CD97
- Known as:
- CD97
- Catalog number:
- 1F-267-T025
- Product Quantity:
- 25 tests
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- CD97
Related genes to: CD97
- 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
Related products to: CD97
Related articles to: CD97
- CD97 is an adhesion G-protein-coupled receptor encoded by that integrates extracellular signals (including cell adhesion, ligand binding, and mechanical stimulation) with intracellular signal transduction. Recent structural studies have further elucidated tethered/intramolecular agonist (TIA)/Stachel recognition and engagement of the seven-transmembrane domain (7TMD), activation-associated 7TMD conformational changes, and G-protein coupling, including the structural basis for the preferential coupling of CD97 to G13. Currently, antibody-drug conjugates (ADCs) targeting CD97 are supported by in vitro proof-of-concept evidence, whereas chimeric antigen receptor (CAR) strategies have shown antitumor activity in animal models of glioblastoma (GBM) and acute myeloid leukemia (AML). Existing research indicates that CD97 is involved in maintaining stem-like states, invasion and metastasis, metabolic adaptation, and stress survival in certain tumors, and its function varies depending on tumor type and cellular environment. Because CD97 is also expressed in normal immune cells and various nonhematopoietic tissues, systemic targeted therapy may be limited by on-target/off-tumor toxicity. This article reviews the latest advances in CD97 structure and signal transduction, and explores its tumor-related functions, biomarker value, evidence for ADC and CAR-related therapies, as well as early exploratory directions involving RNA-mediated downregulation and structure-guided interventions. - Source: PubMed
Publication date: 2026/09/03
Lei YuhongZhang YuanWang YufengLi Lingyu - Allergic asthma results from an uncontrolled type 2 immune response to inhaled allergens. Here, we investigate the function of CD97/ADGRE5, expressed in mouse and human immune and lung epithelial cells, in this disease. Female Cd97 mice exhibit an exacerbated asthmatic phenotype across multiple models, primarily due to CD97 loss on immune cells. A single CD97 antibody treatment before allergen sensitization worsens allergic responses, highlighting a role for CD97 in early immune regulation. Post-sensitization, Cd97 mice display higher frequencies of lung conventional type 2 and monocyte-derived dendritic cells (DCs). Allergen-pulsed Cd97 bone marrow-derived DCs are more activated, promote enhanced proliferation and type 2 cytokine secretion by CD4⁺ OT-II cells, and induce stronger airway inflammation. Consistently, ADGRE5 expression is reduced in airway mucosa-derived mononuclear phagocyte subsets in human asthmatics after allergen-induced exacerbation. These results identify CD97 as an important regulator of DC-driven type 2 allergic responses and a potential target in asthma. - Source: PubMed
Publication date: 2026/08/28
Aust GabrielaHoh Anna-LenaAlladina JehanSmith Neal PHöhna FlorianWang BingyuKerner ChristianeWagner MaritaKrohn KnutPierzchalski ArkadiuszHäussler NeleVillani Alexandra ChloeCho Josalyn LMedoff Benjamin DZenclussen Ana CSteinert MatthiasHamann JörgQuaas MariannePolte Tobias - Intracerebral hemorrhage (ICH) is a severe stroke subtype with high mortality and limited treatment options. This study evaluated the safety and therapeutic potential of human placenta-derived mesenchymal stem cells (PD-MSCs) in acute ICH. PD-MSCs were isolated, characterized, and assessed for tumorigenicity by subcutaneous implantation in nude mice. Acute ICH was induced in rats by collagenase injection, followed by in situ PD-MSC transplantation. Neurological function, brain water content, and hematoma volume were evaluated, and perihematomal biological changes were examined using immunofluorescence staining, ELISA, and transcriptomic sequencing. PD-MSCs displayed typical mesenchymal stem cell characteristics and showed no evidence of tumorigenicity under the present experimental conditions. In ICH rats, PD-MSC transplantation reduced brain edema and hematoma volume and partially improved neurological outcomes compared with those in untreated controls. PD-MSC treatment also modulated astrocytic responses, as reflected by altered glial fibrillary acidic protein expression and astrocyte morphology, and decreased the proinflammatory cytokines interleukin-6 and tumor necrosis factor-α. Transcriptomic analysis indicated that PD-MSCs influenced inflammation-related and immune-regulatory pathways in perihematomal tissues. AKR1B1, SNAI2, and ADGRE5 were identified as candidate genes potentially associated with PD-MSC-mediated responses after ICH. These findings provide preliminary evidence that PD-MSCs are nontumorigenic and may attenuate acute brain injury after ICH, although longer follow-up, expanded behavioral testing, dose optimization, and mechanistic validation are needed to confirm their long-term safety and therapeutic efficacy. SIGNIFICANCE STATEMENT: Acute intracerebral hemorrhage lacks effective therapeutic options, and secondary neuroinflammatory injury contributes substantially to neurological deterioration. This study provides preliminary evidence that placenta-derived mesenchymal stem cells may attenuate acute brain injury and modulate inflammation-associated responses after experimental intracerebral hemorrhage, supporting further investigation of placenta-derived mesenchymal stem cell-based therapeutic strategies for hemorrhagic stroke. - Source: PubMed
Publication date: 2026/07/08
Hu KunLiu HuiDing LuLi JiahuiGu ShueZhang XuGuo Songlin - Ischemic stroke (IS) is a cerebrovascular disease with high mortality and disability rates, currently lacking effective therapeutic targets. The STING inhibitor SN-011 shows potential in IS treatment, but its mechanism of action remains unclear. This study aims to explore the key molecular mechanisms of SN-011 in treating IS through bioinformatics approaches. IS transcriptome datasets were analyzed to identify differentially expressed genes. Mendelian randomization using brain eQTL and IS-GWAS data identified genes with causal relationships to IS. Single-cell transcriptome, pseudo-time trajectory, intercellular communication, and transcription factor regulatory network analyzes were performed. Molecular docking and DARTS-WB assay validated SN-011 binding to transcription factors. Transcriptomic analysis identified 77 intersecting genes. Mendelian randomization revealed ADGRE5 as a protective gene for IS (OR < 1), significantly downregulated in venous endothelial cells (vECs) during disease progression. Cell communication analysis showed ADGRE5-high vECs interact with immune, glial, and stromal cells via LAMININ (Lamb2-CD44, Lamb2-Itga6+Itgb1, Lamb2-Dag1 pair) and JAM signaling pathways. Transcription factor analysis identified JUNB as a negative regulator of ADGRE5. Molecular docking (-6.8 kcal/mol) combined with an in vitro DARTS-WB assay confirmed the interaction between SN-011 and JUNB. In OGD-induced endothelial cell injury models, SN-011 suppressed JUNB expression, restored ADGRE5 expression inhibited by JUNB overexpression, reversed the downregulation of LAMB2 and CD44, and reduced the expression of the pro-inflammatory cytokines IL-6 and IL-1β. Notably, blockade of LAMB2 largely abolished these protective effects, indicating that the anti-inflammatory and endothelial-protective activities of SN-011 are mediated, at least in part, through restoration of the LAMB2-CD44 signaling axis. ADGRE5 downregulation in vECs may impair vascular repair by disrupting LAMININ-mediated intercellular communication. SN-011 may exert neuroprotective effects by targeting JUNB to upregulate ADGRE5 expression and restore the vEC-centered cellular communication network, providing a theoretical basis for SN-011 as a potential IS therapeutic. - Source: PubMed
Ou XiangLingGong ZunKe - Acute inflammatory conditions in the intestine of preterm infants are linked to increased susceptibility due to the immature degree of the gut's epithelial barrier, microbiota, and pattern recognition receptors. Toll-like receptor 4 (TLR4) plays a pivotal role in recognizing lipopolysaccharides (LPS) from gram-negative bacteria, triggering pro-inflammatory cytokine responses (TNF-α, IL-1β, CXCL1) via nuclear factor kappa B (NF-κB) signaling. These processes are implicated in necrotizing enterocolitis (NEC), a severe gastrointestinal condition in premature infants. CD97, an adhesion G-protein coupled receptor (aGPCR), has emerged as a modulator of immune responses influencing inflammatory signaling pathways. CD97 expression is typically low in intestinal epithelial cells (IECs); however, protective effects of increased CD97 levels have been described in experimentally induced colitis. In this study, we examined the role of CD97 in modulating the inflammatory response in the immature gut, utilizing wild-type (WT) and transgenic CD97-overexpressing mice (TgCD97) with epithelial-specific expression in the intestinal epithelium. LPS was administered to IECs and organ segments isolated from the small intestine of mice of specific ages, modeling certain stages of human perinatal/postnatal gut development. CD97 overexpression attenuated LPS-induced TNF-α expression in IECs during early intestinal development while IECs from adult mice remained unaffected. This effect was attributed specifically to ileal tissue. Attenuation was mediated by β-catenin stabilization, leading to suppressed LPS/NF-κB signaling. Inhibition of β-catenin in TgCD97 IECs reversed the anti-inflammatory phenotype restoring pro-inflammatory gene expression. These findings suggest that CD97 overexpression modulates the inflammatory response in the developing gut by stabilizing β-catenin and interacting with the LPS/NF-κB axis. This effect was restricted to early developmental stages and ileal tissue, highlighting a previously unrecognized role of CD97 in age-dependent endotoxin tolerance. These findings identify a novel CD97-β-catenin-NF-κB regulatory axis in the immature small intestine and highlight its potential as a therapeutic target to protect the immature neonatal gut from inflammatory damage. - Source: PubMed
Publication date: 2026/07/30
Dressler NiklasMayer SteffiWiemers ThomasWeise FlorentineFeng XiaoyanAust GabrielaPeukert NicoleLacher MartinRiedel Jan