Guinea pig CD97 ELISA kit
- Known as:
- Guinea pig CD97 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- e05c0579
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Blue gene shanghai
- Gene target:
- Guinea pig CD97 ELISA kit
Related genes to: Guinea pig CD97 ELISA kit
- Gene:
- ADGRE5 NIH gene
- Name:
- adhesion G protein-coupled receptor E5
- Previous symbol:
- CD97
- Synonyms:
- TM7LN1
- Chromosome:
- 19p13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-29
- Date modifiied:
- 2015-03-03
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- Adhesion G protein-coupled receptors (aGPCRs) constitute a structurally and functionally distinct group within the superfamily of GPCRs. In 2015, the International Union of Pharmacology invited the Adhesion GPCR Consortium to publish a comprehensive review about aGPCRs and establish a unified nomenclature. Since then, substantial progress has been made in delineating the biological roles, molecular architecture, biochemical properties, expression profiles, ligand repertoire, and activation and signaling strategies of aGPCRs. Commensurate with these advances, their relevance to human pathophysiology has become increasingly apparent. In a coordinated effort, the Adhesion GPCR Consortium has reviewed recent progress in this field and provides a comprehensive assessment of the current understanding of aGPCR biology, including a focus on human and mammalian aGPCRs, their evolutionary origins, methodological approaches, and model systems for their investigation, as well as emerging approaches for their therapeutic targeting. SIGNIFICANCE STATEMENT: Adhesion G protein-coupled receptors are versatile cell-surface proteins that integrate structural, biochemical, and physiological functions, with major roles in health and disease. This review summarizes current knowledge of their molecular features, functions in diverse model systems, and emerging opportunities for therapeutic targeting, providing a comprehensive resource that connects basic biology with translational applications across multiple scientific disciplines. - Source: PubMed
Publication date: 2026/01/16
Langenhan TobiasAnderson Garret RAraç DemetAust GabrielaAvila-Zozaya MonserratBagger Sofie MorsingBarth PatrickBerndt SandraBlacklow Stephen CBlanco-Redondo BeatrizBoucard Antony ABridges James PBrodmerkel Lara-SophieCaron Kathleen MChung Yin KwanDates Andrew Nde Araujo Farias VirgineaDel Toro DanielDuman Joseph GEngel Felix BFavara David MFormstone Caroline JFu ChaoyuGarcia De Las Bayonas AlainGeorgiadi AnastasiaGloriam David EHall Randy AHamann JörgHildebrand Peter WHsiao Cheng-ChihHuang Bill XJavitch Jonathan AKim Hee-YongKittel Robert JKleinau GunnarLeduc RichardLiebscher InesLin Hsi-HsienLinnert JoshuaLudwig Marie-GabrielleMartinelli David CMathiasen SigneMatúš DanielMelkumyan MariamMoreno-Salinas Ana LMulder JanNash Michael APal KasturiPederick Daniel TPerry-Hauser Nicole APiao XianhuaPing Yu-QiPlacantonakis Dimitris GPohl FabianPrömel SimoneRosenkilde Mette MSabbagh LaurentSando Richard CScheerer PatrickSchöneberg TorstenSeiradake ElenaSelcho MareikeSeufert FlorianSingh Abhishek KSkiniotis GeorgiosSpiess KatjaSträter NorbertStrutt DavidSüdhof Thomas CSun JinpengTall Gregory GThor DoreenTilley Douglas GTolias Kimberley FVallon MarioVan Meir Erwin GVanhollebeke BenoitWiggin Giselle RWolfrum UweYan JieZaidman Nathan AZou YiminScholz Nicole - B-cell precursor acute lymphoblastic leukemia (B-ALL), the most common pediatric acute leukemia (AL), is frequently characterized by aberrant antigen expression, which aids diagnosis and prognosis. The myeloid antigen CD66c is notably frequent in B-ALL and has been proposed as a marker of disease aggressiveness and treatment response. Evaluating CD66c in Mexican pediatric patients may provide insights into disease biology. A cohort of 128 pediatric patients was referred to the Laboratory of Oncoimmunology and Cytomics of Childhood Cancer (OCL) at Instituto Mexicano del Seguro Social (IMSS) for immunophenotyping tests between March 2022 and November 2023. Additionally, control bone marrow (BM) samples were assessed. Aberrant antigen expression in hematopoietic populations and BM microenvironment stroma phenotyping were performed. In total, 84.38% of B-ALL patients exhibited aberrant expression of ≥1 myeloid antigen. Among CD66c-positive patients, 13.79% had detectable measurable residual disease (MRD) during follow-up and 20.69% died. Mesenchymal stromal cells (MSCs) from patients with positive or low CD66c expression displayed inflammatory profiles. ProB leukemias with low CD66c expression were more likely to exhibit detectable MRD, increased mortality, and reduced survival. Low CD66c expression induces molecular stealth that could favor immune evasion and niche persistence, thereby increasing the risk of relapse and therapeutic failure. - Source: PubMed
Publication date: 2026/02/28
Zamora-Herrera GabrielaRomo-Rodríguez RubíLópez-Blanco Jebea AAlfaro-Hernández LauraCasique-Aguirre DianaNúñez-Enriquez Juan CarlosSchnoor MichaelRamírez-Ramírez DaliaPelayo Rosana - Alveolar echinococcosis (AE), caused by the larval stage of , exhibits infiltrative, tumor-like behavior in the liver and persists within its tolerogenic immune environment. Although T cells are central to host defense, the stage-specific remodeling of their lineage states during AE remains unclear. - Source: PubMed
Publication date: 2026/02/19
Tang JingQin XiaoliHou SiyuHuo YanWu PeijiaoQian BingshuoZhu YazhouLi ZihuaZhao YinqiZhang YangyangLi TaoZhao Wei - OBJECTIVE: Systemic lupus erythematosus (SLE) is a prevalent chronic autoimmune disorder that can affect various organs and tissues throughout the body, with the kidneys being the most commonly involved, often leading to lupus nephritis (LN). Immune cells, notably CD4 + T cells and B cells, are crucial in the development of SLE. Investigating the heterogeneity of CD4 + T cells and B cells in patients with LN using single-cell technology is of significant importance. METHODS: With informed consent, this study explored the profiles of LN CD4 + T and B cells through single-cell transcriptome sequencing of peripheral blood mononuclear cell (PBMC) samples from three LN patients and three Normal Control(NC). Initially, the cells were segregated into immune cell clusters using cellular lineage-based clustering. Subsequently, CD4 + T and B cells were further categorized, and marker genes influencing LN CD4 + T and B cells were identified using differential analysis and publicly available data. The differentially expressed genes in LN patients were then functionally analyzed using Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Set Enrichment Analysis (GSEA) enrichment analyses. Additionally, cell communication analysis was conducted to examine the primary secretory pathways of immune cells, along with the profiles of numerous specific cell subtypes and ligand-receptor pairs. RESULTS: In this study, we successfully mapped PBMC cells through single-cell sequencing of LN, and 69,069 single cells were clustered into 8 immune cell subpopulations using dimensionality reduction. These subpopulations included Neutrophils, NK cells, CD4 + T cells, CD8 + T cells, B cells, Macrophages, and Dendritic cells. Further subdivision of CD4 + T cells and B cells into subpopulations revealed that CD4 + T cells were divided into seven subpopulations, namely Tn, Th2, Th1, Tem, Treg, Tm, and Th17 subpopulations. The marker genes of each subpopulation mainly included CCR7, SELL, LEF1, TCF7, MALAT1, GZMA, IL7R, TGFB1, CCL5, KLRB1, CD4, and STAT3, among others. B cells were further divided into six subpopulations, namely Fo-B, AIM2 + Bcell, TCF4 + Bcell, Unknown (to be defined), B1-ATMBCs, and Trans-Bcell, with marker genes including TCL1A, IGHD, FCER2, AIM2, IGHA1, and JCHAIN.The GO enrichment analysis of each cell subpopulation focused on the regulation of lymphocyte activation, cellular response to type I interferon, and other processes. The KEGG analysis concentrated on the chemokine signaling pathway and cytokine-cytokine receptor interactions. Cell communication analysis revealed that the ligand-receptor pairs of the eight immune cell subpopulations were distributed across 11 signaling pathways, including ANNEXIN, BAFF, BAG, CCL, CXCL, FLT3, GALECTIN, GRN, IL16, MIF, and RESISTIN pathways. Three of these important ligand-receptor pairs were CD74 + CXCR4, CD74 + CD44, and IL16-CD4.Communication analysis of T and B cells revealed two-by-two interactions between CD4 + T, CD8 + T, and B cells, with the strongest interaction strengths observed between CD4 + T and CD8 + T, and between CD8 + T and B cells. CellChat identified 22 ligand-receptor pairs in 3 cell subsets, distributed across 12 signaling pathways, including ADGRE5, CD22, CD45, CD99, CLEC, ICAM, ITGB2, LCK, MHC-I, MIF, SELPG, and SEMA4 pathways. The most prominent signaling pathways were MHC-I, MIF, and CLEC, with major ligand-receptor pairs being HLA-B - CD8B, MIF - (CD74 + CXCR4), and CLEC2C - KLRB1. CONCLUSION: In summary, we clarified the immune cell profile of PBMCs from LN patients, with a focus on characterizing the heterogeneity of CD4 + T cells and B cells. We identified several specific cellular subtypes and ligand-receptor pairs, which suggest potential therapeutic targets for lupus erythematosus. - Source: PubMed
Publication date: 2026/01/15
Cheng Li-LiTang Zhong-FuLi MingChen Jun-JieShang Shuang-ShuangHuang Chuan-Bing - Endoplasmic reticulum (ER) autophagy (ER-phagy) is a vital homeostatic process triggered by multiple signals and plays a crucial role in regulating innate immunity and viral replication. However, the mechanisms by which host proteins utilize ER-phagy to regulate innate immune response during viral infection remains largely unclear. Here, we uncover the regulatory crosstalk between innate immune adapter, ER retention protein Stimulator of Interferon Genes (STING), and the G protein-coupled receptor ADGRE5/CD97 (Cluster of Differentiation 97). Our results demonstrate that CD97 suppresses the STING-mediated type-I interferon (IFN-I) response against DNA virus and cytosolic DNA, thereby promoting herpes simplex virus type 1 (HSV-1) replication in both cells and mice. CD97 facilitates the recruitment of the ER-phagy receptor, FAM134B (family with sequence similarity 134, member B), to initiate ER-phagy, resulting in the degradation of STING subsequent to DNA virus infection. Furthermore, Cd97-deficient mice exhibit higher IFN-I response and greater resistance to HSV-1 infection. Additionally, our findings reveal that inhibiting CD97 with sanguinarine effectively disrupts HSV-1 replication. These findings shed light on the role of CD97 in the innate immune response against DNA virus infections and offer valuable checkpoint for anti-viral STING activation. - Source: PubMed
Publication date: 2025/12/18
Chang HuasongYang RukunQi WenjingHou PeiliXiang AibiaoLiu XiaoyuKang RanWang HongmeiHe Hongbin