Ask about this productRelated genes to: NOTCH1 antibody
- Gene:
- NOTCH1 NIH gene
- Name:
- notch receptor 1
- Previous symbol:
- TAN1
- Synonyms:
- -
- Chromosome:
- 9q34.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-02-13
- Date modifiied:
- 2019-04-23
Related products to: NOTCH1 antibody
Related articles to: NOTCH1 antibody
- Atopic dermatitis (AD) is a chronic inflammatory skin condition marked by immune dysregulation and compromised skin barrier function, with dendritic cells (DCs) playing pivotal roles in its pathogenesis. This study aimed to systematically characterize the heterogeneity of DCs in AD, identify key pathogenic subsets and genes, and elucidate their regulatory mechanisms through advanced methodologies. We conducted integrated single-cell RNA sequencing (scRNA-seq) analyses on both AD lesions and normal skin samples, leading to the identification and functional annotation of distinct DC subtypes. Through deconvolution, pseudotime trajectory, and co-expression network analyses, we screened critical cell populations and candidate genes. Causal associations were assessed using Mendelian randomization and colocalization analyses, while transcription factor activity inference, kNN-DREMI, and motif analysis were employed to explore underlying regulatory mechanisms. Our results revealed five distinct DC subsets, with a notable expansion of CD207 migratory DCs ons, contrasting with the enrichment of IL1B DCs in normal skin. CD207_mDCs exhibited enhanced migratory and antigen-presenting capabilities, with CD1B being significantly upregulated and uniquely enriched within this subset. Integrative analyses suggest that CD1B may play a role in AD pathogenesis, potentially regulated by NOTCH1 signaling. These findings underscore the critical involvement of CD207_mDCs in AD progression and highlight CD1B as a promising candidate gene, implicating the NOTCH1-CD1B axis in Th2 polarization and presenting novel therapeutic targets for intervention in AD. - Source: PubMed
Publication date: 2026/08/26
Huang ChushanChen PengshengChen Xiaosong - - Source: PubMed
Publication date: 2026/09/09
Forsythe Steven DWatts JasmineGolivi YuvasriMobley James AHerring BrendonSaddala Madhu SudhanaNagaraju Ganji PurnachandraZaibaq FarisRobledo MarioChen WeishengMoellering Douglas RDhall DeeptiLee GooGillis AndreaJaskula-Sztul RenataRose J BartChen HerbertGuenter Rachael - Gouty arthritis (GA) is driven by NLRP3 inflammasome-dependent pyroptosis. Stanniocalcin-1 (STC1) is a secreted glycoprotein implicated in inflammatory regulation, but its role in GA is unclear. This study examined whether STC1 promotes MSU-induced NLRP3 activation and pyroptosis via cAMP-PKA signalling and interaction with NOTCH1. MSU-induced GA was established in wild-type and STC1-knockout mice to assess joint swelling, histopathology, cytokines and NLRP3-pyroptosis markers. In vitro, J774A.1 cells were subjected to MSU stimulation with lentiviral STC1 knockdown and NOTCH1 overexpression. cAMP levels, ROS, mitochondrial membrane potential, NF-κB activation, NLRP3 components and pyroptosis were evaluated by ELISA, fluorescent probes, Western blotting, CCK-8 and caspase-1/PI flow cytometry, with KH7 and H89 used to inhibit cAMP and PKA. STC1-NOTCH1 interaction was analyzed by in silico prediction, co-immunoprecipitation and immunofluorescence. STC1 was upregulated in GA ankles, and STC1 deficiency reduced ankle swelling, tissue damage, neutrophilia, uric acid elevation and NLRP3-dependent pyroptosis. Gene Ontology analysis of STC1-related genes highlighted cAMP-mediated signalling and inflammatory responses, and protein-interaction prediction identified NOTCH1 as a putative STC1-binding partner. In J774A.1 cells, STC1 knockdown increased cell viability and reduced apoptosis and pyroptosis, while decreasing ROS, mitochondrial depolarisation, NF-κB activation, LDH release and expression of NLRP3, ASC, cleaved caspase-1, GSDMD-N, IL-1β and IL-18. STC1 knockdown elevated cAMP in vivo and in vitro, whereas the adenylate cyclase inhibitor KH7 or the PKA inhibitor H89 abolished these antioxidant and anti-pyroptotic effects. STC1 physically interacted and colocalised with NOTCH1, and NOTCH1 overexpression in STC1-silenced cells lowered cAMP, reactivated NF-κB/NLRP3 signalling and restored pyroptosis. In conclusion, STC1 cooperates with NOTCH1 to suppress cAMP-PKA signalling and thereby enhance NF-κB-driven NLRP3 inflammasome activation and pyroptosis in GA. - Source: PubMed
Publication date: 2026/09/09
He YueZheng HuiYue ZhiGe TingqiuHu YanqingZhang YuZhong Yandan - CD8 (cluster of differentiation 8) T cells contribute to atherosclerosis, but how they affect VSMCs (vascular smooth muscle cells) is unclear. The protective role of CD8 regulatory T cells (Tregs) and in vivo induction strategies also remain undefined. - Source: PubMed
Publication date: 2026/09/09
Gao WentaoHou YangfengLiu JiaxingHo Cheng KiuCheng Alfred Sze-LokWaldmann HermanZhou BinLau James Y WLui Kathy O - Calcific aortic valve disease (CAVD) is a progressive fibrocalcific illness for which no effective pharmaceutical treatment exists. This study investigated whether carbamoylated high-density lipoprotein (C-HDL), a defective type of HDL that can develop during inflammation, contributes to CAVD progression and the involved molecular pathways. Male ApoE mice were divided into three groups: CAVD model, cyanate-treated, and inhibitor, and analyzed after 12 weeks. C57BL/6 mice on a regular diet served as blank controls. Serum paraoxonase-1 (PON1), aortic valve calcification, cluster of differentiation 31 (CD31), phosphorylated nuclear factor kappa B p65 (p-p65), NOTCH receptor 1 (NOTCH1), and runt-related transcription factor 2 (RUNX2) were evaluated. In parallel, using RNA sequencing (RNA-seq), Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses, protein-protein interaction (PPI) network analysis, and quantitative real-time polymerase chain reaction. Cyanate treatment reduced serum PON1 levels, increased von Kossa-positive calcium deposition, and raised CD31, p-p65, NOTCH1, and RUNX2 levels compared with the model group, but Gly partially corrected these effects. Transcriptomic research identified 270 C-HDL-associated differentially expressed genes (DEGs) enriched in pathways associated with inflammatory signaling and NF-κB activity. Five potential hub genes (BIRC6, PIK3R1, ATM, IFIH1, and DDX58) were discovered and verified using qRT-PCR. These data show that C-HDL may accelerate CAVD by disrupting valve endothelial homeostasis and stimulating inflammatory signaling, and they identify potential molecular targets for future functional validation. - Source: PubMed
Publication date: 2026/09/08
Han MinJiang WangYang YalongChen Ran