ArticleThe Journal of biological chemistry2016
Cooperative Control of Caspase Recruitment Domain-containing Protein 11 (CARD11) Signaling by an Unusual Array of Redundant Repressive Elements.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 37 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
- Recent advancements in the diverse roles of polymerase-associated proteins in the replication and pathogenesis of Newcastle disease virus.Veterinary research · 2025Review
- From syndromic clues to diagnosis: understanding CARD11-driven disorders.Frontiers in immunology · 2025Review
- KLF5‑mediated expression of CARD11 promotes the progression of gastric cancer.Experimental and therapeutic medicine · 2023Article
- Mistuned NF-κB signaling in lymphocytes: lessons from relevant inborn errors of immunity.Clinical and experimental immunology · 2023Article
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- Elevated IgE from attenuated CARD11 signaling: lessons from atopic mice and humans.Current opinion in immunology · 2022Review
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- Bcl10 is required for the development and suppressive function of Foxp3Cellular & molecular immunology · 2021Article
- Reconsidering phosphorylation in the control of inducible CARD11 scaffold activity during antigen receptor signaling.Advances in biological regulation · 2021Review
- Gain-of-function mutations in CARD11 promote enhanced aggregation and idiosyncratic signalosome assembly.Cellular immunology · 2020Article
- 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
- Hypomorphic caspase activation and recruitment domain 11 (CARD11) mutations associated with diverse immunologic phenotypes with or without atopic disease.The Journal of allergy and clinical immunology · 2019Article
- CTD-2020K17.1, a Novel Long Non-Coding RNA, Promotes Migration, Invasion, and Proliferation of Serous Ovarian Cancer Cells In Vitro.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Impaired Control of Epstein-Barr Virus Infection in B-Cell Expansion with NF-κB and T-Cell Anergy Disease.Frontiers in immunology · 2018Review
- A Unique HeterozygousFrontiers in immunology · 2018Article
- Mechanisms of Regulated and Dysregulated CARD11 Signaling in Adaptive Immunity and Disease.Frontiers in immunology · 2018Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Several classes of signaling proteins contain autoinhibitory domains that prevent unwarranted signaling and coordinate the induction of activity in response to external cues. CARD11, a scaffold protein critical for antigen receptor signaling to NF-κB, undergoes autoregulation by a poorly understood inhibitory domain (ID), which keeps CARD11 inactive in the absence of receptor triggering through inhibitory intramolecular interactions. This autoinhibitory strategy makes CARD11 highly susceptible to gain-of-function mutations that are frequently observed in diffuse large B cell lymphoma (DLBCL) and that disrupt ID-mediated autoinhibition, leading to constitutive NF-κB activity, which can promote lymphoma proliferation. Although DLBCL-associated CARD11 mutations in the caspase recruitment domain (CARD), LATCH domain, and coiled coil have been shown to disrupt intramolecular ID binding, surprisingly, no gain-of-function mutations in the ID itself have been reported and validated. In this study, we solve this paradox and report that the CARD11 ID contains an unusual array of four repressive elements that function cooperatively with redundancy to prevent spontaneous NF-κB activation. Our quantitative analysis suggests that potent oncogenic CARD11 mutations must perturb autoinhibition by at least three repressive elements. Our results explain the lack of ID mutations in DLBCL and reveal an unusual autoinhibitory domain structure and strategy for preventing unwarranted scaffold signaling to NF-κB.
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What OpenQuestion holds
Registered trials
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.