CARD8 Antibody
- Known as:
- CARD8 Antibody
- Catalog number:
- 32067
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- CARD8 Antibody
Related genes to: CARD8 Antibody
- Gene:
- CARD8 NIH gene
- Name:
- caspase recruitment domain family member 8
- Previous symbol:
- -
- Synonyms:
- TUCAN, KIAA0955, CARDINAL, NDPP, Dakar
- Chromosome:
- 19q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-03
- Date modifiied:
- 2016-04-25
Related products to: CARD8 Antibody
Related articles to: CARD8 Antibody
- Over one million patients receive cancer immunotherapy annually, yet the mechanisms underlying life-threatening immune-mediated toxicities remain poorly understood. Checkpoint inhibitor pneumonitis (CIP) is the leading cause of immunotherapy-related mortality, with a case fatality rate approaching 10%, and no genetic risk factors have been described to date. We identified Dipeptidyl-peptidase 9 (DPP9) as the first genetic susceptibility gene for CIP in a clinico-genomics cohort of 4,397 patients treated with immune checkpoint inhibitors. Mechanistically, DPP9 suppresses CARD8 inflammasome activation and IL-18 secretion in human monocytes, a pathway which is engaged prior to CIP onset, with IL-18 selectively elevated in the plasma of patients who subsequently develop CIP. Myeloid-restricted ablation of and in mice recapitulated the pulmonary histopathological and immunological hallmarks of CIP, including granuloma formation, accumulation of IFNγ-producing T cells and monocyte-derived macrophages. Each of these phenotypes were driven by excessive IL-18 secretion. Together, these findings establish DPP9 as a genetic determinant of CIP and nominate IL-18 blockade as a mechanistically rational therapeutic strategy. - Source: PubMed
Publication date: 2026/07/02
Brewer J RichardHan AilinNassar Amin HFarhat Elias BouBlackburn Holly NXiao TianliMirza HarisMowel Walter KSefik EsenHartner SaskiaChiorazzi MichaelIto TakeshiOh Min-HeeMadden Matthew ZRangavajhula AthreyaAdib ElioSaleh Mustafa JMachaalani MarcRakaee MehrdadTafavvoghi MasoudQuattropani ClaireGazetos NicoleGerber DavidFattah FarjanaSoRelle Jeffrey AChoo Dominicvon Itzstein Mitchell SBevans-Fonti ShannonGhanbar MohammadSuresh KarthikMazumder ThomasYe Chun JChoueiri Toni KGusev AlexanderFlavell Richard A - Loss of function mutation in the human gene causes Hatipoglu syndrome leading to severe inflammasomopathy. A key feature of the disease is pancytopenia and patients require bone marrow transplantation, but the mechanism of cell loss is unclear since mutant mice have normal hematopoiesis, suggesting that a distinct mechanism of disease occurs in humans. Here, we present a model of human DPP9 deficiency leveraging reverse genetics in the MISTRG6 humanized mice. We found that CRISPR editing of human CD34 hematopoietic stem and progenitor cells (HSPCs) led to very efficient and persistent gene deletion in vivo. Human deletion recapitulated cytopenia in peripheral blood and in the bone marrow, and cell loss was cell intrinsic. However, deletion led to little transcriptional changes suggesting post-transcriptional regulation in human HSPCs. Mechanistically, DPP9 deficiency led to the activation of the CARD8 inflammasome resulting in HSPC pyroptosis, whereas NLRP1 was dispensable for cell death. Thus, our results reveal a unique human mechanism of disease and offer therapeutic insight for this inflammasomopathy. - Source: PubMed
Publication date: 2026/06/30
Xiao TianliBrewer J RichardCarlino MaximilianHan AilinTakabe YamatoLee Chia-YiZhang FengruiChen MiBlackburn Holly NicoleNassar Amin HWang QiankunBrennad KristenShan LiangSefik EsenKrause Diane SFlavell Richard A - Coronary artery calcification (CAC) serves as a significant predictor of cardiovascular events; however, its underlying molecular mechanisms remain incompletely elucidated. PTBP1, an RNA-binding protein with profound regulatory functions, plays a critical role in post-transcriptional regulation. Nevertheless, its function and mechanism in vascular calcification have yet to be fully explored. - Source: PubMed
Publication date: 2026/05/27
Hu HaoZhang FanWu JunMa Likun - - Source: PubMed
Pai Yu-HsuanLin Kan-HsuanYang Shun-ChengHsu Chien-ShengKao Jun-Kai - Lung cancer is the leading cause of cancer-related mortality worldwide, emphasizing the need for innovative therapeutic strategies. This study utilized immunoinformatics and structural bioinformatics approaches to design and evaluate a multi-epitope vaccine targeting pyroptosis-associated antigens (CARD8, NAIP, NLRP1, and NLRP3), which are implicated in lung cancer immunology. Fifteen T-cell and B-cell epitopes were identified, analyzed for their antigenicity, non-toxicity, non-allergenicity, and immune-stimulatory potential, and optimized to construct a vaccine with suitable adjuvants and linkers. The vaccine demonstrated high antigenicity, solubility, and stability, as validated through physicochemical analyses. Its three-dimensional structure was modeled, refined, and validated using molecular modeling approaches. Molecular docking studies revealed stable and strong interactions between the vaccine and key immune receptors (TLR2, TLR4, TLR5, TLR3, TLR7, and TLR8), indicating its potential to activate both innate and adaptive immunity. Molecular dynamics simulations confirmed the vaccine's structural stability and solvent accessibility over 100 ns across ten replicas. Immune simulations demonstrated strong immunogenic responses, including elevated antibody titers, memory cell populations, and cytokine production. Codon optimization and in silico cloning further ensured efficient expression in Escherichia coli, facilitating experimental application. These findings underscore the vaccine's promise as a therapeutic candidate against lung cancer, warranting further in vitro and in vivo investigations. - Source: PubMed
Publication date: 2026/03/19
Nguyen Truc LyKim Heebal