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Post-translational modifications regulate distinct functions of CARMA1 and BCL10.
Trends in Immunology
Activation of the transcription factor nuclear factor (NF)-kappaB is essential for the normal functioning of the immune system. Deregulated NF-kappaB signalling in lymphocytes can lead to immunodeficiency, but also to autoimmunity or lymphomas. Many of the signalling components controlling NF-kappaB activation in lymphocytes are now known, but it is less clear how distinct molecular components of this pathway are regulated. Here, we summarize recent findings on post-translational modifications of intracellular components of this pathway. Phosphorylation of the CARMA1 and BCL10 proteins and ubiquitylation of BCL10 affect the formation and stability of the CARMA1-BCL10-MALT1 (CBM) complex, and also control negative feedback regulation of the NF-kappaB signalling pathway. Moreover, the study of BCL10 phosphorylation isoforms has revealed a new mechanism controlling BCL10 nuclear translocation and an unexpected role for BCL10 in the regulation of the actin cytoskeleton.
Actins/chemistry, Active Transport, Cell Nucleus, Adaptor Proteins, Signal Transducing/physiology, Animals, Apoptosis Regulatory Proteins/physiology, CARD Signaling Adaptor Proteins/physiology, Guanylate Cyclase/physiology, Humans, NF-kappa B/metabolism, Phosphorylation, Protein Kinase C/physiology, Protein Processing, Post-Translational, Ubiquitin/metabolism
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