CD97
- Known as:
- CD97
- Catalog number:
- 1F-267-T100
- Product Quantity:
- 100 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
- During the daily process of healthy cellular turnover in the human body, billions of cells undergo apoptosis. These cells are removed by phagocytic cells, namely macrophages through a process known as efferocytosis, which triggers a cascade of reprogramming events in the cell, with a shift towards a pro-resolving or 'wound healing' phenotype. To date, no study has attempted to investigate these phenotypic changes from a proteomic perspective. Here, we present a novel and robust workflow for the investigation of proteome and secretome changes in bone marrow-derived macrophages (BMDMs) and alveolar macrophages following efferocytosis using stable isotope labelling by amino acids in cell culture (SILAC) combined with data-independent acquisition (DIA) mass spectrometry. Using this workflow, we dissected the mixed proteomes of BMDMs and apoptotic cells to map the reprogramming events occurring in macrophages in the later stages of efferocytosis. Specifically, we identified the adhesion G protein-coupled receptor Adgre5/CD97 as a novel efferocytosis-associated protein and showed that this evolutionary conserved protein plays a role in the uptake of apoptotic cells (ACs) by macrophages from mouse, human and fly. Additionally, we show that CD97 may act as a co-receptor for ACs with other efferocytic receptors such as MerTK. Our results provide an unprecedented view of the efferocytic landscape of macrophages and will aid in further understanding this important immunological process in the larger context of immune homeostasis and inflammatory disorders. - Source: PubMed
Publication date: 2026/09/29
Raymond Benjamin Bernard ArmandoNovenstern JasminDannoura AbeerMeng MeihanFrey Andrew MichaelSneperger TamaraZechini LuigiScopelliti AlessandroWood WillTrost Matthias - 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
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