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Wegener, E. ; Krappmann, D.

CARD-Bcl10-Malt1 Signalosomes: Missing Link to NF-B.

Sci. Signal. 384, p21. (2007)

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Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.

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Cytokines, pathogens, and antigens signal through NF-{kappa}B (nuclear factor {kappa}B) transcription factors to regulate the expression of genes that mediate the inflammatory response. Stimulation of G protein–coupled receptors (GPCRs) has also been shown to trigger inflammatory responses by activating the canonical NF-{kappa}B pathway, which involves the phosphorylation and degradation of cytosolic NF-{kappa}B inhibitors (I{kappa}Bs) that depend on the I{kappa}B kinase (IKK). However, genetic data about the molecular links between GPCR-proximal events and activation of IKK and, thereby, of NF-{kappa}B have remained elusive. Recent studies by Klemm et al., McAllister-Lucas et al., and Wang et al. now present compelling evidence that signaling complexes containing the adaptor proteins Bcl10 (B cell chronic lymphocytic leukemia and/or lymphoma 10) and Malt1 [mucosa-associated lymphoid tissue (MALT) lymphoma translocation gene 1], constitute the missing link between GPCRs and IKK and NF-{kappa}B activation (1–3). A separate study by Gross et al. reports an intriguing finding, that Dectin-1–mediated antifungal immunity in dendritic cells is also regulated by the Bcl10-Malt1 module (4). GPCR- and Dectin-1–induced NF-{kappa}B activation depends on the interaction of the Bcl10-Malt1 module with specific Bcl10-binding CARD (caspase recruitment domain)–containing scaffold proteins (2, 4). Together with previous data establishing a crucial role for CARD11 [also known as CARMA1, for CARD-MAGUK (membrane-associated guanylate kinase)] association with Bcl10-Malt1 in lymphocytes, these results suggest that diverse receptor systems use distinct CARD scaffolds and conserved Bcl10-Malt1 modules to stimulate IKK and NF-{kappa}B signaling (Fig. 1).

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