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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Caspase recruitment domain family, member 11

CARMA1, CARD11, Bimp3
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. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: BCL10, Eco, NF-kappaB, PrP, CAN
Papers on CARMA1
Oncogenic CARMA1 couples NF-κB and β-catenin signaling in diffuse large B-cell lymphomas.
Krappmann et al., München, Germany. In Oncogene, Feb 2016
Recurrent oncogenic mutations are found in the scaffold protein CARMA1 (CARD11) that connects B-cell receptor (BCR) signaling to the canonical NF-κB pathway.
Diffuse large B-cell lymphoma patient-derived xenograft models capture the molecular and biologic heterogeneity of the disease.
Shipp et al., Boston, United States. In Blood, Feb 2016
Six of the eight DLBCL models were ABC-type tumors that exhibited ABC-associated mutations such as MYD88, CD79B, CARD11 and PIM1.
Frequent MYD88 L265P and CD79B Mutations in Primary Breast Diffuse Large B-Cell Lymphoma.
Yoshino et al., Isehara, Japan. In Am J Surg Pathol, Feb 2016
ABC-like DLBCL was reported to have gain-of-function mutations in MYD88, CD79B, CARD11, and TNFAIP3, resulting in constitutive activation of the NFκB pathway.
CARMA1- and MyD88-dependent activation of Jun/ATF-type AP-1 complexes is a hallmark of ABC diffuse large B-cell lymphomas.
Thome et al., Lausanne, Switzerland. In Blood, Feb 2016
UNASSIGNED: A hallmark of the diffuse large B-cell lymphoma (DLBCL) of the activated B-cell (ABC) type, a molecular subtype characterized by adverse outcome, is constitutive activation of the transcription factor NF-κB, which controls expression of genes promoting cellular survival and proliferation.
T-Cell-Specific Deletion of Map3k1 Reveals the Critical Role for Mekk1 and Jnks in Cdkn1b-Dependent Proliferative Expansion.
Gallagher et al., London, United Kingdom. In Cell Rep, Feb 2016
Mekk1 regulates Jnk activation in iNKT cells and binds and transfers Lys63-linked poly-ubiquitin onto Carma1.
Unravelling the immunological roles of dipeptidyl peptidase 4 (DPP4) activity and/or structure homolog (DASH) proteins.
von Hörsten et al., Stuttgart, Germany. In Clin Exp Immunol, Jan 2016
UNASSIGNED: Dipeptidyl peptidase 4 (CD26, DPP4) is a multifunctional protein involved in T-cell activation by co-stimulation via its association with ADA, Caveolin-1, CARMA-1, CD45, M6P/IGFII-R and CXC-R4.
Genomic profiling of Sézary syndrome identifies alterations of key T cell signaling and differentiation genes.
Duvic et al., Houston, United States. In Nat Genet, Dec 2015
Frequent somatic alterations were identified in TP53, CARD11, CCR4, PLCG1, CDKN2A, ARID1A, RPS6KA1 and ZEB1.
The mutational landscape of cutaneous T cell lymphoma and Sézary syndrome.
Palomero et al., New York City, United States. In Nat Genet, Dec 2015
Mutation analysis identified a broad spectrum of somatic mutations in key genes involved in epigenetic regulation (TET2, CREBBP, KMT2D (MLL2), KMT2C (MLL3), BRD9, SMARCA4 and CHD3) and signaling, including MAPK1, BRAF, CARD11 and PRKG1 mutations driving increased MAPK, NF-κB and NFAT activity upon T cell receptor stimulation.
TCR signaling to NF-κB and mTORC1: Expanding roles of the CARMA1 complex.
Sun et al., Baoding, China. In Mol Immunol, Dec 2015
A central mediator of the TCR and CD28 signals is the scaffold protein CARMA1, which functions by forming a complex with partner proteins, Bcl10 and MALT1.
Integrated molecular analysis of adult T cell leukemia/lymphoma.
Ogawa et al., Kyoto, Japan. In Nat Genet, Nov 2015
Other notable features include a predominance of activating mutations (in PLCG1, PRKCB, CARD11, VAV1, IRF4, FYN, CCR4 and CCR7) and gene fusions (CTLA4-CD28 and ICOS-CD28).
Genetic errors of the human caspase recruitment domain-B-cell lymphoma 10-mucosa-associated lymphoid tissue lymphoma-translocation gene 1 (CBM) complex: Molecular, immunologic, and clinical heterogeneity.
Puel et al., Madrid, Spain. In J Allergy Clin Immunol, Nov 2015
Three members of the caspase recruitment domain (CARD) family of adaptors (CARD9, CARD10, and CARD11) are known to form heterotrimers with B-cell lymphoma 10 (BCL10) and mucosa-associated lymphoid tissue lymphoma-translocation gene 1 (MALT1).
Integration of gene mutations in risk prognostication for patients receiving first-line immunochemotherapy for follicular lymphoma: a retrospective analysis of a prospective clinical trial and validation in a population-based registry.
Weigert et al., München, Germany. In Lancet Oncol, Sep 2015
FINDINGS: We established a clinicogenetic risk model (termed m7-FLIPI) that included the mutation status of seven genes (EZH2, ARID1A, MEF2B, EP300, FOXO1, CREBBP, and CARD11), the Follicular Lymphoma International Prognostic Index (FLIPI), and Eastern Cooperative Oncology Group (ECOG) performance status.
Immunological loss-of-function due to genetic gain-of-function in humans: autosomal dominance of the third kind.
Casanova et al., New York City, United States. In Curr Opin Immunol, Feb 2015
Remarkably, six of the 17 genes concerned also harbor monoallelic (STAT3), biallelic (C3, CFB, CARD11, PIK3R1) or both monoallelic and biallelic (STAT1) LOF alleles in patients with other clinical phenotypes.
Primary Immunodeficiencies Associated with EBV Disease.
Cohen, Bethesda, United States. In Curr Top Microbiol Immunol, 2014
These include diseases due to mutations in PIK3CD, PIK3R1, CTPS1, STK4, GATA2, MCM4, FCGR3A, CARD11, ATM, and WAS.
Positive feedback within a kinase signaling complex functions as a switch mechanism for NF-κB activation.
Okada-Hatakeyama et al., Yokohama, Japan. In Science, 2014
We show that the CARD-containing MAGUK protein 1 (CARMA1, also called CARD11)-TAK1 (MAP3K7)-inhibitor of NF-κB (IκB) kinase-β (IKKβ) module is a switch mechanism for NF-κB activation in B cell receptor (BCR) signaling.
Protein kinase C-δ negatively regulates T cell receptor-induced NF-κB activation by inhibiting the assembly of CARMA1 signalosome.
Shu et al., Wuhan, China. In J Biol Chem, 2012
PKCdelta is a negative regulator in T cell activation through inhibiting the assembly of CARMA1 signalosome.
CARMA1 controls Th2 cell-specific cytokine expression through regulating JunB and GATA3 transcription factors.
Lin et al., Houston, United States. In J Immunol, 2012
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.
Cutting edge: the "death" adaptor CRADD/RAIDD targets BCL10 and suppresses agonist-induced cytokine expression in T lymphocytes.
Ruley et al., Nashville, United States. In J Immunol, 2012
We show that CRADD interacts with BCL10 through its caspase recruitment domain and suppresses interactions between BCL10 and CARMA1
CARMA1 is necessary for optimal T cell responses in a murine model of allergic asthma.
Medoff et al., Boston, United States. In J Immunol, 2012
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.
PKCθ synergizes with TLR-dependent TRAF6 signaling pathway to upregulate MUC5AC mucin via CARMA1.
Li et al., Rochester, United States. In Plos One, 2011
TLR-dependent TRAF6-MKK3-p38 MAPK signaling pathway synergizes with PKCtheta;-MEK-ERK signaling pathway. CARMA1 plays a crucial role in mediating this synergistic effect via TRAF6.
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