in IKK recruitment or activation and was dispensable for RelA induction and proliferation. MALT1 selectively activated c-Rel to control a distinct subprogram. Our results provide mechanistic insights into B cell receptor-induced survival and proliferation signals and demonstrate the selective control of c-Rel in the canonical NF-kappaB pathway.
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| http://dx.doi.org/10.1038/ni1493 | DOI Listing |
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