ArticleiScience2022
Mechanistic impact of oligomer poisoning by dominant-negative CARD11 variants.
Article in iScience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
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Who cites it
11 citing papers in PubMed, 15 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
- Dominant interfering CARD11 variants disrupt JNK signaling to promote GATA3 expression in T cells.The Journal of experimental medicine · 2025Article
- QRICH1 mediates an intracellular checkpoint for CD8Science immunology · 2025Article
- From syndromic clues to diagnosis: understanding CARD11-driven disorders.Frontiers in immunology · 2025Review
- A20 intrinsically influences human effector T-cell survival and function by regulating both NF-κB and JNK signaling.European journal of immunology · 2024Article
- A new-disease-causing dominant-negative variant in CARD11 gene in a Chinese case with recurrent fever.Scientific reports · 2024Article
- Biochemical, structural, and computational analyses of two new clinically identified missense mutations of ALDH7A1.Chemico-biological interactions · 2024Article
- Mistuned NF-κB signaling in lymphocytes: lessons from relevant inborn errors of immunity.Clinical and experimental immunology · 2023Article
- Elevated IgE from attenuated CARD11 signaling: lessons from atopic mice and humans.Current opinion in immunology · 2022Review
- CARD11 signaling in regulatory T cell development and function.Advances in biological regulation · 2022Review
- Expanding spectrum, intrafamilial diversity, and therapeutic challenges from 15 patients with heterozygous CARD11-associated diseases: A single center experience.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The CARD11 scaffold controls antigen receptor signaling to NF-κB, JNK, and mTOR. Three classes of germline mutations in CARD11 cause Primary Immunodeficiency, including homozygous loss-of-function (LOF) mutations in CARD11 deficiency, heterozygous gain-of-function (GOF) mutations in BENTA disease, and heterozygous dominant-negative LOF mutations in CADINS. Here, we characterize LOF CARD11 mutants with a range of dominant-negative activities to identify the mechanistic properties that cause these variants to exert dominant effects when heterozygous. We find that strong dominant negatives can poison signaling from mixed wild-type:mutant oligomers at two steps in the CARD11 signaling cycle, at the Opening Step and at the Cofactor Association Step. Our findings provide evidence that CARD11 oligomer subunits cooperate in at least two steps during antigen receptor signaling and reveal how different LOF mutations in the same oligomeric signaling hub may cause disease with different inheritance patterns.
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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.