Disease relevance of Card11

• Compared with wild-type controls, CARMA1(-/-) mice did not develop airway eosinophilia, had no significant T cell recruitment into the airways, and had no evidence for T cell activation in the lung or draining lymph nodes [1].
• In addition, the CARMA1(-/-) mice had significantly decreased levels of IL-4, IL-5, and IL-13, did not produce IgE, and did not develop airway hyperresponsiveness or mucus cell hypertrophy [1].

High impact information on Card11

• The mutant TCR poorly recruits the protein adaptor Carma-1 and is subsequently impaired in activating NF-kappaB [2].
• The mutation alters a conserved leucine in the coiled-coil domain of CARMA-1/CARD11, a member of the MAGUK protein family implicated in organizing multimolecular signaling complexes [3].
• Identifying the MAGUK protein Carma-1 as a central regulator of humoral immune responses and atopy by genome-wide mouse mutagenesis [3].
• We report that genetic inactivation of the MAGUK family protein CARD11/Carma1/Bimp3 results in a complete block in T and B cell immunity [4].
• The activation of lymphocytes is in their CARMA [5].

Biological context of Card11

• A lacZ reporter gene knocked into the CARMA1 locus confirmed lymphocyte-specific expression of CARMA1 [6].
• First, CARMA1-deficient B cells show defective cell-cycle progression [7].

Anatomical context of Card11

• Together, these results show that CARMA1 has a central role in antigen receptor signaling that results in activation and proliferation of both B and T lymphocytes [8].
• Requirement for CARMA1 in antigen receptor-induced NF-kappa B activation and lymphocyte proliferation [8].
• These findings also uncover a function of the CARMA, Bcl10, and MALT1 proteins in cells outside the immune system [9].
• However, adoptive transfer of wild-type Th2 cells into CARMA1(-/-) mice restored eosinophilic airway inflammation, cytokine production, airway hyperresponsiveness, and mucus production [1].

Associations of Card11 with chemical compounds

• CARMA1 (originally called CARD11) is a membrane-associated guanylate kinase family member that is required for T cell receptor (TCR)-induced NF-kappa B activation in T cell leukemia lines [6].

Regulatory relationships of Card11

• We report that Carma1 is essential for peptide-induced interleukin 2 and interferon gamma production, but dispensable for proliferation in T cells [10].
• The molecular adapter Carma1 controls entry of IkappaB kinase into the central immune synapse [10].

Other interactions of Card11

• Yet, Card9 is dispensable for antigen receptor signalling that uses Carma1 as a link to Bcl10-Malt1 [11].
• Carma1 (also known as caspase recruitment domain [CARD]11, Bimp3) is a CARD-containing membrane-associated guanylate kinase family protein that plays an essential role in antigen receptor-induced nuclear factor kappaB activation [10].
• Branches of the B cell antigen receptor pathway are directed by protein conduits Bam32 and Carma1 [12].

References