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IKKbeta is involved in membrane fusion, and serves as a critical protein kinase required for initial formation and the regulation of the CARMA1/MALT1/Bcl10/CBM complex in platelets.
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this study shows that Malt1 protease activity plays an important role in the activation of innate immune cells via FcgammaR, and the development of FcgammaR-mediated autoimmune diseases
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the importance of MALT1-mediated inflammation and T cell activation to control ERA virus, providing new insights in the biology of MALT1 and rabies virus infection.
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MALT1 as a key molecule that contributes to immune tolerance at steady-state while facilitating immune reactivity under stress conditions.
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Data show that inhibition of the protease activity of MALT1 might be a strategy to treat inflammatory bowel disease and the NLRP3 inflammasome and NF-kappaB activation are critical components in MALT1 signaling cascades in this disease model.
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Thrombin-mediated MALT1 protease activation triggers acute disruption of endothelial barrier integrity via CYLD cleavage.
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MALT1 function is required in B cells for germinal center formation.
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Studies indicate an important role for mucosa associated lymphoid tissue lymphoma translocation gene 1 protein (MALT1) in the development of experimental autoimmune encephalomyelitis (EAE)
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Targeting MALT1 proteolytic activity in autoimmune disease and B-cell lymphoma might not be a successful strategy. (Review)
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TCR-induced alternative splicing augments MALT1 scaffolding to enhance downstream signalling and to promote optimal T-cell activation.
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MALT1-dependent NF-kappaB activation is crucial for the development of EGFR-associated solid-tumor progression
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By regulating linear ubiquitination, MALT1 is both a positive and negative pleiotropic regulator of the canonical NF-kappaB pathway.
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Results demonstrate that MALT1 protease activity plays key roles in both innate and adaptive immune responses, and in regulating immune homeostasis in vivo.
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data demonstrate that MALT1 ubiquitination is critical for the engagement of CBM and IKK complexes, thereby directing platelet signals to the NF-kappaB pathway.
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Malt1 protease inactivation efficiently dampens immune responses but causes spontaneous autoimmunity.
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These results reveal distinct threshold and modulatory functions of Malt1 that differentially control lymphocyte differentiation and activation pathways.
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data suggest that Carma1 and MALT1 play previously unappreciated roles in the activation of mTOR signaling in T cells after engagement of the TCR.
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Trehalose 6,6'-dimycolate-induced Mincle expression is dependent on Dectin-3-mediated NF-kappaB activation through the CARD9-BCL10-MALT1 complex.
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Upon recognition of antigen by the T cell antigen receptor (TCR), roquin and regnase-1 proteins were cleaved by the paracaspase MALT1.
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TCR-stimulated activation of NF-kappaB requires the assembly of cytosolic p62-Bcl10-Malt1-IKK signalosomes, which may ensure highly regulated activation of NF-kappaB in response to TCR engagement.
