CARD14 Antibody
Description
Introduction to CARD14 Antibody
CARD14 (Caspase Recruitment Domain Family Member 14) antibodies are specialized reagents designed to detect and study the CARD14 protein, a key regulator of inflammatory signaling pathways. These antibodies enable researchers to investigate CARD14's role in immune responses, skin disorders like psoriasis, and cancer biology through techniques such as Western blotting (WB), immunohistochemistry (IHC), and functional assays .
Key Applications of CARD14 Antibodies
CARD14 antibodies are pivotal in both basic and translational research:
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Dermatological Research: Detecting CARD14 overexpression in psoriatic lesions and studying its role in NF-κB/MAPK pathway activation .
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Cancer Studies: Analyzing associations between CARD14 expression and tumor progression, particularly in prostate, lung, and renal cancers .
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Mechanistic Studies: Investigating CARD14-BCL10-MALT1 (CBM) complex formation and downstream signaling .
Role in Psoriasis Pathogenesis
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Upregulation in Lesional Skin: CARD14 expression is 2–3× higher in psoriatic epidermis compared to healthy skin, confirmed via IHC and qPCR .
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Mechanistic Insights: Gain-of-function CARD14 mutations (e.g., E138A) drive IL-23/IL-17 axis activation and neutrophil recruitment via NF-κB .
Cancer Associations
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Prognostic Marker: Elevated CARD14 correlates with poor survival in adrenocortical carcinoma (ACC) and renal cancer (KIRC) but better outcomes in sarcoma and lung cancer .
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Immune Modulation: CARD14 expression positively correlates with neutrophil infiltration in tumors, mediated by chemokines like CXCL1–3 .
Inflammatory Signaling
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CBM Complex Activation: Antibodies have confirmed CARD14’s interaction with BCL10 and MALT1, which induces proteolytic MALT1 activity and inflammatory cytokine production .
Technical Considerations
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Validation: Ensure antibodies are tested in relevant models (e.g., keratinocytes for skin studies) .
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Cross-Reactivity: Some antibodies may detect splice variants (e.g., isoform 3, which lacks NF-κB activation capacity) .
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Functional Assays: Pair with siRNA knockdown to study CARD14’s role in cell survival and inflammation .
Future Directions
CARD14 antibodies will remain critical for:
Product Specs
Target Background
- Research has shown that RNF7 interacts with CARMA2, influencing its NF-kappaB-activating capacity. RNF7 exerts this control by modulating the ubiquitination state of MALT1 and the NF-kappaB-regulatory molecule NEMO. Interestingly, CARMA2short (CARMA2sh) mutants, linked to psoriasis susceptibility, evade the negative regulation imposed by RNF7. PMID: 29194363
- ULK2, a serine/threonine kinase, binds to and phosphorylates CARMA2sh. PMID: 28230860
- Inhibition of MALT1 deficiency or its catalytic activity pharmacologically suppresses pathogenic mutant CARD14-induced cytokine and chemokine expression in human primary keratinocytes. PMID: 27113748
- The CARD14/MALT1-mediated signaling pathway in keratinocytes plays a significant role in psoriasis. [review] PMID: 27939769
- Findings suggest that the common CARD14 p.Arg820Trp variant may significantly impact the response to anti-TNF therapies among patients with psoriasis. Additionally, rare CARD14 missense variants could also predispose individuals to a better response. PMID: 26854129
- Research suggests that both familial and sporadic Pityriasis Rubra Pilaris Type V may be caused by CARD14 mutations. PMID: 27760266
- Psoriasis mutations disrupt CARD14 autoinhibition, promoting BCL10-MALT1-dependent NF-kappaB activation. PMID: 27071417
- Genetic evidence suggests an association between the CARD14 single nucleotide polymorphism rs11652075 and other rare mutations in this gene with psoriasis. A meta-analysis has confirmed a significant association between the CARD14 rs11652075 polymorphism and psoriasis. PMID: 27706581
- The SNP c.C2458T may have significant effects on the heritability of psoriasis vulgaris in the Chinese population. The CC genotype was more prevalent in familial cases compared to sporadic cases. PMID: 26249641
- Observations provide further insights into the genetics of psoriasis and functional information on novel CARD14 mutational variants observed in cases from Tunisia and other populations. PMID: 26358359
- Genetic interactions of SNPs in CARD14, SENP1, and VEGFA may represent a functional mechanism in the pathogenesis of high altitude polycythemia. PMID: 26852650
- Analysis of 105 individuals with generalized pustular psoriasis (GPP) identified a low-frequency variant (p.Asp176His) that causes constitutive CARD14 oligomerization. PMID: 26203641
- CARD14 protein missense mutation has been found in patients diagnosed with psoriasis. PMID: 25989471
- No definitive causative genetic mutation in CARD14 was identified in familial pityriasis rubra pilaris after screening 8 non-familial patients of type I, type III, and type IV pityriasis rubra pilaris. PMID: 24577624
- The study identified the DEP domain-containing protein DEPDC7 as a cellular binding partner of CARMA2 and CARMA3 proteins. PMID: 25541973
- CARD14 mutations may be responsible for the activation of the NF-kB signaling pathway in patients with pityriasis rubra pilaris. PMID: 25734815
- Transfection of dermal ECs with psoriasis-associated CARD14 mutations resulted in increased expression of several chemokines, including CXCL10, IL-8, and CCL2. PMID: 25369198
- Variant analysis of CARD14 in a Chinese Han population with psoriasis vulgaris and generalized pustular psoriasis suggests that CARD14 may play a role in the pathogenesis of generalized pustular psoriasis. PMID: 24999592
- Due to the relatively small number of cases analyzed in this study, the possibility that CARD14 mutations may be an exceptional cause of sporadic pityriasis rubra pilaris, as previously found in sporadic psoriasis, cannot be ruled out. PMID: 24359224
- Mutations and variants are causal or disease susceptibility factors of psoriasis vulgaris, generalized pustular psoriasis, or pityriasis rubra pilaris. [review] PMID: 24656634
- Chromosome 17q25 harbors a susceptibility locus for psoriasis. Non-parametric linkage analysis revealed a linkage peak lying close to a novel cluster of genes from the immunoglobulin (Ig) superfamily. PMID: 12483297
- Our results confirmed the published linkage with the PSORS1 locus, as well as the PSORS2 locus, which has not been previously shown in the Chinese population. PMID: 12709815
- These results fail to support rs734232 as a psoriasis susceptibility factor in German psoriasis patients. PMID: 15654961
- PSORS2 alleles are not susceptibility factors in arthritis psoriatic patients of Italian origin. PMID: 16733365
- Results show genetic heterogeneity of psoriasis in the Tunisian population, provide confirmatory evidence for a novel psoriasis locus at chromosome 2p12 and reveal a psoriasis family with a mutation at PSORS2. PMID: 23013406
- Pityriasis rubra pilaris autosomal dominant family is an allelic disease to certain genetic forms of familial psoriasis. PMID: 23328365
- CARD14 c.526G>C (p.Asp176His) may have a role in generalized pustular psoriasis with psoriasis vulgaris in Japanese patients. PMID: 24476623
- The association between SNP rs11652075 at the CARD14 gene and psoriasis. PMID: 23905699
- Three different heterozygous mutations in CARD14 have been identified as causing familial pityriasis rubra pilaris. PMID: 22703878
- Rare, highly penetrant mutations in CARD14 have been shown to cause psoriasis. PMID: 22521418
- A range of NF-kB responses in the skin are mediated by CARD14, and a subset of rare CARD14 variants leads to psoriasis and psoriatic arthritis. PMID: 22521419
- Results demonstrate that multiple transcripts encoding several CARMA2 isoforms exist in vivo and regulate NF-kappaB activation and apoptosis. PMID: 21302310
