ArticleMolecular and cellular biology2008
The protein kinase C-responsive inhibitory domain of CARD11 functions in NF-kappaB activation to regulate the association of multiple signaling cofactors that differentially depend on Bcl10 and MALT1 for association.
Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 68 citations in OpenAlex.
- Potentiation of noncanonical NF-κB signaling and marginal zone B cell expansion by CARD11-mediated regulation of p100 processing.Cell reports · 2025Article
- QRICH1 mediates an intracellular checkpoint for CD8Science immunology · 2025Article
- From syndromic clues to diagnosis: understanding CARD11-driven disorders.Frontiers in immunology · 2025Review
- A new-disease-causing dominant-negative variant in CARD11 gene in a Chinese case with recurrent fever.Scientific reports · 2024Article
- The role of the CBM complex in allergic inflammation and disease.The Journal of allergy and clinical immunology · 2022Review
- BCL10 Mutations Define Distinct Dependencies Guiding Precision Therapy for DLBCL.Cancer discovery · 2022Article
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- Reconsidering phosphorylation in the control of inducible CARD11 scaffold activity during antigen receptor signaling.Advances in biological regulation · 2021Review
- Identification and Characterization of a Germline Mutation in CARD11 From a Chinese Case of B Cell Expansion With NF-κB and T Cell Anergy.Frontiers in immunology · 2021Article
- Coordinated regulation of scaffold opening and enzymatic activity during CARD11 signaling.The Journal of biological chemistry · 2019Article
- Structures of autoinhibited and polymerized forms of CARD9 reveal mechanisms of CARD9 and CARD11 activation.Nature communications · 2019Article
- CARMA3: Scaffold Protein Involved in NF-κB Signaling.Frontiers in immunology · 2019Review
- Mechanisms of Regulated and Dysregulated CARD11 Signaling in Adaptive Immunity and Disease.Frontiers in immunology · 2018Review
- BCL10-CARD11 Fusion Mimics an Active CARD11 Seed That Triggers Constitutive BCL10 Oligomerization and Lymphocyte Activation.Frontiers in immunology · 2018Article
- Post-translational Modifications of the CARMA1-BCL10-MALT1 Complex in Lymphocytes and Activated B-Cell Like Subtype of Diffuse Large B-Cell Lymphoma.Frontiers in oncology · 2018Review
- Impaired Control of Epstein-Barr Virus Infection in B-Cell Expansion with NF-κB and T-Cell Anergy Disease.Frontiers in immunology · 2018Review
- Germline hypomorphic CARD11 mutations in severe atopic disease.Nature genetics · 2017Article
- Intrinsic Plasma Cell Differentiation Defects in B Cell Expansion with NF-κB and T Cell Anergy Patient B Cells.Frontiers in immunology · 2017Article
- Molecular Determinants of Scaffold-induced Linear Ubiquitinylation of B Cell Lymphoma/Leukemia 10 (Bcl10) during T Cell Receptor and Oncogenic Caspase Recruitment Domain-containing Protein 11 (CARD11) Signaling.The Journal of biological chemistry · 2016Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The activation of NF-kappaB by T-cell receptor (TCR) signaling is critical for T-cell activation during the adaptive immune response. CARD11 is a multidomain adapter that is required for TCR signaling to the IkappaB kinase (IKK) complex. During TCR signaling, the region in CARD11 between the coiled-coil and PDZ domains is phosphorylated by protein kinase Ctheta (PKCtheta) in a required step in NF-kappaB activation. In this report, we demonstrate that this region functions as an inhibitory domain (ID) that controls the association of CARD11 with multiple signaling cofactors, including Bcl10, TRAF6, TAK1, IKKgamma, and caspase-8, through an interaction that requires both the caspase recruitment domain (CARD) and the coiled-coil domain. Consistent with the ID-mediated control of their association, we demonstrate that TRAF6 and caspase-8 associate with CARD11 in T cells in a signal-inducible manner. Using an RNA interference rescue assay, we demonstrate that the CARD, linker 1, coiled-coil, linker 3, SH3, linker 4, and GUK domains are each required for TCR signaling to NF-kappaB downstream of ID neutralization. Requirements for the CARD, linker 1, and coiled-coil domains in signaling are consistent with their roles in the association of CARD11 with Bcl10, TRAF6, TAK1, caspase-8, and IKKgamma. Using Bcl10- and MALT1-deficient cells, we show that CARD11 can recruit signaling cofactors independently of one another in a signal-inducible manner.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.