CARD9 Rabbit Polyclonal Antibody
- Known as:
- CARD9 Rabbit Polyclonal Antibody
- Catalog number:
- APO-2515
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- CARD9 Rabbit Polyclonal Antibody
Related genes to: CARD9 Rabbit Polyclonal Antibody
- Gene:
- CARD9 NIH gene
- Name:
- caspase recruitment domain family member 9
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 9q34.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-08-13
- Date modifiied:
- 2019-04-23
Related products to: CARD9 Rabbit Polyclonal Antibody
Related articles to: CARD9 Rabbit Polyclonal Antibody
- Crohn's disease (CD) is a chronic inflammatory disease mainly characterized by chronic and relapsing intestinal inflammation. The pathogenesis of CD involves dysregulation of the immune response to commensal gut pro-inflammatory microbiota. Genome-wide association studies (GWAS) identified many genetic susceptibility loci associated with CD, such as , and , etc. These risk genes are associated with the relative abundance of particular bacteria. The combined risk score was found to be predictive of disease severity. Moreover, the exact composition of microbiota is known to determine host phenotypes, including metabolic and immunological phenotypes. In this study, we elucidated the association between host genetics, gut microbiota, and host phenotypes. We propose that the pathogenesis of Crohn's disease is mediated by pro-inflammatory microbiota in genetically susceptible individuals. - Source: PubMed
Publication date: 2026/06/03
Gong DaweiZhang ShanshanZhu HengLv JicaiSun LiguoChen ZiyingZhang LeishengZhang Shumin - - Source: PubMed
Publication date: 2026/06/10
Gowda Shreya KKumar BhoopendraXess ImmaculataDixit SonaliGupta Somesh - The human mycobiome comprising commensal fungi such as Saccharomyces, Candida, Malassezia and others constitutes less than 0.1 percent of total gut microbes yet exerts outsized influence on host immune homeostasis. Fungal cell-wall components (β-glucans, mannans, chitin) engage C-type lectin receptors (Dectin-1/2), Toll-like receptors and NOD-like receptors to initiate Syk-CARD9, NF-κB and inflammasome signaling. These pathways shape both pro-inflammatory Th17/IL-22 responses that reinforce mucosal barrier integrity and anti-inflammatory IL-10/Treg circuits that promote immunotolerance. Commensal yeasts such as Saccharomyces boulardii secrete short-chain fatty acids that expand Foxp3 regulatory T cells and bolster mucus production, while Malassezia indoles activate the aryl hydrocarbon receptor to induce tolerogenic dendritic cells. Conversely, Candida-derived prostaglandins and oxylipins dampen Th1-mediated defenses, skewing immunity toward a regulatory phenotype. In murine models of inflammatory bowel disease, type 1 diabetes, and rheumatoid arthritis, supplementation with fungal -glucans and live yeasts indicates potential reductions in disease severity by modulating cytokine networks. Clinical studies further support these findings, with probiotic yeast administration lowering relapse rates in ulcerative colitis and Crohn's disease and improving systemic inflammation markers in multiple sclerosis. While mycobiome dysbiosis correlates with autoimmune flares, strategic restoration of fungal balance offers a novel avenue for therapeutic intervention. Collectively, current research underscores the mycobiome's integral role in immune regulation and highlight fungal metabolites and cell-wall ligands as promising targets for the prevention and treatment of autoimmune diseases. - Source: PubMed
Publication date: 2026/06/05
Ahmad SaleemUsman MuhammadBibi MaryamAftab Muhammad NaumanAslam Muhammad Shahbaz - Pancreatic cancer (PC) cells suppress dendritic cell (DC) maturation and function through multiple pathways, further impairing antitumor activity of CD8 T cells. Our previous study revealed that caspase-recruitment domain-containing protein 9 (CARD9) deficiency led to DC dysfunction and exacerbated PC progression, yet the precise mechanism underlying CARD9 downregulation in DCs remains elusive. In this study, we observed that CARD9 expression was progressively downregulated in PC tumors and associated with advanced clinicopathological stages and DC dysfunction. Functionally, PC cells reduced CARD9 expression, impaired DC maturation and weakened CD8 T cell activation, with these suppressive effects attenuated in CARD9-deficient DCs and reversed when CARD9 was restored. Then, we identified YY1 as a critical upstream transcription factor that bound to the promoter of CARD9 and repressed it, accompanied with DC dysfunction and tumor growth. Mechanistically, tumor-derived lactate induced YY1 lactylation at lysine 183, facilitating YY1 nuclear entry and strengthening its combination with CARD9 promoter. Furthermore, we identified p300 as the "writer" catalyzing YY1-K183 lactylation, and HDAC2 as its enzymatic "eraser". Lactylation enhanced YY1 stability by limiting ubiquitination, sustaining YY1 activation and reinforcing CARD9 suppression. Overall, our findings define a lactate-p300/HDAC2-YY1 lactylation-CARD9 regulatory axis that restricts DC function and promotes immune escape in PC. - Source: PubMed
Publication date: 2026/05/01
Ding LingyanTian ChengFeng YitingXu RuochenLi SenlinZheng MengzhuWang XiaoyanXu QianqianXiang Ming - Little is known about the long-term prognosis of patients with talaromycosis and inborn errors of immunity (IEI). - Source: PubMed
Publication date: 2026/05/13
Lu QianLi XianghuiJiang ZhiwenLi TiantianLi BingkunHuang LanHuang QihuaHu DongmeiLv ChunyingLiu GuoqunZhong JialingLin JingjingLiao LiuweiQin QianfengQin ShaShao HaotianWang ZhiyiLi XiuyingJiang LiZhang XinyuWei LiliLiang JiarongZheng DongyanWang ShuangjieWu WeixuanPan KaisuZheng YanqingLi YanningTang QingJiang MinLiao WanqingCao Cunwei