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single amino acid oncogenic CARD11 mutations can perturb or bypass the action of redundant inhibitory REs to achieve the level of hyperactive CARD11 signaling required to support lymphoma growth.
Cooperative Control of Caspase Recruitment Domain-containing Protein 11 (CARD11) Signaling by an Unusual Array of Redundant Repressive Elements.
CARMA1- and MyD88 (show MYD88 Proteins)-dependent activation of Jun (show JUN Proteins)/ATF-type AP-1 (show FOSB Proteins) complexes is a hallmark of ABC (show ABCB6 Proteins) diffuse large B-cell lymphomas.
Data show that caspase recruitment domain-containing protein 11/B-cell CLL/lymphoma 10 (show BCL10 Proteins)/mucosa-associated lymphoid tissue lymphoma translocation gene 1 (show MALT1 Proteins) signaling drives lymphoproliferation (show FAS Proteins) through NF-kappa B (show NFKB1 Proteins) and c-Jun N-terminal kinase activation.
CARD11-mediated alterations in NF-kappaB (show NFKB1 Proteins) signaling may be an early event in the development of cutaneous squamous cell carcinoma
Taken together, our data indicate that miR (show MLXIP Proteins)-539 is a novel regulator of migration and invasion in human thyroid cancer cells by targeting CARMA1.
CARMA1 clustering through SH3-GUK domain interactions is required for its activation of NF-kappaB (show NFKB1 Proteins) signalling
Both carried homozygous germline mutations in CARD11 (p.Cys150*), impairing NF-kappaB (show NFKB1 Proteins) signaling and IL-2 (show IL2 Proteins) production
Three patients have been described with mild B-cell lymphocytosis and a CARD11 C49Y missense mutation.
Overexpression of CARMA-BCL10 (show BCL10 Proteins)-MALT in T-ALL may contribute to the constitutive cleavage and inactivation of A20 (show TNFAIP3 Proteins), which enhances NF-kappaB (show NFKB1 Proteins) signaling and may be related to T-ALL pathogenesis.
synergistic activity of Card11 mutant and Bcl6 (show BCL6 Proteins) in the development of diffuse large B-cell lymphoma in a mouse model
data suggest that Carma1 and MALT1 play previously unappreciated roles in the activation of mTOR signaling in T cells after engagement of the TCR.
CARMA1 CARD shows the first homo-dimeric structure of CARD formed by a disulfide bond and reveals a possible biologically important homo-dimerization mechanism
Data indicate that caspase recruitment domain-containing protein 11 (CARD11) is involved in the pathogenesis of collagen-induced arthritis (CIA (show NCOA5 Proteins)) by formation of the CARD11/Bcl10 (show BCL10 Proteins) complex and enhancement of the Th17 cell response.
Genetic approach demonstrates a critical role for the CARD function of CARMA1 in Treg cell development in vivo.
both CARMA1 CARD and BCL10 CARD easily self-oligomerized under physiological conditions.
Findings show that regulation of CARD11 signaling is a critical switch governing the decision between death and proliferation in antigen-stimulated mature B cells.
TCR/CARMA1/NF-kappaB (show NFKB1 Proteins) controls completion of Th17 differentiation.
These studies provide molecular insight into the assembly of CARMA1 and BCL10.
The protein encoded by this gene belongs to the membrane-associated guanylate kinase (MAGUK) family, a class of proteins that functions as molecular scaffolds for the assembly of multiprotein complexes at specialized regions of the plasma membrane. This protein is also a member of the CARD protein family, which is defined by carrying a characteristic caspase-associated recruitment domain (CARD). This protein has a domain structure similar to that of CARD14 protein. The CARD domains of both proteins have been shown to specifically interact with BCL10, a protein known to function as a positive regulator of cell apoptosis and NF-kappaB activation. When expressed in cells, this protein activated NF-kappaB and induced the phosphorylation of BCL10.
caspase recruitment domain family, member 11
, caspase recruitment domain-containing protein 11-like
, CARD-containing MAGUK protein 1
, bcl10-interacting maguk protein 3
, carma 1
, caspase recruitment domain-containing protein 11