Polyclonal CARD9
- Known as:
- Polyclonal CARD9
- Catalog number:
- pc-525
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- Polyclonal CARD9
Related genes to: Polyclonal CARD9
- 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: Polyclonal CARD9
Related articles to: Polyclonal CARD9
- Inflammatory bowel disease (IBD) and IgA nephropathy (IgAN) share features of mucosal immune dysregulation, but the genetic basis of their relationship and the contribution of specific IBD subtypes remain unclear. - Source: PubMed
Publication date: 2026/08/04
Su TaoLiang MengjunGao XiaohangLin RuiWu HongzhenWu LuyingZhang MinLiu TaoPeng XiangZhao JunzhangDeng JunYao JiayinZhi Min - Metritis is a major cause of infertility, contributing to repeat breeding, early embryonic loss, fetal mortality, and abortion. - Source: PubMed
Publication date: 2026/07/22
Alqhtani Haifa AliElsayed Ahmed AAl-Hazani Tahani M IElkhidr Rasha YassinAbdelnaby Elshymaa AAlmubarak Adel IAl-Rasheed MohammedEmam Ibrahim ASafhi Fatmah AhmedZarah Rowa KAteya AhmedMarzok Mohamed - Innate immune signaling plays a key role in host response to infection, yet the pattern recognition receptors that detect non-model gut-associated yeasts remain poorly defined. Here, we investigated macrophage sensing of , a food-derived yeast that we found to be enriched within intestinal ulcers of Crohn disease (CD) patients. Using a cell surface receptor antibody screen of bone marrow-derived macrophages infected with a CD patient isolate of , we showed that -induced macrophage activation characterized by increased expression of co-stimulatory molecules, MHC-II, and pattern recognition receptors, including the C-type lectin receptor Dectin-1. Antibody blockade experiments showed both Dectin-1 and complement receptor 3 subunit CD11b were required for phagocytosis of , while Dectin-1 was uniquely required for production of the pro-inflammatory cytokine tumor necrosis factor (Tnf). CRISPR-Cas9-mediated deletion of Dectin-1 phenocopied antibody neutralization effects on phagocytosis. Furthermore, deletion of Dectin-1 or its downstream signaling adaptor molecule Card9 resulted in reduced Tnf secretion in response to . Dectin-1-mediated uptake of was observed in primary bone marrow-derived macrophage and dendritic cells, as well as across the spectrum of macrophage polarization states. Together, these findings define the role of Dectin-1-Card9 signaling axis in innate immune cell sensing of . These findings support the emerging relevance of innate immune recognition of a yeast in Crohn disease pathogenesis. - Source: PubMed
Publication date: 2026/08/04
Newhall Kevin PMcNeer Sarah KEspenschied Scott TDolan Elora GZhou Julie YHogan Deborah AStappenbeck Thaddeus S - Subchondral bone remodeling in the early stages of osteoarthritis (OA) is characterized by elevated bone turnover and is closely associated with osteocyte function within the subchondral bone. However, beyond the canonical role of gasdermin D (GSDMD) in mediating pyroptosis in immune cells, its function in osteocytes remains poorly understood. Accordingly, this study aimed to determine whether osteocyte-derived GSDMD regulates subchondral bone homeostasis or contributes to pathological remodeling during osteoarthritis progression. GSDMD expression was evident in osteocytes within the subchondral bone in both clinical and experimental models of OA, as well as in osteocytes co-cultured with stimulated chondrocytes, suggesting a potential role for osteocyte-derived GSDMD in the bone microenvironment. Remarkably, specific deletion of Gsdmd in osteocytes led to increased bone remodeling, which was accompanied by cartilage degeneration in an OA model, as well as bone loss in an osteoporosis model. Mechanistically, Gsdmd-deficient osteocytes displayed enhanced activation of CARD9/NF-κB signaling under inflammatory stimulation, leading to increased production of inflammatory mediators and osteoclastogenic factors that disrupted osteoblast-osteoclast coupling. These changes induced high-turnover subchondral bone remodeling, altered joint mechanical properties, and accelerated cartilage degeneration. Collectively, our findings identify osteocyte-derived GSDMD as an important regulator of subchondral bone remodeling and suggest that loss of this regulatory mechanism exacerbates OA progression. These results further indicate that therapeutic strategies targeting GSDMD should be approached with caution due to potential effects on bone remodeling and inflammatory signaling. - Source: PubMed
Publication date: 2026/07/28
Ogawa YukiEbata TakuTokuhiro TaikiChen LiyileSuzuki RyotaFujie YukiNakajo MasayaEndo TsutomuAlhasan HendHamasaki MasanariTakahashi DaisukeIwasaki KojiKadoya KenOnodera TomohiroIwasaki NorimasaTerkawi M Alaa - Thalamic hemorrhage is a severe subtype of intracerebral hemorrhage in which secondary neuroinflammation contributes to tissue injury and neurological deterioration. N-acetyltransferase 10 (NAT10), an RNA N4-acetylcytidine writer, has been implicated in inflammatory regulation and neurological disorders. However, inflammation-related transcriptomic changes associated with Remodelin treatment after thalamic hemorrhage remain unclear - Source: PubMed
Publication date: 2026/07/07
Wang ZiLi YaqunXiao YinggangGao JuHuang Tianfeng