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anti-Human CARD11 Antibodies:
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Human Polyclonal CARD11 Primary Antibody for IHC (p), WB - ABIN541216
Fanning, Anderson: Protein modules as organizers of membrane structure. in Current opinion in cell biology 1999
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Human Polyclonal CARD11 Primary Antibody for IHC (p), IHC - ABIN249816
Rajasekaran, Kumar, Schuldt, Peterson, Vanhaesebroeck, Dixit, Thakar, Malarkannan: Signaling by Fyn-ADAP via the Carma1-Bcl-10-MAP3K7 signalosome exclusively regulates inflammatory cytokine production in NK cells. in Nature immunology 2013
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Human Polyclonal CARD11 Primary Antibody for IHC, ELISA - ABIN1030313
Cheng, Hamilton, Kane: Phosphorylation of Carma1, but not Bcl10, by Akt regulates TCR/CD28-mediated NF-κB induction and cytokine production. in Molecular immunology 2014
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Human Polyclonal CARD11 Primary Antibody for IHC (p), ELISA - ABIN547040
Bertin, Wang, Guo, Jacobson, Poyet, Srinivasula, Merriam, DiStefano, Alnemri: CARD11 and CARD14 are novel caspase recruitment domain (CARD)/membrane-associated guanylate kinase (MAGUK) family members that interact with BCL10 and activate NF-kappa B. in The Journal of biological chemistry 2001
MALT1 activation by TRAF6 in lymphocytes needs neither BCL10 nor CARD11.
CARMA1 forms CARMA1-BCL10-MALT1-TRAF6 signalosome.CARMA1, the BCL10 nucleator, serves as a hub for formation of star-shaped filamentous networks of BCL10 and significantly decreases the lag period of BCL10 polymerization.
study results suggest variations in the inflammasome, particularly in NLRP1 and CARD11, may be associated with chronic Chagas cardiomyopathy
CARD11, a scaffold protein required for B-cell receptor (BCR)-induced NF-kappaB activation, was screened in an additional 173 MCL samples and mutations were observed in 5.5% of cases.
CARMA1 may be aberrantly upregulated in T-ALL, leading to disease progression and migration of leukemic cells to the CNS
findings indicate that a single hypomorphic mutation in CARD11 can cause potentially correctable cellular defects that lead to atopic dermatitis
NF-kappaB and beta-catenin signaling by gain-of-function mutations in CARMA1 augments WNT stimulation and is required for regulating the expression of distinct NF-kappaB target genes to trigger cell-intrinsic and extrinsic processes that promote DLBCL lymphomagenesis
CARD11 mutations are rare in patients with CD5+ DLBCL.
results define molecular determinants that control the production of Lin(Ub)n-Bcl10, an important signaling intermediate in TCR and oncogenic CARD11 signaling.
We evaluated the relationship between rs4722404 polymorphism in the CARD11 gene, and the risk and clinical features of psoriasis vulgaris in a southern Chinese Han cohort.We identified no association between the SNP and risk of psoriasis vulgaris.
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-dependent activation of Jun/ATF-type AP-1 complexes is a hallmark of ABC diffuse large B-cell lymphomas.
Data show that caspase recruitment domain-containing protein 11/B-cell CLL/lymphoma 10/mucosa-associated lymphoid tissue lymphoma translocation gene 1 signaling drives lymphoproliferation through NF-kappa B and c-Jun N-terminal kinase activation.
CARD11-mediated alterations in NF-kappaB signaling may be an early event in the development of cutaneous squamous cell carcinoma
Taken together, our data indicate that miR-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 signalling
Both carried homozygous germline mutations in CARD11 (p.Cys150*), impairing NF-kappaB signaling and IL-2 production
Three patients have been described with mild B-cell lymphocytosis and a CARD11 C49Y missense mutation.
Overexpression of CARMA-BCL10-MALT in T-ALL may contribute to the constitutive cleavage and inactivation of A20, which enhances NF-kappaB signaling and may be related to T-ALL pathogenesis.
CARD11-BCL10-MALT1 (CBM) signaling mediates TCR-induced NF-kappaB activation in Tregs and controls the conversion of resting Tregs to effector Tregs under homeostatic conditions. However, in inflammatory milieus, cytokines can bypass the CBM requirement for this differentiation step.
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.
LRRK1 physically interacted and potently synergized with CARMA1 to enhance NF-kappaB activation.
synergistic activity of Card11 mutant and Bcl6 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) by formation of the CARD11/Bcl10 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 controls completion of Th17 differentiation.
These studies provide molecular insight into the assembly of CARMA1 and BCL10.
Upregulation of CARMA1 in vivo results in Th2 cell-mediated inflammation. Mice expressing constitutively active CARMA1 have elevated IL-4, IL-5, and IL-10 and spontaneously develop pulmonary inflammation and eosinophilia.
We show that CRADD interacts with BCL10 through its caspase recruitment domain and suppresses interactions between BCL10 and CARMA1
Adoptive transfer of T helper cell (Th)2-polarized OX40+CARMA1-deficient antigen-specific CD4+ T cells into wild-type mice induces less airway inflammation in response to antigen challenge than does the transfer of wild-type Th2 cells.
Decreased T-cell receptor signaling through CARD11 differentially compromises Foxp3 regulatory T-cell suppression that result in selective Th2 dysregulation and allergic disease.
CARMA1 regulates IL-2 receptor signaling and controls the IL-2-stimulated maturation of Treg precursors to mature Tregs
the ADAP CARMA1 binding site is required for IKK gamma ubiquitination; both TAK1 and CARMA1 binding sites are required for IkappaB alpha phosphorylation and degradation and NF-kappaB nuclear translocation
found that antigen receptor-activated CARMA1 underwent lysine 48 (K48) polyubiquitination and proteasome-dependent degradation.
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.
CARD-containing MAGUK protein 1
, bcl10-interacting maguk protein 3
, carma 1
, caspase recruitment domain-containing protein 11
, caspase recruitment domain family, member 11
, caspase recruitment domain-containing protein 11-like