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Showing ADGRE2 — EMR2 is a alias.

ADGRE2

Adhesion G protein-coupled receptor E2 · UniProt Q9UHX3

Length
823 aa
Mass
90.5 kDa
Annotated
2026-06-09
37 papers in source corpus 20 papers cited in narrative 20 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ADGRE2 (EMR2/CD312) is a myeloid-restricted adhesion G protein-coupled receptor of the EGF-TM7 family that links extracellular glycosaminoglycan recognition to proinflammatory signaling (PMID:10903844, PMID:12829604). Its extracellular region carries five tandem EGF-like modules, and the fourth EGF module mediates Ca2+- and sulfation-dependent binding to chondroitin sulfate and the variant dermatan sulfate, defining a ligand specificity distinct from its paralog CD97/CD55 (PMID:12829604, PMID:15498814, PMID:15693006). The receptor matures by autocatalytic intramolecular cis-proteolysis at the His-Leu↓Ser518 GPS site within the ER, an N-terminal-nucleophile-hydrolase-like reaction requiring a Ser/Thr/Cys at P+1 and the full extracellular stalk, generating a non-covalent extracellular α-subunit/transmembrane β-subunit heterodimer (PMID:12860403, PMID:15150276). Ligation or antibody-mediated activation drives subunit translocation into lipid raft microdomains, which is required for downstream signaling and cytokine output (PMID:22310662). The activated receptor couples broadly to G proteins, including Gα16 and Gαq/11, to engage a PLC-β → Ca2+/PKC → PI3K/Akt → MAPK/NF-κB cascade (PMID:28421075, PMID:31969668, PMID:32222457). Functionally this potentiates neutrophil adhesion, migration, superoxide production and degranulation (PMID:17928360), promotes monocyte/macrophage differentiation, cytokine secretion and NLRP3 inflammasome activation (PMID:28421075, PMID:33488598), and in AML sustains an MEK/ERK→AP1→DUSP1→DNAJB1-HSP70 proteostasis axis whose disruption is antileukemic (PMID:39082681). A heterozygous p.C492Y variant that destabilizes the autoinhibitory α–β subunit interaction causes autosomal dominant vibratory urticaria by sensitizing mast cells to mechanical, IgE-independent degranulation (PMID:26841242, PMID:32222457).

Mechanistic history

Synthesis pass · year-by-year structured walk · 20 steps
  1. 2000 Medium

    Established ADGRE2/EMR2 as a distinct myeloid-restricted EGF-TM7 class B GPCR, separating it from its ubiquitous paralog CD97 and asking what its ligand and function are.

    Evidence Genomic mapping, cloning, monoclonal antibody and flow cytometry on leukocytes, with ligand-binding assays showing no CD55 interaction

    PMID:10903844

    Open questions at the time
    • Ligand identity unknown at this stage
    • No signaling mechanism defined
    • Functional consequences of expression not addressed
  2. 2002 Medium

    Showed the receptor exists at the cell surface as a two-subunit heterodimer (extracellular α + 7TM β), establishing the architecture later linked to autoproteolysis and autoinhibition.

    Evidence Reciprocal immunoprecipitation and flow cytometry with the 2A1 mAb on primary leukocytes and cell lines

    PMID:11994511

    Open questions at the time
    • Mechanism generating the heterodimer not yet defined
    • Subunit interaction strength/regulation unknown
  3. 2003 High

    Identified chondroitin sulfate as the molecular ligand and localized binding to the fourth EGF module, answering what ADGRE2 recognizes extracellularly.

    Evidence Multivalent protein probes, GAG-biosynthesis-deficient CHO mutants, enzymatic GAG removal and dose-dependent inhibition

    PMID:12829604

    Open questions at the time
    • Physiological cellular source of CS ligand in vivo not defined
    • Signaling consequence of ligation not yet measured
  4. 2003 High

    Defined the GPS cleavage site at Leu517-Ser518 and showed the full extracellular stalk (not the GPS motif alone) is required, with alternative splicing controlling whether cleavage occurs.

    Evidence Site-directed mutagenesis, biochemical and cell-free cleavage assays, analysis of spliced isoforms

    PMID:12860403

    Open questions at the time
    • Catalytic chemistry of cleavage not yet established
    • Functional role of cleavage in signaling unaddressed
  5. 2004 High

    Demonstrated GPS proteolysis is an autocatalytic intramolecular reaction occurring in the ER, mechanistically resembling N-terminal nucleophile hydrolases.

    Evidence Mutagenesis of P+1/P-2 residues and cell-free spontaneous hydrolysis of slow-processing precursors

    PMID:15150276

    Open questions at the time
    • Link between cleavage and receptor activation not yet demonstrated
    • Fate of subunits after cleavage unclear
  6. 2005 Medium

    Extended ligand recognition to a cellular context, showing EGF4-mediated CS binding targets B cells, implying immune cell–cell interactions.

    Evidence Recombinant protein-coated beads and isoform-specific mAbs on primary leukocytes

    PMID:15498814

    Open questions at the time
    • Functional consequence of the EMR2–B cell interaction not tested
    • In vivo relevance not established
  7. 2005 Medium

    Connected ADGRE2 to inflammatory disease by identifying dermatan sulfate as a ligand and showing elevated EMR2 on activated macrophages/DCs in rheumatoid synovium.

    Evidence Immunohistochemistry, immunofluorescence colocalization and multivalent probe binding on synovial tissue

    PMID:15693006

    Open questions at the time
    • Causal role in RA pathogenesis not demonstrated
    • Downstream signaling in synovial cells not measured
  8. 2006 Medium

    Showed ADGRE2 expression is dynamically regulated during myeloid differentiation and induced by LPS and IL-10, framing it as an inducible inflammatory receptor.

    Evidence Flow cytometry, qPCR and cytokine stimulation of primary myeloid cells

    PMID:17174274

    Open questions at the time
    • Transcriptional regulators not identified
    • Functional output of regulated expression not tested here
  9. 2007 High

    Provided the first direct functional evidence that receptor ligation drives effector responses, establishing ADGRE2 as a proinflammatory neutrophil receptor.

    Evidence Anti-EMR2 antibody ligation with adhesion, migration, superoxide, degranulation assays and live imaging of receptor translocation

    PMID:17928360

    Open questions at the time
    • G protein and second-messenger pathway not defined
    • Endogenous ligand-triggered responses not tested
  10. 2011 Medium

    Identified additional neutrophil outcomes of ligation, including suppression of LPS-induced survival and altered cytokine secretion.

    Evidence 2A1 mAb ligation with apoptosis, ROS and cytokine ELISA assays

    PMID:22035891

    Open questions at the time
    • Single-lab functional study with limited mechanistic depth
    • Signaling intermediates not mapped
  11. 2012 High

    Linked GPS autoproteolysis to signaling by showing ligation drives subunit translocation and colocalization in lipid rafts, which is required for cytokine production.

    Evidence Lipid raft fractionation, co-IP, live imaging, GPS-mutant constructs and macrophage cytokine assays

    PMID:22310662

    Open questions at the time
    • Identity of raft-resident signaling partners not defined
    • G protein specificity not yet resolved
  12. 2016 High

    Established a Mendelian disease link, showing the p.C492Y variant destabilizes the α–β interaction and causes autosomal dominant vibratory urticaria via mast cell sensitization.

    Evidence Cosegregation in two kindreds plus mast cell degranulation and subunit-interaction biochemistry

    PMID:26841242

    Open questions at the time
    • Downstream mechanotransduction signaling not yet dissected
    • How subunit destabilization couples to force sensing unclear
  13. 2017 High

    Defined the canonical signaling cascade in monocytes, placing Gα16 upstream of sequential Akt/ERK/JNK/NF-κB activation driving differentiation and proinflammatory mediator expression.

    Evidence Anti-EMR2 mAb stimulation with siRNA knockdown and inhibitors of pathway nodes in THP-1 cells

    PMID:28421075

    Open questions at the time
    • Direct receptor–Gα16 coupling biochemistry not shown here
    • Endogenous ligand-driven cascade not tested
  14. 2018 Medium

    Refined post-cleavage receptor biology by showing site-specific GAIN-domain N-glycosylation and an amphipathic helix control membrane association of the N-terminal fragment.

    Evidence Glycosylation-site mutagenesis, subcellular fractionation and domain deletion analysis

    PMID:29540735

    Open questions at the time
    • Functional consequence of NTF membrane anchoring for signaling unknown
    • Single-lab biochemical study
  15. 2020 Medium

    Confirmed ADGRE2 is a functional GPCR with broad G protein coupling, including Gα16 and PTX-insensitive Gαz, distinguishing it from CD97's narrower coupling.

    Evidence Yeast chimeric G protein assay, cAMP inhibition, IP1 accumulation and NFAT reporter with pertussis toxin

    PMID:31969668

    Open questions at the time
    • Coupling tested with truncated/activated forms, not native ligand
    • Physiological G protein usage in primary cells not confirmed
  16. 2020 High

    Mechanistically dissected the disease pathway, showing variant-receptor mechanoactivation on dermatan sulfate triggers PLC/Ca2+/PKC/PI3K/ERK signaling and PGD2 synthesis driving degranulation.

    Evidence Vibration stimulation of mast cells on dermatan sulfate with calcium imaging, pathway inhibitors, pertussis toxin and PGD2 ELISA

    PMID:32222457

    Open questions at the time
    • Direct force-sensing molecular event not resolved
    • Contribution of specific Gα subunits to mechanosignaling only partially defined
  17. 2019 Medium

    Used SGD→RGD swap to show ADGRE2 lacks the integrin motif of CD97 and does not promote angiogenesis, clarifying functional divergence from its paralog.

    Evidence Site-directed mutagenesis with endothelial tube formation, CAM assay and MMP-9/VEGF analysis

    PMID:31594642

    Open questions at the time
    • Endogenous angiogenic role of wild-type EMR2 remains negative/uncharacterized
    • Single-lab gain-of-function study
  18. 2021 Medium

    Extended the Gα16/PLC-β cascade to innate immune activation, showing EMR2 stimulation licenses the NLRP3 inflammasome second signal via Akt/MAPK/NF-κB, Ca2+ and K+ efflux.

    Evidence 2A1 mAb stimulation with siRNA, inhibitors, K+ efflux and Ca2+ assays in THP-1 and primary monocytes

    PMID:33488598

    Open questions at the time
    • Endogenous ligand triggering of inflammasome not tested
    • Single-lab study
  19. 2024 High

    Revealed a pro-leukemic role in AML, linking the PLC-β/PKC/MEK/ERK→AP1→DUSP1 axis to DNAJB1-HSP70 chaperone function and proteostasis maintenance.

    Evidence siRNA/shRNA knockdown, MEK/AP1/DUSP1 inhibitors, DUSP1 Ser16 phospho-analysis, DNAJB1-HSP70 co-IP and xenograft models in patient-derived AML cells

    PMID:39082681

    Open questions at the time
    • Upstream ligand/activation trigger in AML cells not defined
    • Whether autoproteolysis is required for the leukemic axis untested
  20. 2024 Medium

    Identified a direct intracellular interaction with Gα15/GNA15 and a T-cell-associated pro-leukemic effect in ALL, supporting G protein engagement and microenvironmental immune modulation.

    Evidence Co-IP/affinity assay for CD312-GNA15, knockdown/overexpression, BrdU proliferation and flow cytometry of immune subsets

    PMID:39656442

    Open questions at the time
    • Single Co-IP for the CD312-GNA15 interaction
    • Mechanism of T-cell-mediated leukemia support beyond MAPK phosphorylation unclear

Open questions

Synthesis pass · forward-looking unresolved questions
  • How endogenous chondroitin/dermatan sulfate ligation, mechanical force, and subunit dissociation are integrated into a unified activation mechanism, and whether autoproteolysis is required across all disease contexts, remains unresolved.
  • No structural model of the activated ligand-bound receptor
  • Force-sensing molecular event not defined
  • Native-ligand-driven (vs antibody-driven) signaling incompletely characterized

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060089 molecular transducer activity 3 GO:0098631 cell adhesion mediator activity 3 GO:0016787 hydrolase activity 2 GO:0140096 catalytic activity, acting on a protein 2
Localization
GO:0005886 plasma membrane 3 GO:0005783 endoplasmic reticulum 1
Pathway
R-HSA-162582 Signal Transduction 3 R-HSA-1643685 Disease 3 R-HSA-168256 Immune System 3 R-HSA-392499 Metabolism of proteins 1
Partners
GNA15

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2000 EMR2 (ADGRE2) is a member of the EGF-TM7 family of class B GPCRs, contains five tandem EGF-like domains coupled to a seven-span transmembrane domain via a mucin-like spacer, and expresses multiple protein isoforms via alternative RNA splicing. Expression is restricted to monocytes/macrophages and granulocytes, unlike the ubiquitously expressed paralog CD97. EMR2 fails to interact with CD55, the cellular ligand for CD97, indicating distinct ligand specificity. Genomic mapping, molecular cloning, monoclonal antibody generation, flow cytometry, ligand-binding assays Genomics Medium 10903844
2002 EMR2 is expressed as a heterodimeric receptor on the cell surface, consisting of an extracellular alpha subunit and a seven-pass transmembrane/cytoplasmic beta subunit. Expression is restricted to myeloid cells (highest on CD16+ monocytes, macrophages, and BDCA-3+ myeloid DC), and EMR2 does not interact with CD55 (the CD97 ligand), confirming non-redundant functions for the two molecular twins. Monoclonal antibody generation (2A1), immunoprecipitation, flow cytometry on primary blood leukocytes, hematopoietic cell lines, and in situ tissue analysis Journal of leukocyte biology Medium 11994511
2003 The largest EMR2 isoform (containing 5 EGF-like modules) mediates cell attachment through binding to chondroitin sulfate (CS) glycosaminoglycans. The fourth EGF-like module is the major ligand-binding site. The interaction is Ca2+- and sulphation-dependent. Mutant CHO cell lines defective in GAG biosynthesis and enzymatic removal of cell-surface GAGs demonstrated that CS is the molecular identity of the EMR2 ligand. Exogenous CS GAGs blocked the interaction in a dose-dependent manner. Multivalent protein probes, antibody-blocking studies, mutant CHO cell lines (GAG biosynthesis-deficient), enzymatic GAG removal, dose-dependent inhibition assays Blood High 12829604
2003 Proteolytic cleavage of EMR2 occurs at Leu517-Ser518 within the GPS motif and is independent of the transmembrane domains. The non-covalent association of the resulting extracellular alpha-subunit and transmembrane beta-subunit requires a minimum of eight amino acids in the beta-subunit. The GPS motif is necessary but not sufficient for cleavage; the entire extracellular stalk is required. An alternatively spliced EMR2 isoform with a truncated stalk fails to undergo proteolytic cleavage, demonstrating that alternative splicing regulates GPS cleavage. Site-directed mutagenesis, biochemical cleavage assays, analysis of alternatively spliced isoforms, cell-free system FEBS letters High 12860403
2004 GPS proteolysis of EMR2 is an autocatalytic intramolecular reaction. Cleavage occurs at the conserved His-Leu↓Ser518 site inside the endoplasmic reticulum, producing two protein subunits that associate non-covalently as a heterodimer. The P(+1) Ser518 residue (Ser, Thr, or Cys) is absolutely required for efficient proteolysis. Substitution of the P(-2) His residue produces slow-processing precursor proteins that spontaneously hydrolyze in a cell-free system, indicating the mechanism is similar to N-terminal nucleophile hydrolases performing cis-proteolysis. Site-directed mutagenesis of cleavage site residues, cell-free proteolysis assay, biochemical characterization of processing intermediates The Journal of biological chemistry High 15150276
2004 The fourth EGF domain of both CD97 and EMR2 is expressed on activated lymphocytes and myeloid cells and mediates binding to chondroitin sulfate specifically found on B cells within peripheral blood, suggesting a role in interaction of activated T cells, dendritic cells, and macrophages with B cells. Fluorescent beads coated with recombinant CD97 and EMR2 protein, isoform-specific monoclonal antibodies, flow cytometry on primary leukocytes Journal of leukocyte biology Medium 15498814
2005 Dermatan sulfate (a chondroitin sulfate variant) is identified as the ligand of the largest isoforms of EMR2 and CD97 in rheumatoid synovial tissue. EMR2 is expressed on macrophages and dendritic cells expressing costimulatory molecules and TNF-α in RA synovium. EMR2 expression in the synovial sublining is significantly higher in RA patients compared with OA and ReA controls. Immunohistochemistry with anti-EMR2 mAb, digital image analysis, double immunofluorescence microscopy, multivalent fluorescent probe binding assays on synovial tissue sections Arthritis and rheumatism Medium 15693006
2006 EMR2 receptor expression is up-regulated during differentiation and maturation of macrophages, and down-regulated during dendritic cell maturation. In monocytes and macrophages, EMR2 is specifically up-regulated by LPS and IL-10 via an IL-10-mediated pathway. Alternative splicing and glycosylation of EMR2 are regulated during myeloid differentiation. Flow cytometry, quantitative PCR, functional stimulation assays with LPS and cytokines, analysis of primary myeloid cells during differentiation Biochemical and biophysical research communications Medium 17174274
2007 Ligation of EMR2 via a specific antibody increases neutrophil adhesion and migration, augments superoxide production and proteolytic enzyme degranulation, and potentiates the effects of proinflammatory mediators. Upon neutrophil activation, EMR2 is rapidly translocated to membrane ruffles and the leading edge of the cell. The transmembrane region is critical for adhesion-GPCR function. Anti-EMR2 antibody ligation, superoxide assay, degranulation assay, neutrophil adhesion and migration assays, live-cell imaging of receptor translocation FASEB journal High 17928360
2012 GPS autoproteolysis of EMR2 generates two distinct receptor complexes: a noncovalent α-β heterodimer and two completely independent receptor subunits. These distribute differentially in membrane raft microdomains. Receptor ligation induces subunit translocation and colocalization within lipid rafts, leading to receptor signaling and inflammatory cytokine production by macrophages. GPS autoproteolysis is critical for mediating receptor signaling and cell activation. Lipid raft fractionation, co-immunoprecipitation, live-cell imaging, cytokine ELISA, GPS-mutant receptor constructs, macrophage stimulation assays Molecular and cellular biology High 22310662
2011 EMR2 ligation suppresses LPS-induced neutrophil survival (pro-apoptotic effect). EMR2 ligation also changes the secretion profiles of multiple cytokines, including IL-6, IL-8, and MCP-1, in LPS-treated neutrophils. Anti-EMR2 mAb (2A1) ligation, flow cytometry (annexin-V/PI apoptosis), ELISA for cytokine secretion, reactive oxygen species assay Chang Gung medical journal Medium 22035891
2016 A missense variant in ADGRE2 (p.C492Y) cosegregates with autosomal dominant vibratory urticaria in two large kindreds. The ADGRE2 receptor undergoes autocatalytic cleavage producing an extracellular subunit that noncovalently binds a transmembrane subunit. The p.C492Y variant destabilizes the autoinhibitory subunit interaction, sensitizing mast cells to IgE-independent vibration-induced degranulation. Genetic cosegregation analysis in human kindreds, functional studies of variant receptor in mast cells (degranulation assays), biochemical analysis of subunit interaction The New England journal of medicine High 26841242
2017 Activation of EMR2 via a receptor-specific monoclonal antibody promotes differentiation of human THP-1 monocytic cells and induces expression of pro-inflammatory mediators (IL-8, TNF-α, MMP-9). EMR2-mediated signaling is initiated by Gα16, followed by sequential activation of Akt, ERK, JNK, and NF-κB. siRNA knockdown of specific signaling intermediates confirmed the pathway. Anti-EMR2 mAb stimulation, siRNA knockdown of signaling intermediates, specific signaling inhibitors, ELISA, western blotting, THP-1 differentiation assays Frontiers in immunology High 28421075
2018 The membrane association of the EMR2 N-terminal fragment (NTF) after GPS autoproteolysis is regulated by site-specific N-glycosylation within the GAIN domain, occurring in post-ER compartments. A unique amphipathic α-helix in the GAIN domain serves as a putative membrane anchor for the membrane-associated NTF subtype. Glycosylation site mutagenesis, subcellular fractionation, biochemical characterization of NTF subtypes, domain deletion analysis Scientific reports Medium 29540735
2020 ADGRE2/EMR2 and ADGRE5/CD97 are functionally G protein-coupled receptors. Using activated truncated receptor forms in a yeast-based assay with chimeric G proteins, EMR2 showed broad G protein-coupling, while CD97 coupled more specifically to Gα12, Gα13, Gα14, and Gαz chimeras. Both receptors induced pertussis-toxin insensitive inhibition of cAMP, suggesting coupling to Gαz. EMR2 signals via Gα16 and a Gα16/Gαz chimera to stimulate IP1 accumulation. A polyclonal antibody was identified that activates EMR2 G protein signaling in vitro. Yeast-based GPCR/chimeric G protein coupling assay, cAMP inhibition assay in mammalian cells, IP1 accumulation assay, NFAT reporter assay, pertussis toxin treatment Scientific reports Medium 31969668
2020 Mechanical activation (vibration) of mast cells expressing p.C492Y-ADGRE2 attached to dermatan sulfate triggers phospholipase C activation, transient cytosolic calcium increases, and downstream activation of PI3K and ERK1/2, mediated by Gβγ, Gαq/11, and through Gαi/o-independent mechanisms. Degranulation was dependent on PLC pathways (calcium, PKC, PI3K) and pertussis toxin-sensitive signals. Mechanoactivation also stimulated prostaglandin D2 synthesis via ERK1/2, calcium, PKC, and PI3K. Vibration stimulation of human mast cells on dermatan sulfate substrate, calcium imaging, pharmacological inhibitors of PLC/PKC/PI3K/ERK, pertussis toxin treatment, prostaglandin D2 ELISA, degranulation assay The Journal of investigative dermatology High 32222457
2019 EMR2/ADGRE2 contains an SGD sequence (corresponding to the RGD integrin-binding motif in CD97). Unlike CD97, EMR2 fails to induce angiogenesis or upregulate MMP-9. However, a single change of the SGD to RGD sequence in EMR2 allows it to up-regulate MMP-9 expression, leading to enhanced angiogenesis. MMP-9 promotes HUVEC proliferation, migration, and invasion by modulating VEGF, PIGF, and bFGF levels. MMP-9 expression is modulated by N-cadherin, which is upregulated by both CD97 and EMR2/RGD. Site-directed mutagenesis (SGD→RGD), in vitro endothelial tube formation assay, in ovo chick chorioallantoic membrane assay, MMP-9 expression analysis, VEGF/PIGF/bFGF measurement Biochemical and biophysical research communications Medium 31594642
2021 EMR2 stimulation by its agonistic 2A1 monoclonal antibody activates the NLRP3 inflammasome second signal in THP-1 monocytic cells and primary monocytes via a Gα16-dependent PLC-β activation pathway, inducing downstream Akt, MAPK, NF-κB activation and Ca2+ mobilization, ultimately leading to K+ efflux. Anti-EMR2 mAb (2A1) stimulation, siRNA knockdown, pharmacological inhibitors, K+ efflux measurement, Ca2+ mobilization assay, NLRP3 inflammasome activation assay in THP-1 and primary monocytes Frontiers in immunology Medium 33488598
2024 ADGRE2 activates phospholipase Cβ/protein kinase C/MEK/ERK signaling to enhance expression of AP1 transcription factor, which transcriptionally drives DUSP1 (a protein phosphatase). DUSP1 dephosphorylates Ser16 in the J-domain of co-chaperone DNAJB1, facilitating the DNAJB1-HSP70 interaction and maintenance of proteostasis in AML. Silencing ADGRE2 exerts antileukemic effects in AML cell lines and patient-derived cells in vitro, and delays AML progression in xenograft models. siRNA/shRNA knockdown, xenograft mouse models, pharmacological inhibitors of MEK/AP1/DUSP1, phosphorylation analysis (DUSP1 Ser16), co-immunoprecipitation (DNAJB1-HSP70), transcriptional reporter assays Cancer research High 39082681
2024 CD312/ADGRE2 interacts with GNA15 (Gα15) via its transmembrane intracellular segment. CD312 knockdown reduces Treg cell proportion while increasing CTL proportion in the ALL bone marrow immune microenvironment. Overexpression of CD312 in CD3+ T cells enhances leukemia cell proliferation via phosphorylation of ERK, JNK, and p38, while GNA15 knockdown decreases this proliferative effect. Co-immunoprecipitation/affinity assay for CD312-GNA15 interaction, CD312 knockdown and overexpression, GNA15 siRNA, BrdU proliferation assay, flow cytometry for immune subsets Journal of cellular and molecular medicine Medium 39656442

Source papers

Stage 0 corpus · 37 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2004 Autocatalytic cleavage of the EMR2 receptor occurs at a conserved G protein-coupled receptor proteolytic site motif. The Journal of biological chemistry 172 15150276
2003 The epidermal growth factor-like domains of the human EMR2 receptor mediate cell attachment through chondroitin sulfate glycosaminoglycans. Blood 172 12829604
2016 Vibratory Urticaria Associated with a Missense Variant in ADGRE2. The New England journal of medicine 151 26841242
2000 Human EMR2, a novel EGF-TM7 molecule on chromosome 19p13.1, is closely related to CD97. Genomics 85 10903844
2017 miR-99a reveals two novel oncogenic proteins E2F2 and EMR2 and represses stemness in lung cancer. Cell death & disease 84 29072692
2007 Ligation of the adhesion-GPCR EMR2 regulates human neutrophil function. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 82 17928360
2004 Expression of the largest CD97 and EMR2 isoforms on leukocytes facilitates a specific interaction with chondroitin sulfate on B cells. Journal of leukocyte biology 73 15498814
2002 CD97, but not its closely related EGF-TM7 family member EMR2, is expressed on gastric, pancreatic, and esophageal carcinomas. American journal of clinical pathology 73 12428789
2002 The human EGF-TM7 family member EMR2 is a heterodimeric receptor expressed on myeloid cells. Journal of leukocyte biology 57 11994511
2003 Proteolytic cleavage of the EMR2 receptor requires both the extracellular stalk and the GPS motif. FEBS letters 54 12860403
2012 Activation of myeloid cell-specific adhesion class G protein-coupled receptor EMR2 via ligation-induced translocation and interaction of receptor subunits in lipid raft microdomains. Molecular and cellular biology 50 22310662
2015 Expression of CD11c and EMR2 on neutrophils: potential diagnostic biomarkers for sepsis and systemic inflammation. Clinical and experimental immunology 47 26153037
2017 Activation of Adhesion GPCR EMR2/ADGRE2 Induces Macrophage Differentiation and Inflammatory Responses via Gα16/Akt/MAPK/NF-κB Signaling Pathways. Frontiers in immunology 43 28421075
2005 Identification of the epidermal growth factor-TM7 receptor EMR2 and its ligand dermatan sulfate in rheumatoid synovial tissue. Arthritis and rheumatism 43 15693006
2006 CD312, the human adhesion-GPCR EMR2, is differentially expressed during differentiation, maturation, and activation of myeloid cells. Biochemical and biophysical research communications 42 17174274
2006 An unusual mode of concerted evolution of the EGF-TM7 receptor chimera EMR2. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 41 17068111
2010 Leukocyte adhesion-GPCR EMR2 is aberrantly expressed in human breast carcinomas and is associated with patient survival. Oncology reports 39 21174063
2020 G Protein-Coupling of Adhesion GPCRs ADGRE2/EMR2 and ADGRE5/CD97, and Activation of G Protein Signalling by an Anti-EMR2 Antibody. Scientific reports 27 31969668
2020 Critical Signaling Events in the Mechanoactivation of Human Mast Cells through p.C492Y-ADGRE2. The Journal of investigative dermatology 25 32222457
2016 Increased EMR2 expression on neutrophils correlates with disease severity and predicts overall mortality in cirrhotic patients. Scientific reports 20 27905560
2011 EMR2 receptor ligation modulates cytokine secretion profiles and cell survival of lipopolysaccharide-treated neutrophils. Chang Gung medical journal 20 22035891
2010 Differential expression of the EGF-TM7 family members CD97 and EMR2 in lipid-laden macrophages in atherosclerosis, multiple sclerosis and Gaucher disease. Immunology letters 17 20167235
2003 Detection of alternatively spliced EMR2 mRNAs in colorectal tumor cell lines but rare expression of the molecule in colorectal adenocarcinomas. Virchows Archiv : an international journal of pathology 17 12761622
2021 Stimulation of Vibratory Urticaria-Associated Adhesion-GPCR, EMR2/ADGRE2, Triggers the NLRP3 Inflammasome Activation Signal in Human Monocytes. Frontiers in immunology 16 33488598
2019 The role of the RGD motif in CD97/ADGRE5-and EMR2/ADGRE2-modulated tumor angiogenesis. Biochemical and biophysical research communications 12 31594642
2024 Adhesion GPCR ADGRE2 Maintains Proteostasis to Promote Progression in Acute Myeloid Leukemia. Cancer research 10 39082681
2018 Membrane-association of EMR2/ADGRE2-NTF is regulated by site-specific N-glycosylation. Scientific reports 10 29540735
2004 Crystallization and preliminary X-ray diffraction analysis of three EGF domains of EMR2, a 7TM immune-system molecule. Acta crystallographica. Section D, Biological crystallography 10 15103144
2011 Comparative domain modeling of human EGF-like module EMR2 and study of interaction of the fourth domain of EGF with chondroitin 4-sulphate. Journal of biomedical research 5 23554678
2024 Research Progress of EMR2 Receptor Function in Glioma and its Potential Application as Therapeutic Target. Current health sciences journal 3 40144939
2017 Affinity Binding of EMR2 Expressing Cells by Surface-Grafted Chondroitin Sulfate B. Biomacromolecules 3 28437084
2025 Long-lasting changes in circulating dendritic cell and monocyte subsets, and altered expression of EMR2, CD97 and EMR3 on these cells in the posttraumatic course. Clinical & translational immunology 2 40529451
2024 CD312 Promotes Paediatric Acute Lymphoblastic Leukaemia Through GNA15-Mediated Non-Classical GPCR Signalling Pathway. Journal of cellular and molecular medicine 2 39656442
2023 The Posttraumatic Increase of the Adhesion GPCR EMR2/ADGRE2 on Circulating Neutrophils Is Not Related to Injury Severity. Cells 2 37998392
2024 Investigating the role of non-synonymous variant D67N of ADGRE2 in chronic myeloid leukemia. BMC cancer 1 39501172
2020 Author Correction: G Protein-Coupling of Adhesion GPCRs ADGRE2/EMR2 and ADGRE5/CD97, and Activation of G Protein Signalling by an Anti-EMR2 Antibody. Scientific reports 1 32184438
2026 Myeloid-driven inflammation highlights ADGRE2 as a biomarker in prurigo nodularis: Integrated multiomics analysis. The Journal of investigative dermatology 0 41544890

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