Affinage

CARD14

Caspase recruitment domain-containing protein 14 · UniProt Q9BXL6

Length
1004 aa
Mass
113.3 kDa
Annotated
2026-06-09
74 papers in source corpus 22 papers cited in narrative 21 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CARD14 (CARMA2) is a CARD-MAGUK scaffold protein, predominantly expressed in the basal and suprabasal epidermis, that nucleates inflammatory signaling in keratinocytes by assembling a CARD14–BCL10–MALT1 (CBM) complex (PMID:11278692, PMID:22521418, PMID:22521419, PMID:27939769). Its CARD domain engages BCL10, recruiting and activating the paracaspase MALT1 to drive NF-κB and p38/JNK/ERK MAPK signaling and proinflammatory cytokine/chemokine expression (PMID:11278692, PMID:27113748, PMID:27071417). Complex assembly is normally restrained by the linker region, which autoinhibits BCL10 binding; psoriasis-associated gain-of-function mutations (e.g., G117S, E138A) disrupt this autoinhibition, producing constitutive BCL10/MALT1 recruitment, enhanced MALT1 protease activity, and elevated expression of psoriasis genes such as CCL20 and IL8 (PMID:22521418, PMID:22521419, PMID:27113748, PMID:27071417). Active CARD14 signalosomes recruit the ubiquitin ligases HOIP and TRAF6 to ubiquitinate BCL10—an event essential for NF-κB and MAPK activation—while CARD14 additionally localizes to early endosomes via the AP2 adaptor complex to activate mTORC1 and stimulate keratinocyte metabolism and proliferation (PMID:39145956). Multiple negative regulators tune this output, including RNF7 (ubiquitination of MALT1/NEMO), A20/ABIN1 (CARD14 turnover), UBAC1/TANK, and PLK1 binding the linker region (PMID:29194363, PMID:33316896, PMID:39145956, PMID:38797267). In vivo, keratinocyte-intrinsic CARD14 gain-of-function drives IL-23–IL-17A axis-dependent psoriatic skin disease that is reversed by MALT1, TNF, or IL-23 blockade (PMID:29980436, PMID:29689250, PMID:32343482, PMID:32597759), and CARD14 mediates IL-17A signaling itself by associating with the ACT1–TRAF6 complex (PMID:29980436). Dominant-negative loss-of-function CARD14 mutations reduce keratinocyte NF-κB signaling and are associated with severe atopic dermatitis (PMID:30248356). Beyond skin, CARD14 gain-of-function disrupts intestinal epithelial homeostasis (PMID:41131424) and promotes osteoclast differentiation through a MYC-dependent pathway (PMID:40971787).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 2001 High

    Established CARD14's founding molecular activity—how it could trigger inflammatory signaling—by showing its CARD domain binds BCL10 and activates NF-κB.

    Evidence Reciprocal domain-mapping Co-IP and NF-κB reporter assays in transfected cells

    PMID:11278692

    Open questions at the time
    • Did not identify downstream effectors beyond BCL10
    • No endogenous/physiological trigger defined
    • No disease link yet
  2. 2011 High

    Resolved isoform-specific function by showing a short CARMA2 isoform localizes to cytosol, binds TRAF2, activates NF-κB and is anti-apoptotic, indicating splicing diversifies CARD14 signaling.

    Evidence Isoform RT-PCR, fluorescence localization, Co-IP, NF-κB reporter and apoptosis assays

    PMID:21302310

    Open questions at the time
    • Physiological role of cardless isoform unclear
    • TRAF2 dependence not tied to keratinocyte biology
  3. 2012 High

    Connected CARD14 to human disease by demonstrating gain-of-function mutations enhance NF-κB and induce psoriasis-associated genes in keratinocytes where CARD14 is expressed.

    Evidence Genomic sequencing, NF-κB reporter, keratinocyte expression profiling, immunohistochemistry

    PMID:22521418 PMID:22521419

    Open questions at the time
    • Did not define the effector complex downstream of mutant CARD14
    • Mechanism of mutational hyperactivation unresolved
  4. 2014 Medium

    Expanded the interactome and cellular context by identifying DEPDC7 as a required cofactor for CARMA2-dependent NF-κB and showing CARD14 acts in dermal endothelial cells as well as keratinocytes.

    Evidence Yeast two-hybrid, Co-IP, shRNA knockdown; immunofluorescence co-localization and mutant transfection in endothelial cells

    PMID:25369198 PMID:25541973

    Open questions at the time
    • DEPDC7 mechanism single-lab
    • Endothelial contribution to psoriasis in vivo untested
  5. 2016 High

    Defined the core effector mechanism and its autoinhibition: CARD14 recruits MALT1 via BCL10 to drive NF-κB/MAPK, the linker region autoinhibits assembly, and psoriasis mutations relieve this to boost MALT1 protease activity.

    Evidence Co-IP, MALT1 protease assays, linker-region deletion mutagenesis, MAPK and reporter assays in primary keratinocytes

    PMID:27071417 PMID:27113748 PMID:27939769

    Open questions at the time
    • Structural basis of linker autoinhibition not solved
    • MALT1 substrates in keratinocytes not enumerated
  6. 2017 Medium

    Identified a negative regulator, showing RNF7 dampens CARMA2 NF-κB output via MALT1/NEMO ubiquitination and that mutants escape this control.

    Evidence Yeast two-hybrid, Co-IP, ubiquitination assays, NF-κB reporter

    PMID:29194363

    Open questions at the time
    • Single-lab interaction
    • In vivo relevance of RNF7 regulation untested
  7. 2018 High

    Provided definitive in vivo causation, linking CARD14 self-aggregation to IL-23/IL-17A-axis-driven psoriasis and to IL-17A signaling via the ACT1-TRAF6 complex, with concurrent demonstration of IL-23 dependence.

    Evidence Card14 gain-of-function knock-in and knockout mice, IL-23p19 neutralization, Co-IP of ACT1-TRAF6, cytokine measurements

    PMID:29689250 PMID:29980436

    Open questions at the time
    • Cell type initiating disease not yet isolated
    • Mechanism coupling aggregation to ACT1-TRAF6 unclear
  8. 2018 Medium

    Showed the bidirectional disease spectrum—dominant-negative CARD14 mutations reduce keratinocyte NF-κB and cause severe atopic dermatitis—establishing signaling dosage as the determinant.

    Evidence NF-κB reporter, immunohistochemistry of patient tissue, keratinocyte ELISA, sequencing

    PMID:30248356

    Open questions at the time
    • No animal model of loss-of-function allele
    • Innate mediator dysregulation mechanism incomplete
  9. 2019 Medium

    Linked CARD14 to TLR3 antiviral signaling by showing CARMA2sh/TANK/MALT1 complexes are required for poly(I:C)-induced NF-κB while repressing the TBK1/IRF3 arm.

    Evidence Co-IP, siRNA knockdown, NF-κB and TBK1/IRF3 pathway assays in keratinocytes

    PMID:31486084

    Open questions at the time
    • Physiological role of IRF3 repression untested
    • Single-lab
  10. 2020 High

    Pinpointed keratinocyte-intrinsic CARD14/MALT1 signaling as causal and druggable, showing MALT1 deletion/inhibition, TNF blockade, and adaptive-immune-independence all shape disease.

    Evidence Keratinocyte-specific and inducible CARD14E138A mice, conditional MALT1 KO, MALT1 inhibitor, anti-TNF, immunodeficient crosses, histology

    PMID:32343482 PMID:32597759

    Open questions at the time
    • Innate effector circuit downstream of keratinocytes not fully mapped
    • Systemic pustular phenotype mechanism partial
  11. 2020 Medium

    Added a further negative regulator, UBAC1, which K63-ubiquitinates TANK within the CARMA2sh/TANK complex to restrain TLR3-induced NF-κB.

    Evidence Yeast two-hybrid, Co-IP, K63-ubiquitination assay, siRNA, reporter in keratinocytes

    PMID:33316896

    Open questions at the time
    • Single-lab
    • In vivo significance untested
  12. 2021 Medium

    Revealed an unexpected genome-stability consequence: pathogenic CARD14 mutations increase DSBs under replication stress and favor break-induced replication, explaining revertant mosaicism.

    Evidence DSB quantification, replication stress and origin-firing assays, patient tissue analysis

    PMID:34004138

    Open questions at the time
    • Mechanistic link between CARD14 signaling and replication stress unclear
    • Single-lab
  13. 2024 High

    Defined the ubiquitin-driven activation circuit and a proliferative arm: HOIP/TRAF6 ubiquitinate BCL10 for NF-κB/MAPK, A20/ABIN1 drive CARD14 turnover, and AP2-mediated endosomal localization activates mTORC1 to promote keratinocyte proliferation.

    Evidence AP-MS, Co-IP, ubiquitination assays, endosome fractionation, AP2 inhibition, mTORC1 assays, in vivo rapamycin

    PMID:39145956

    Open questions at the time
    • How AP2 selectively routes mTORC1 but not NF-κB activation unresolved
    • Structural basis of endosomal signalosome unknown
  14. 2024 High

    Identified PLK1 as a phospho-dependent linker-region binder that negatively regulates CARD14 inflammatory signaling, coupling the scaffold to cell-cycle kinase control.

    Evidence AP-MS, Co-IP, linker-motif and CARD-domain mutagenesis, confocal localization, proinflammatory gene expression

    PMID:38797267

    Open questions at the time
    • Whether PLK1 phosphorylates CARD14 directly unestablished
    • Physiological/in vivo role of PLK1 regulation untested
  15. 2025 Medium

    Extended CARD14 function beyond skin by showing intestinal epithelial gain-of-function causes inflammation, reduced motility, Paneth cell/antimicrobial defects, and dysbiosis.

    Evidence IEC-specific CARD14E138A transgenic mice, motility and antimicrobial assays, IEC RNA-seq, bacterial challenge

    PMID:41131424

    Open questions at the time
    • Effector pathway in IECs not dissected
    • Single study
  16. 2026 Medium

    Implicated CARD14 in bone biology by showing it interacts with MYC and promotes osteoclast differentiation alongside NF-κB/MAPK activation.

    Evidence Co-IP, adenoviral overexpression in BM macrophages, BM-specific Card14 KO mice, micro-CT, TRAP and resorption assays

    PMID:40971787

    Open questions at the time
    • Mechanism coupling CARD14 to MYC in osteoclasts unclear
    • Single lab, novel context

Open questions

Synthesis pass · forward-looking unresolved questions
  • How distinct CARD14 outputs (NF-κB/MAPK inflammation, endosomal mTORC1 proliferation, replication-stress, MYC-dependent osteoclastogenesis) are selectively wired from a single scaffold, and the structural basis of linker autoinhibition, remain unresolved.
  • No structure of autoinhibited vs. active CARD14 signalosome
  • Determinants of output selectivity (NF-κB vs mTORC1 vs MYC) unknown
  • Cross-tissue regulatory differences uncharacterized

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 4 GO:0098772 molecular function regulator activity 3
Localization
GO:0005829 cytosol 2 GO:0005768 endosome 1
Pathway
R-HSA-162582 Signal Transduction 3 R-HSA-1643685 Disease 3 R-HSA-168256 Immune System 3
Partners
BCL10DEPDC7HOIPMALT1PLK1TANKTRAF2TRAF6
Complex memberships
ACT1-TRAF6 complexCARMA2sh-TANK-MALT1 complexCBM complex (CARD14-BCL10-MALT1)

Evidence

Reading pass · 21 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2001 CARD14 (CARMA2) is a CARD-containing MAGUK family protein whose CARD domain specifically associates with the CARD domain of BCL10, and when expressed in cells, activates NF-κB and induces phosphorylation of BCL10. Co-immunoprecipitation, cell-based NF-κB reporter assay, transfection The Journal of biological chemistry High 11278692
2011 Alternative splicing of CARD14/CARMA2 produces a short isoform (CARMA2sh) containing CARD, coiled-coil, and PDZ domains, and a cardless isoform (CARMA2cl); CARMA2sh localizes to the cytosol, interacts with TRAF2, and activates NF-κB in a TRAF2-dependent manner, and also protects cells from apoptosis. RT-PCR/isoform identification, fluorescence microscopy (localization), co-immunoprecipitation (TRAF2 interaction), NF-κB reporter assay, apoptosis assay Journal of cellular physiology High 21302310
2012 Gain-of-function mutations in CARD14 (p.Gly117Ser, p.Glu138Ala) lead to enhanced NF-κB activation and upregulation of psoriasis-associated genes (CCL20, IL8) in keratinocytes; CARD14 is localized mainly to the basal and suprabasal layers of the epidermis. Genomic sequencing, NF-κB luciferase reporter assay, gene expression profiling in keratinocytes, immunohistochemistry (localization) American journal of human genetics High 22521418 22521419
2014 DEPDC7 (a DEP domain-containing protein) binds to CARMA2 (CARD14) and CARMA3 in the cytosol and is required for NF-κB activation downstream of G protein-coupled receptor stimulation; shRNA-mediated knockdown of DEPDC7 impairs CARMA2/CARMA3-dependent but not CARMA1-dependent NF-κB activation. Yeast two-hybrid screening, co-immunoprecipitation, shRNA knockdown, NF-κB reporter assay, subcellular localization PloS one Medium 25541973
2014 CARD14 is expressed in dermal CD31+ endothelial cells in addition to epidermal keratinocytes; transfection of dermal endothelial cells with psoriasis-associated CARD14 mutations results in increased expression of chemokines CXCL10, IL-8, and CCL2, and phosphorylated NF-κB is detected in psoriatic CARD14+ endothelial cells. Two-color immunofluorescence co-localization, transfection with mutant CARD14 constructs, gene expression assays, immunohistochemistry PloS one Medium 25369198
2016 CARD14 physically interacts with the paracaspase MALT1, and activates NF-κB, p38, and JNK MAP kinase pathways in keratinocytes; all three pathways are dependent on MALT1. Psoriasis-associated CARD14 mutations enhance CARD14-MALT1 interaction and MALT1 proteolytic activity, and MALT1 deficiency or pharmacological inhibition reduces mutant CARD14-induced cytokine/chemokine expression in human primary keratinocytes. Co-immunoprecipitation (CARD14-MALT1 interaction), MALT1 protease activity assay, MALT1 knockdown/inhibitor experiments, NF-κB and MAPK signaling assays, cytokine expression in primary keratinocytes EMBO reports High 27113748
2016 Psoriasis mutants CARD14(E138A) and CARD14(G117S) constitutively interact with BCL10 and MALT1; the CARD14 linker region (LR) normally exerts an autoinhibitory effect on NF-κB activation by preventing BCL10 binding, and mutations disrupt this autoinhibition. CARD14(E138A) also stimulates MALT1 paracaspase activity and activates ERK1/2 and p38α MAP kinases. Co-immunoprecipitation (constitutive BCL10/MALT1 binding), linker region deletion mutagenesis, NF-κB reporter assay, MALT1 paracaspase activity assay, MAPK phosphorylation assay, keratinocyte gene expression The Biochemical journal High 27071417
2016 CARD14-mediated activation of MALT1 protease activity in keratinocytes drives psoriasis-associated inflammatory gene expression; CARD14 forms a CBM (CARD14-BCL10-MALT1) signaling complex whose assembly and MALT1 activation are enhanced by psoriasis-associated mutations. MALT1 protease assay, co-immunoprecipitation, gene expression analysis, pharmacological inhibition of MALT1 The Journal of investigative dermatology Medium 27939769
2017 The E3 ubiquitin ligase RNF7 interacts with CARMA2 (CARD14) and negatively regulates its NF-κB-activating capacity by modulating ubiquitination of MALT1 and NEMO; psoriasis-associated CARMA2sh mutants escape this negative regulation by RNF7. Yeast two-hybrid screening (RNF7 as CARMA2 interactor), co-immunoprecipitation, ubiquitination assays, NF-κB reporter assay International journal of molecular sciences Medium 29194363
2018 Card14 gain-of-function (E138A/+, ΔQ136/+) mice develop spontaneous psoriasis-like skin inflammation through constitutive CARMA2 self-aggregation, which leads to enhanced activation of the IL-23–IL-17A cytokine axis; CARMA2 associates with the ACT1-TRAF6 signaling complex and mediates IL-17A-induced NF-κB and MAPK signaling in keratinocytes. Card14-/- mice show attenuated IMQ-induced skin inflammation due to impaired IL-17A signaling. Knock-in mouse models (spontaneous disease), Card14 knockout mice (loss-of-function), co-immunoprecipitation (ACT1-TRAF6 complex), NF-κB and MAPK signaling assays, cytokine measurements Immunity High 29980436
2018 Heterozygous Card14ΔE138 gain-of-function mutation in mice is sufficient to drive chronic psoriatic skin disease with IL-23/IL-17 axis-dependent pathogenesis; neutralization of IL-23p19 significantly reduced skin lesions and proinflammatory gene expression. Knock-in mouse model (Card14ΔE138 heterozygous), IL-23p19 neutralizing antibody treatment, histology, cytokine/chemokine expression analysis The Journal of investigative dermatology High 29689250
2018 Loss-of-function mutations in CARD14 (dominant negative effect) result in decreased NF-κB signaling in keratinocytes and are associated with severe atopic dermatitis; CARD14-deficient or mutant-expressing keratinocytes display abnormal secretion of innate immunity mediators. Dual luciferase reporter assay (NF-κB), immunohistochemistry (p65/CARD14), direct sequencing, keratinocyte functional assays (ELISA) The Journal of allergy and clinical immunology Medium 30248356
2019 CARMA2sh (CARD14 short isoform) and TANK form a complex with MALT1 in human keratinocytes; CARMA2sh and TANK are both required for NF-κB activation following TLR3 stimulation with poly(I:C), while CARMA2sh functions as a repressor of the TBK1/IRF3 pathway downstream of TLR3. Psoriasis-associated CARMA2sh mutants bind less efficiently to TANK and are less effective in suppressing the TBK1/IRF3 pathway. Co-immunoprecipitation (CARMA2sh-TANK-MALT1 complex), siRNA knockdown, NF-κB reporter assay, TBK1/IRF3 pathway assays, poly(I:C) stimulation Journal of cellular physiology Medium 31486084
2020 Keratinocyte-specific expression of CARD14E138A in mice rapidly induces psoriatic skin inflammation; keratinocyte-specific MALT1 deletion or pharmacological MALT1 protease inhibition strongly reduces CARD14E138A-induced psoriatic skin disease, demonstrating a keratinocyte-intrinsic causal role of CARD14/MALT1 signaling in psoriasis. Inducible keratinocyte-specific CARD14E138A transgenic mice, conditional MALT1 knockout in keratinocytes, MALT1 pharmacological inhibitor (oral), histology, gene expression analysis EMBO reports High 32343482
2020 CARD14E138A-induced skin inflammation and systemic disease are independent of adaptive immune cells, ameliorated by blocking TNF, and induced specifically by CARD14E138A signaling in keratinocytes (demonstrated by knock-in allowing tamoxifen-inducible keratinocyte expression); homozygous CARD14E138A induces systemic disease resembling acute generalized pustular psoriasis exacerbations. Tamoxifen-inducible knock-in mouse model, anti-TNF treatment, immunodeficient mouse crosses, histology, gene expression eLife High 32597759
2020 UBAC1 (non-catalytic subunit of the KPC E3 ubiquitin ligase complex) interacts with CARMA2sh and participates in the CARMA2sh/TANK complex; UBAC1 promotes K63-linked ubiquitination of TANK and negatively regulates the NF-κB-activating capacity of CARMA2sh following TLR3 stimulation in human keratinocytes. Yeast two-hybrid screening, co-immunoprecipitation, K63-ubiquitination assay, siRNA knockdown, NF-κB reporter assay, poly(I:C) stimulation of keratinocytes International journal of molecular sciences Medium 33316896
2021 Pathogenic CARD14 mutations increase DNA double-strand breaks under replication stress conditions and suppress new origin firings without promoting crossover events, preferentially driving break-induced replication (BIR); this altered replication stress response underlies recombination-induced revertant mosaicism in CARD14-mutant patients. DNA damage assays (DSB quantification), replication stress assays, origin firing analysis, crossover analysis, patient tissue analysis American journal of human genetics Medium 34004138
2024 CARD14E138A associates with HOIP (M1-specific ubiquitin E3 ligase) and TRAF6 (K63-specific ubiquitin E3 ligase), which promote BCL10 ubiquitination and are essential for NF-κB and MAP kinase activation. A20 and ABIN1 negatively regulate signaling by inducing CARD14E138A turnover. CARD14E138A localizes to early endosomes via association with the AP2 adaptor complex; AP2 function is required for CARD14E138A activation of mTORC1 (but not NF-κB or MAP kinase), which stimulates keratinocyte metabolism and proliferation. Rapamycin (mTORC1 inhibitor) ameliorates CARD14E138A-induced keratinocyte proliferation and epidermal acanthosis in mice. Affinity purification–mass spectrometry (AP-MS), co-immunoprecipitation, ubiquitination assays, subcellular fractionation/early endosome localization, AP2 inhibition, mTORC1 signaling assays, rapamycin treatment in vivo, mouse model The Biochemical journal High 39145956
2024 PLK1 (polo-like kinase 1) is a novel CARD14-binding protein; the interaction is mediated by a consensus phospho-dependent PLK1-binding motif in the CARD14 linker region (LR), independent of the CARD domain. CARD14E138A expression recruits PLK1 to CARD14-containing signalosomes in interphase keratinocytes. Disruption of the PLK1-binding motif in CARD14E138A increases CARD14-induced proinflammatory signaling and gene expression, indicating PLK1 negatively regulates CARD14 signaling. Affinity purification–mass spectrometry (AP-MS), co-immunoprecipitation, CARD domain deletion mutagenesis, linker region motif mutagenesis, subcellular localization (confocal imaging in interphase vs. mitotic cells), proinflammatory gene expression assays Biochemical pharmacology High 38797267
2025 Gain-of-function CARD14(E138A) expression specifically in intestinal epithelial cells (IEC) induces mild intestinal inflammation, drastic reduction in intestinal motility, decreased Paneth cell antimicrobial peptide expression, microbial dysbiosis, and increased susceptibility to enteric bacterial infection; transcriptome analysis confirms cell-autonomous IEC signaling. IEC-specific CARD14(E138A) transgenic mouse model, intestinal motility assays, enteric neuron analysis, RNA-seq of IEC, antimicrobial peptide assays, bacterial infection challenge EMBO molecular medicine Medium 41131424
2026 CARD14 interacts with MYC and regulates osteoclast differentiation through a MYC-dependent pathway while simultaneously activating NF-κB and MAPK signaling; adenoviral CARD14 overexpression in bone marrow-derived macrophages markedly increases osteoclast differentiation and activity, and bone marrow-specific Card14 knockout mice show reduced osteoclast activity, improved trabecular bone microarchitecture, and increased BMD. Co-immunoprecipitation (CARD14-MYC interaction), adenoviral CARD14 overexpression in bone marrow macrophages, BM-specific Card14 knockout mice, micro-CT, TRAP staining, resorption pit assay, serum bone metabolism markers Journal of bone and mineral research Medium 40971787

Source papers

Stage 0 corpus · 74 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2012 PSORS2 is due to mutations in CARD14. American journal of human genetics 321 22521418
2001 CARD11 and CARD14 are novel caspase recruitment domain (CARD)/membrane-associated guanylate kinase (MAGUK) family members that interact with BCL10 and activate NF-kappa B. The Journal of biological chemistry 296 11278692
2012 Rare and common variants in CARD14, encoding an epidermal regulator of NF-kappaB, in psoriasis. American journal of human genetics 285 22521419
2012 Familial pityriasis rubra pilaris is caused by mutations in CARD14. American journal of human genetics 192 22703878
2018 Gain-of-Function Mutation of Card14 Leads to Spontaneous Psoriasis-like Skin Inflammation through Enhanced Keratinocyte Response to IL-17A. Immunity 132 29980436
2018 CARD14-associated papulosquamous eruption: A spectrum including features of psoriasis and pityriasis rubra pilaris. Journal of the American Academy of Dermatology 97 29477734
2015 Activating CARD14 Mutations Are Associated with Generalized Pustular Psoriasis but Rarely Account for Familial Recurrence in Psoriasis Vulgaris. The Journal of investigative dermatology 89 26203641
2014 The genetic background of generalized pustular psoriasis: IL36RN mutations and CARD14 gain-of-function variants. Journal of dermatological science 89 24656634
2018 CARD14 Gain-of-Function Mutation Alone Is Sufficient to Drive IL-23/IL-17-Mediated Psoriasiform Skin Inflammation In Vivo. The Journal of investigative dermatology 81 29689250
2017 Pityriasis Rubra Pilaris Type V as an Autoinflammatory Disease by CARD14 Mutations. JAMA dermatology 63 27760266
2018 Loss-of-function mutations in caspase recruitment domain-containing protein 14 (CARD14) are associated with a severe variant of atopic dermatitis. The Journal of allergy and clinical immunology 62 30248356
2018 Clinical and Genetic Heterogeneity of CARD14 Mutations in Psoriatic Skin Disease. Frontiers in immunology 62 30386326
2011 Alternative splicing of CARMA2/CARD14 transcripts generates protein variants with differential effect on NF-κB activation and endoplasmic reticulum stress-induced cell death. Journal of cellular physiology 62 21302310
2016 The paracaspase MALT1 mediates CARD14-induced signaling in keratinocytes. EMBO reports 61 27113748
2016 Psoriasis mutations disrupt CARD14 autoinhibition promoting BCL10-MALT1-dependent NF-κB activation. The Biochemical journal 55 27071417
2014 CARD14 expression in dermal endothelial cells in psoriasis. PloS one 46 25369198
2018 CARD14/CARMA2 Signaling and its Role in Inflammatory Skin Disorders. Frontiers in immunology 37 30319628
2017 Beneficial effect of ustekinumab in familial pityriasis rubra pilaris with a new missense mutation in CARD14. The British journal of dermatology 34 28301045
2017 Essential Role of CARD14 in Murine Experimental Psoriasis. Journal of immunology (Baltimore, Md. : 1950) 32 29150564
2015 CARD14 alterations in Tunisian patients with psoriasis and further characterization in European cohorts. The British journal of dermatology 32 26358359
2016 CARD14-Mediated Activation of Paracaspase MALT1 in Keratinocytes: Implications for Psoriasis. The Journal of investigative dermatology 29 27939769
2019 Whole exome sequencing approach to childhood onset familial erythrodermic psoriasis unravels a novel mutation of CARD14 requiring unusual high doses of ustekinumab. Pediatric rheumatology online journal 28 31286971
2020 CARD14E138A signalling in keratinocytes induces TNF-dependent skin and systemic inflammation. eLife 27 32597759
2013 SNP rs11652075 in the CARD14 gene as a risk factor for psoriasis (PSORS2) in a Spanish cohort. DNA and cell biology 25 23905699
2018 Caspase recruitment domain (CARD) family (CARD9, CARD10, CARD11, CARD14 and CARD15) are increased during active inflammation in patients with inflammatory bowel disease. Journal of inflammation (London, England) 24 30008619
2016 Common and rare CARD14 gene variants affect the antitumour necrosis factor response among patients with psoriasis. The British journal of dermatology 23 26854129
2014 The Dishevelled, EGL-10 and pleckstrin (DEP) domain-containing protein DEPDC7 binds to CARMA2 and CARMA3 proteins, and regulates NF-κB activation. PloS one 22 25541973
2020 MALT1 targeting suppresses CARD14-induced psoriatic dermatitis in mice. EMBO reports 20 32343482
2005 Lack of evidence for genetic association to RUNX1 binding site at PSORS2 in different German psoriasis cohorts. The Journal of investigative dermatology 19 15654961
2006 Investigation of the chromosome 17q25 PSORS2 locus in atopic dermatitis. The Journal of investigative dermatology 18 16374479
2015 CARD14 gene polymorphism c.C2458T (p.Arg820Trp) is associated with clinical features of psoriasis vulgaris in a Chinese cohort. The Journal of dermatology 17 26249641
2020 Regulation and dysregulation of CARD14 signalling and its physiological consequences in inflammatory skin disease. Cellular immunology 16 32593012
2019 Histopathologic findings characteristic of CARD14-associated papulosquamous eruption. Journal of cutaneous pathology 16 31849081
2015 CARD14 Glu138 mutation in familial pityriasis rubra pilaris does not warrant differentiation from familial psoriasis. The Journal of dermatology 16 26130407
2017 The E3 Ubiquitin Ligase RNF7 Negatively Regulates CARD14/CARMA2sh Signaling. International journal of molecular sciences 14 29194363
2016 Intra-familial Variation in Clinical Phenotype of CARD14-related Psoriasis. Acta dermato-venereologica 13 26984337
2020 UBAC1/KPC2 Regulates TLR3 Signaling in Human Keratinocytes through Functional Interaction with the CARD14/CARMA2sh-TANK Complex. International journal of molecular sciences 12 33316896
2016 The common CARD14 gene missense polymorphism rs11652075 (c.C2458T/p.Arg820Trp) is associated with psoriasis: a meta-analysis. Genetics and molecular research : GMR 12 27706581
2019 Gain of function p.E138A alteration in Card14 leads to psoriasiform skin inflammation and implicates genetic modifiers in disease severity. Experimental and molecular pathology 11 31323190
2023 Correlation of IL36RN and CARD14 mutations with clinical manifestations and laboratory findings in patients with generalised pustular psoriasis. Indian journal of dermatology, venereology and leprology 10 36331855
2015 Interaction of CARD14, SENP1 and VEGFA polymorphisms on susceptibility to high altitude polycythemia in the Han Chinese population at the Qinghai-Tibetan Plateau. Blood cells, molecules & diseases 10 26852650
2020 Knockdown of CARD14 Inhibits Cell Proliferation and Migration in Breast Cancer Cells. Anticancer research 9 32234884
2020 Two cases of CARD14-associated papulosquamous eruption from India. Pediatric dermatology 9 32323375
2017 Acute generalized exanthematous pustulosis and polyarthritis associated with a novel CARD14 mutation. The Australasian journal of dermatology 9 28776328
2016 Variants of CARD14 gene and psoriasis vulgaris in southern Chinese cohort. Anais brasileiros de dermatologia 9 26982778
2021 Altered replication stress response due to CARD14 mutations promotes recombination-induced revertant mosaicism. American journal of human genetics 8 34004138
2022 Association of PSORS1C3, CARD14 and TLR4 genotypes and haplotypes with psoriasis susceptibility. Genetics and molecular biology 7 36382932
2021 Identification of a pathogenic CARD14 mutation in a 70-year-old woman with pityriasis rubra pilaris: when genetic diagnosis influences choice of treatment strategy. BMJ case reports 7 33431438
2019 CARD14/CARMA2sh and TANK differentially regulate poly(I:C)-induced inflammatory reaction in keratinocytes. Journal of cellular physiology 7 31486084
2018 Nuclear Factor κB Activation in a Type V Pityriasis Rubra Pilaris Patient Harboring Multiple CARD14 Variants. Frontiers in immunology 7 30018619
2024 Case report: Successful treatment with biologics in a pediatric patient with a severe inflammatory skin disease and novel CARD14 mutation. Frontiers in medicine 6 38375322
2023 Case report: Infantile generalized pustular psoriasis with IL36RN and CARD14 gene mutations. Frontiers in genetics 6 36704338
2022 Association between CARD14 gene polymorphisms and psoriasis vulgaris in Hainan Han population based on exon sequencing: A case-control study. Medicine 6 36221432
2006 PSORS2 markers are not associated with psoriatic arthritis in the Italian population. Human heredity 6 16733365
2022 CARD14 Missense Variant Underlying CARD14-Associated Papulosquamous Eruption with Beneficial Response to Secukinumab. JID innovations : skin science from molecules to population health 5 36699196
2024 CARD14 signalosome formation is associated with its endosomal relocation and mTORC1-induced keratinocyte proliferation. The Biochemical journal 3 39145956
2023 A novel mutation in a CARD14-associated papulosquamous eruption. Pediatric dermatology 3 36724903
2022 Association of CARD14 Single-Nucleotide Polymorphisms with Psoriasis. International journal of molecular sciences 3 36012602
2025 Similar Molecular Features in Two Cases of CARD14-Associated Papulosquamous Eruption. The Australasian journal of dermatology 2 40084598
2025 Clinical Characteristics of CARD14-Associated Papulosquamous Eruption and Evaluation of Therapeutic Efficacy of Secukinumab. Journal of inflammation research 2 40433052
2021 CARD14-associated papulosquamous eruption (CAPE) in a toddler responding to treatment with acitretin. Pediatric dermatology 2 34075616
2020 Updating and identifying three novel variants of the CARD14 gene in Chinese Han patients with psoriasis. Journal of genetics 2 33622988
2026 CARD14-mediated MYC interaction promotes osteoclastogenesis and bone density reduction in adolescent idiopathic scoliosis. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 1 40971787
2025 Neonatal CARD14-Associated Papulosquamous Eruption: Response to Secukinumab During Infancy. Pediatric dermatology 1 40525499
2025 Case Report: Successful treatment of a novel variant of CARD14-mutated juvenile Pityriasis rubra pilaris with ixekizumab. Frontiers in medicine 1 40766060
2024 Polo-like kinase 1 (PLK1) is a novel CARD14-binding protein in keratinocytes. Biochemical pharmacology 1 38797267
2024 A case of revertant mosaic-like normal-looking spots in a patient with erythroderma with IL36RN and CARD14 heterozygous mutations. The Journal of dermatology 1 39373130
2023 Clinical features of acute generalized exanthematous pustulosis caused by hydroxychloroquine in rheumatology patients and exploration of CARD14 gene mutations. Frontiers in medicine 1 37089611
2023 Acute generalized exanthematous pustulosis caused by hydroxychloroquine in a patient with rheumatoid arthritis and CARD14 mutation: Case report. Medicine 1 38013380
2022 Cutaneous and Developmental Effects of CARD14 Overexpression in Zebrafish. Biomedicines 1 36551948
2026 CARD14-Associated Papulosquamous Eruption (CAPE): An Updated Review of Pathogenesis and Treatment. International journal of dermatology 0 41845528
2026 Case Report: Successful treatment of dystrophic epidermolysis bullosa pruriginosa with upadacitinib in a patient with COL7A1, CARD14, and G6PD gene mutations. Frontiers in medicine 0 42180729
2025 Impact of CARD14 rs34367357 Mutation, Nutrition Status, and Seasonality on the Response to Biologic Therapy in Psoriasis-A Retrospective Observational Single-Center Study. Journal of clinical medicine 0 41010661
2025 CARD14 signaling in intestinal epithelial cells induces intestinal inflammation and intestinal transit delay. EMBO molecular medicine 0 41131424

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