ArticleThe Biochemical journal2016
Psoriasis mutations disrupt CARD14 autoinhibition promoting BCL10-MALT1-dependent NF-κB activation.
Article in The Biochemical journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 70 citations in OpenAlex.
- Genotype-phenotype correlations in autoimmune and autoinflammatory diseases: An NGS-based immunogenetic cohort study.Immunogenetics · 2026Article
- NF‑κB signaling drives Th17‑mediated lacrimal gland injury and tear dysfunction in a murine model of primary Sjögren's syndrome.Molecular medicine reports · 2026Article
- CARD14 signaling in intestinal epithelial cells induces intestinal inflammation and intestinal transit delay.EMBO molecular medicine · 2025Article
- Pathophysiology and Treatment of Psoriasis: From Clinical Practice to Basic Research.Pharmaceutics · 2025Review
- Bioinformatic analysis of molecular characteristics and oncogenic features of CARD14 in human cancer.Scientific reports · 2024Article
- CARD14 signalosome formation is associated with its endosomal relocation and mTORC1-induced keratinocyte proliferation.The Biochemical journal · 2024Article
- Insights into mechanisms of MALT1 allostery from NMR and AlphaFold dynamic analyses.Communications biology · 2024Article
- Genetic and Immunological Pathogenesis of Atopic Dermatitis.The Journal of investigative dermatology · 2024Review
- Case report: Successful treatment with biologics in a pediatric patient with a severe inflammatory skin disease and novelFrontiers in medicine · 2024Article
- Article
- Association of CARD14 Single-Nucleotide Polymorphisms with Psoriasis.International journal of molecular sciences · 2022Article
- CARD14 Signalling Ensures Cell Survival and Cancer Associated Gene Expression in Prostate Cancer Cells.Biomedicines · 2022Article
- Novel role for caspase recruitment domain family member 14 and its genetic variant rs11652075 in skin filaggrin homeostasis.The Journal of allergy and clinical immunology · 2022Article
- Integrative analysis of macrophage ribo-Seq and RNA-Seq data define glucocorticoid receptor regulated inflammatory response genes into distinct regulatory classes.Computational and structural biotechnology journal · 2022Article
- Genetic Variants of the NF-κB Pathway: Unraveling the Genetic Architecture of Psoriatic Disease.International journal of molecular sciences · 2021Review
- Purinergic Signaling and Inflammasome Activation in Psoriasis Pathogenesis.International journal of molecular sciences · 2021Review
- Analysis of the Potential Genetic Links between Psoriasis and Cardiovascular Risk Factors.International journal of molecular sciences · 2021Review
- Molecular mechanisms of phenotypic variability in monogenic autoinflammatory diseases.Nature reviews. Rheumatology · 2021Review
- Immune responses and therapeutic options in psoriasis.Cellular and molecular life sciences : CMLS · 2021Review
- "Autoinflammatory psoriasis"-genetics and biology of pustular psoriasis.Cellular & molecular immunology · 2021Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Inherited and de novo mutations in the CARD14 gene promote the development of psoriasis, an inflammatory disease of the skin. Caspase recruitment domain-containing protein 14 (CARD14) is a member of the CARMA protein family that includes the structurally related CARD11 adaptor that mediates NF-κB activation by antigen receptors. We investigated the mechanism by which CARD14 mutation in psoriasis activates NF-κB. In contrast with wild-type CARD14, CARD14(E138A) and CARD14(G117S) psoriasis mutants interacted constitutively with BCL10 and MALT1, and triggered BCL10- and MALT1-dependent activation of NF-κB in keratinocytes. These alterations disrupted the inhibitory effect of the CARD14 linker region (LR) on NF-κB activation by facilitating BCL10 binding. Therefore, psoriasis mutations activated CARD14 by a mechanism analogous to oncogenic CARD11 mutations in non-Hodgkin B cell lymphomas. CARD14(E138A) also stimulated MALT1 paracaspase activity and activated both ERK1/2 and p38α MAP kinases. Inhibition of MALT1 with mepazine reduced CARD14(E138A)-induced expression of specific psoriasis-associated transcripts in keratinocytes. Our results establish the mechanism whereby gain-of-function CARD14 variants, which induce psoriatic disease in affected individuals, activate pro-inflammatory signalling.
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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.