CARD14 Antibody
- Known as:
- CARD14 Antibody
- Catalog number:
- XW-7890
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- CARD14 Antibody
Related genes to: CARD14 Antibody
- Gene:
- CARD14 NIH gene
- Name:
- caspase recruitment domain family member 14
- Previous symbol:
- PSORS2
- Synonyms:
- CARMA2, BIMP2
- Chromosome:
- 17q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-09-19
- Date modifiied:
- 2019-04-23
Related products to: CARD14 Antibody
Related articles to: CARD14 Antibody
- Generalized pustular psoriasis (GPP) is a rare, severe, and potentially life-threatening inflammatory dermatosis increasingly recognized as a distinct disease entity rather than a variant of plaque psoriasis. Emerging evidence indicates that GPP is primarily driven by dysregulation of the interleukin-36 (IL-36) signaling axis, leading to amplification of proinflammatory cascades in keratinocytes and a predominantly innate, neutrophil-driven immune response. This promotes rapid neutrophil recruitment, sterile pustule formation, and abrupt cutaneous and systemic inflammation. Consistent with this, GPP demonstrates a greater predominance of innate immune and neutrophil-driven inflammation, whereas plaque psoriasis is more strongly associated with IL-23/Th17-mediated adaptive immune responses. Transcriptomic and genetic studies further support this distinction, demonstrating enrichment of IL-36-associated and neutrophil-related signatures, activation of MyD88-dependent pathways, and mutations in genes regulating the IL-36 axis, including , , and . Consequently, conventional systemic therapies and biologics targeting TNF-α, IL-17, and IL-23 pathways show variable efficacy and may act more slowly in GPP. In contrast, IL-36 receptor inhibitors represent a more mechanism-aligned approach and have demonstrated rapid and clinically meaningful responses in acute flares. However, important gaps remain, including the lack of validated biomarkers and limited data on long-term treatment outcomes. This review provides an integrated perspective on IL-36-driven inflammation in GPP, including comparison with plaque psoriasis, and outlines its implications for mechanism-based therapeutic approaches. - Source: PubMed
Publication date: 2026/05/15
Andrzejczak KlaraKucharczyk EmiliaSternak AgataBiliński KarolMaj JoannaPonikowska Małgorzata - Dystrophic epidermolysis bullosa pruriginosa (DEB-Pr) is a rare subtype of dystrophic epidermolysis bullosa (DEB) characterized by intensely pruritic blisters, prurigo-like nodules, and scarring on the extensor aspects of the extremities. We present a 43-year-old female patient with a 30-year history of recurrent erythematous plaques, nodules, and blisters, which was accompanied by severe pruritus affecting the scalp, back, and extremities. Whole-exome sequencing identified a heterozygous likely pathogenic variant in (c.6760G>A, p.Gly2254Arg), a heterozygous variant of uncertain significance (VUS) in (c.2172C>A, p.Tyr724*), and a heterozygous pathogenic variant in (c.1388G>A, p.Arg463His). Combined with the patient's clinical manifestations, histopathological findings, direct immunofluorescence results, negative results for pemphigus and pemphigoid autoantibodies, genetic testing results, and past medical history, the patient was diagnosed with refractory DEB-Pr and glucose-6-phosphate dehydrogenase (G6PD) deficiency. To the best of our knowledge, the co-occurrence of these three distinct variants in a patient with DEB-Pr has not been previously reported in the literature. Oral upadacitinib (initiated at 15 mg once daily) induced rapid and substantial relief of pruritus as well as improvement of cutaneous lesions. Clinical symptoms continued to improve during subsequent gradual dose tapering, and maintenance therapy with 15 mg once weekly has been administered since month 16 of treatment, with a 7-month follow-up to date. No treatment-related adverse events were observed throughout the entire 22-month follow-up period. This case suggests that Janus kinase (JAK) inhibitors may represent a feasible therapeutic option for patients with similar refractory DEB-Pr. - Source: PubMed
Publication date: 2026/05/08
Li HaoZhang YuLin XuewenYan TianmengWu XiaoyanZhang Zhenying - Primary Sjögren's syndrome (pSS) is a systemic autoimmune disorder characterized by chronic inflammation of exocrine glands, resulting in lacrimal gland dysfunction, reduced tear secretion and dry eye manifestations. The nuclear factor κB (NF‑κB) signaling pathway is a central regulator of inflammatory responses; however, its role in lacrimal gland injury in pSS remains incompletely defined. The present study investigated the contribution of NF‑κB signaling to lacrimal gland damage and tear secretion in non‑obese diabetic (NOD)/Ltj mice, an established model of pSS. Histopathological alterations were evaluated by hematoxylin and eosin staining. Transcriptomic profiling was performed using mRNA sequencing and validated by western blotting analysis. Pharmacological inhibition of NF‑κB was achieved using JSH‑23. T helper 17 (Th17) cell differentiation, inflammatory cytokine production, apoptosis and tear secretion were assessed by immunohistochemistry, flow cytometry, enzyme‑linked immunosorbent assay, terminal deoxynucleotidyl transferase dUTP nick end labeling staining and the phenol red thread test. NF‑κB signaling was markedly activated in the lacrimal glands of NOD/Ltj mice. Inhibition of NF‑κB reduced Th17 cell differentiation, decreased proinflammatory cytokine expression, attenuated apoptosis, restored tear secretion and partially normalized the expression levels of differentially expressed genes, including and transcripts and their corresponding proteins, CARD14 and CCL19. These findings indicated that NF‑κB signaling contributes to Th17‑mediated lacrimal gland injury in pSS and suggested that pharmacological targeting of this pathway may represent a potential therapeutic strategy for pSS‑associated dry eye. - Source: PubMed
Publication date: 2026/05/22
Xie JiajunZhang HuinaShen WenyueYe Juan - Esophageal squamous cell carcinoma (ESCC) lacks effective targeted therapies. The tumor suppressor ZNF750 is frequently inactivated, yet the primary mechanism and its therapeutic implications remain poorly defined. - Source: PubMed
Publication date: 2026/05/03
Bi YanghuiWang MengyaoZhang YongCui HeyangCheng CaixiaSong BinZhang LingKong PengzhouYang BinYuan FajiaZhang RuipingCui Yongping - Genetic studies mutations (IL36RN, CARD14 and AP1S3) account for only 28.6% of generalised pustular psoriasis (GPP) leaving much of its pathogenesis remained to be elucidated. Emerging evidence suggests Th17-mediated inflammation, potentially driven by specific HLA class alleles, may underlie dysregulated IL-36 signalling. This study explores the genotypic and phenotypic features of autochthonous GPP in Sarawak. A cross-sectional case-control study was conducted in Sarawak's three main dermatology centres. GPP patients (n = 43) fulfilling ERASPEN criteria between 1997 and June 2024 were included (23 with GPP alone); 20 with concomitant psoriasis vulgaris. HLA genotyping (HLA-A, -B, -C, -DR) was performed via polymerase chain reaction and sequence-specific oligonucleotide probe hybridisation (PCR-SSO) methods at the Institute of Medical Research (IMR). HLA frequencies were compared to 90 Sarawakian controls from Malaysian Stem Cell Registry. Female predominance was noted (1:4.4). Median age at GPP onset was 29 years. Family history of psoriasis was reported in 30.2%, with 16% females developing GPP during pregnancy. Treatment responses: corticosteroids (100%), ciclosporin (82.1%), acitretin (60%) and methotrexate (50%). While biologics were effective in 10 patients. Common alleles included HLA-DRB1*12:02, HLA-A*11:01 and HLA-C*07:02 while HLA-C06:02 was not observed. HLA-A*02:07 and HLA-B*46:01 were observed only in concomitant psoriasis patients. HLA-A*11:02 was seen in patients with ciclosporin non-response, HLA-A*24:02 in those with poorer responses to acitretin and methotrexate and HLA-B*38:02 in psoriatic arthritis. Lower frequencies of HLA-B*35:05 and HLA-C*04:01 were observed among Dayak patients. The absence of HLA-C*06:02 and variation in allele frequencies in this cohort may reflect population-specific patterns but require validation in larger studies. - Source: PubMed
Ting Ingrid Pao LinTeo Hock GinKoay Bee TeeKhairul-Fahmy NorfarhanaArip MasitaMustafa NorhazlinTang Min Moon