Affinage

Showing AGER — RAGE is a alias.

AGER

Advanced glycosylation end product-specific receptor · UniProt Q15109

Length
404 aa
Mass
42.8 kDa
Annotated
2026-06-09
100 papers in source corpus 23 papers cited in narrative 23 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

AGER (RAGE) is a multiligand cell-surface receptor that couples recognition of damage-associated ligands to inflammatory and pro-tumorigenic signaling, and it additionally serves as a defining marker and functional determinant of alveolar type 1 (AT1) cell identity in the lung (PMID:30011373, PMID:34466790). AGER engages a spectrum of ligands released during cell stress and death—S100B (PMID:16341840), HMGB1 (PMID:29079726), decorin (DCN) released during ferroptosis (PMID:34964698), and NCOA4 secreted by activated macrophages (PMID:38916095)—and transduces these signals through PKC/oxidative-stress, ERK, and NF-κB cascades to drive prostaglandin production, cytokine release, and pyroptotic inflammation (PMID:16341840, PMID:29796842, PMID:38916095). In innate immunity, AGER is required for caspase-11 inflammasome activation through ALOX5-mediated lipid peroxidation, enabling gasdermin D cleavage, IL-1β maturation, and pyroptosis, such that AGER deletion protects mice from LPS-induced septic death (PMID:31440260); it also routes HMGB1 and NCOA4 signals into STING1- and NFKBIA-degradation-dependent NF-κB activation during sepsis and regulated cell death (PMID:33992959, PMID:38916095). In cancer, AGER supports tumorigenesis by sustaining autophagic flux that promotes IL-6–driven STAT3 phosphorylation and mitochondrial bioenergetics (PMID:22722139), by establishing a hexosamine/O-GlcNAc–c-Jun autoregulatory loop under high glucose (PMID:26825459), and by interacting with the formin DIAPH1 to drive RAC1-dependent macropinocytosis that confers resistance to KRAS-G12D inhibition (PMID:39879317). A soluble ectodomain (sRAGE), generated by C-terminal proteolytic truncation, adopts a J-shaped monomer that homodimerizes through its V domains in a concentration- and Ca²⁺-dependent manner (PMID:15381690, PMID:21865159), and acts both as a decoy that sequesters ligands to dampen inflammation and, in certain contexts, as a direct agonist of monocyte survival and migration (PMID:20574008, PMID:29079726, PMID:29796842). AGER expression is governed by a YAP/KLF5/NFIB/NKX2-1 transcriptional network in alveolar cells (PMID:34466790), by promoter and coding polymorphisms that modulate expression and sRAGE output (PMID:22860029, PMID:27755550), and post-transcriptionally by miRNAs and competing endogenous RNAs (PMID:31396332, PMID:29752466).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 2004 Medium

    Established the biochemical origin of soluble RAGE, resolving how the decoy form is generated and distributed.

    Evidence Purification and biochemical characterization of mouse sRAGE (glycosylation, disulfide pattern, heparin binding)

    PMID:15381690

    Open questions at the time
    • Did not identify the protease responsible for C-terminal truncation
    • Human sRAGE generation (splicing vs shedding) not directly resolved here
  2. 2005 Medium

    Linked ligand engagement of AGER to a defined downstream output, showing S100B drives COX-2/PGE2 via PKC and oxidative stress.

    Evidence RT-PCR, Western blot, PGE2 immunoassay and PKC/oxidant inhibitors in human pancreatic islets

    PMID:16341840

    Open questions at the time
    • Did not establish direct receptor occupancy versus indirect activation
    • Limited to islet context
  3. 2010 Medium

    Showed sRAGE is not purely a decoy but can directly engage immune cells, complicating the simple competitive-sequestration model.

    Evidence Direct binding, migration, cytokine assays and Akt/Erk/NF-κB immunoblots in human monocytes/macrophages, with intratracheal administration

    PMID:20574008

    Open questions at the time
    • The cell-surface receptor mediating sRAGE binding to monocytes not identified
    • Agonist versus decoy balance in vivo unresolved
  4. 2011 High

    Defined the solution architecture of sRAGE, explaining how V-domain-mediated, Ca²⁺-dependent dimerization underlies oligomeric signaling.

    Evidence Synchrotron SAXS structure determination and concentration-dependent oligomerization assays

    PMID:21865159

    Open questions at the time
    • No ligand-bound structure
    • Full-length transmembrane receptor architecture not resolved
  5. 2012 High

    Demonstrated a cell-intrinsic oncogenic mechanism for AGER, coupling autophagy to IL-6/STAT3 mitochondrial bioenergetics in pancreatic tumorigenesis.

    Evidence Ager-/- in KRAS-driven mouse model, autophagic flux assays, pSTAT3 immunoblotting, mitochondrial fractionation and ATP measurement

    PMID:22722139

    Open questions at the time
    • Ligand driving the autophagy-STAT3 loop not defined
    • How AGER mechanistically promotes autophagic flux unclear
  6. 2016 Medium

    Uncovered a metabolic autoregulatory loop in which AGER drives O-GlcNAc-dependent c-Jun activity that feeds back to enhance its own transcription under hyperglycemia.

    Evidence Gain/loss-of-function in HCC cells, Ser73 O-GlcNAcylation mapping, ChIP and reporter assays

    PMID:26825459

    Open questions at the time
    • Direct vs indirect AGER control of hexosamine pathway not dissected
    • In vivo confirmation of the loop limited
  7. 2016 Medium

    Provided functional consequence for a coding polymorphism, showing rs2070600 (Gly82Ser) reduces ligand-induced sRAGE generation.

    Evidence Allele-specific RAGE variant transfection in airway cells with HMGB1 stimulation and sRAGE ELISA plus cohort association

    PMID:27755550

    Open questions at the time
    • Mechanism by which Ser82 impairs shedding not defined
    • Single cell-line overexpression system
  8. 2017 High

    Showed AGER governs the inflammatory polarization of macrophages in diabetes, with its deletion restoring reparative inflammation and angiogenesis.

    Evidence Ager-/- and Glo1 transgenic mice, hindlimb ischemia model, flow cytometry, macrophage-endothelial co-culture

    PMID:28642238

    Open questions at the time
    • Ligand driving the high-glucose inflammatory shift not pinpointed
    • Downstream transcriptional program incompletely mapped
  9. 2017 Medium

    Established HMGB1/RAGE signaling in dendritic cells as a driver of Th17/neutrophilic asthma, antagonized by sRAGE.

    Evidence Murine asthma model, intratracheal sRAGE, adoptive DC transfer, in vitro Th17 polarization

    PMID:29079726

    Open questions at the time
    • Direct DC receptor-level signaling steps to IL-23 not fully resolved
    • Single lab
  10. 2018 Medium

    Identified AGER as a marker and functional determinant of AT1 cell identity, upregulated during AT2-to-AT1 repair.

    Evidence Ager-CreERT2 knock-in lineage tracing and DTA ablation in mice

    PMID:30011373

    Open questions at the time
    • Whether AGER is causal for AT1 differentiation or merely a marker unresolved
    • Signaling role in AT1 cells not addressed
  11. 2018 Medium

    Showed AGER drives cardiomyocyte and stem-cell pathology via PKC-ERK-NF-κB/NLRP3 and JNK-ROS axes, with miRNA control of AGER tuning these outcomes.

    Evidence H9C2 Ang II model with sRAGE blockade; AGER siRNA and miR-5591-5p modulation in ADSCs with ROS/apoptosis and JNK readouts plus diabetic wound model

    PMID:29752466 PMID:29796842

    Open questions at the time
    • Cardiomyocyte work is in vitro only
    • Direct ligand engagement not demonstrated
  12. 2019 Medium

    Connected AGER to lung cancer cell behavior through ceRNA/miRNA regulation and NF-κB, while revealing context-dependent tumor-suppressive effects in NSCLC.

    Evidence Luciferase reporter validation of miR-182-5p targeting AGER, LINC00173 ceRNA experiments, proliferation/migration assays

    PMID:31396332

    Open questions at the time
    • Reconciliation of pro- vs anti-tumor AGER roles across cancers unresolved
    • NF-κB suppression mechanism only partially defined
  13. 2019 High

    Defined a molecular requirement for AGER in caspase-11 inflammasome activation through ALOX5-mediated lipid peroxidation, establishing it as a driver of pyroptotic sepsis.

    Evidence Global and myeloid-conditional Ager-/-, ALOX5 pathway inhibition, caspase-11/gasdermin D cleavage assays, in vivo LPS sepsis

    PMID:31440260

    Open questions at the time
    • How AGER physically couples to ALOX5 lipid peroxidation not structurally defined
    • Upstream nDAMP ligand identity incomplete
  14. 2021 High

    Identified DCN and HMGB1 from regulated cell death as AGER ligands that route into NF-κB and STING1 inflammatory signaling in macrophages.

    Evidence DCN-AGER binding/Co-IP, AGER knockout and inhibition in pancreatitis; genetic dissection of HMGB1-AGER-STING1 in alkaliptosis with cytokine ELISA

    PMID:33992959 PMID:34964698

    Open questions at the time
    • Binding sites on AGER for DCN/HMGB1 not mapped
    • How AGER engages STING1 mechanistically unclear
  15. 2021 Medium

    Mapped the transcriptional control of AGER, placing it under a YAP-anchored KLF5/NFIB/NKX2-1 network that specifies AT1 over AT2 fate.

    Evidence YAP gain/loss transgenic mice, ATAC-seq, transcriptomics, motif enrichment

    PMID:34466790

    Open questions at the time
    • Direct binding of each factor to the AGER locus not individually validated
    • Relationship to AGER signaling output not addressed
  16. 2024 High

    Discovered NCOA4 as an AGER ligand released by macrophages that activates NF-κB via NFKBIA degradation to drive lethal sepsis, defining a therapeutically targetable axis.

    Evidence Co-IP NCOA4-AGER, Ager-/- and ATG5/MCOLN1/GSDMD knockouts, neutralizing antibodies, endotoxemia and polymicrobial sepsis models

    PMID:38916095

    Open questions at the time
    • Structural basis of NCOA4-AGER recognition unknown
    • Selectivity of AGER over TLR4 only functionally inferred
  17. 2025 High

    Revealed a non-classical AGER mechanism in cancer drug resistance: an AGER-DIAPH1 interaction drives RAC1-dependent macropinocytosis and nutrient scavenging that defeats KRAS-G12D inhibition.

    Evidence Co-IP of AGER-DIAPH1, RAC1 activity and macropinocytosis assays, PDX and GEMM models with pharmacological inhibitors

    PMID:39879317

    Open questions at the time
    • How ligand binding (if any) regulates the AGER-DIAPH1 interaction unclear
    • Structural interface with DIAPH1 not defined

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how AGER's opposing roles—pro-tumorigenic in pancreatic and hepatocellular cancer versus tumor-suppressive in NSCLC—are determined, and how ligand identity, cell type, and the membrane versus soluble forms dictate which downstream program (NF-κB, STAT3/autophagy, macropinocytosis, pyroptosis) is engaged.
  • No unified structural model of ligand-specific receptor activation
  • Context determinants of agonist vs decoy sRAGE function undefined
  • Cross-pathway selectivity (NF-κB vs STING1 vs DIAPH1/RAC1) unexplained

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060089 molecular transducer activity 3 GO:0098772 molecular function regulator activity 3 GO:0038024 cargo receptor activity 2
Localization
GO:0005576 extracellular region 3 GO:0005886 plasma membrane 3 GO:0005829 cytosol 1
Pathway
R-HSA-168256 Immune System 4 R-HSA-162582 Signal Transduction 3 R-HSA-1266738 Developmental Biology 2 R-HSA-1643685 Disease 2 R-HSA-5357801 Programmed Cell Death 2 R-HSA-9612973 Autophagy 1
Partners
DCNDIAPH1HMGB1NCOA4S100BSTING1

Evidence

Reading pass · 23 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2004 Mouse soluble RAGE (sRAGE) is produced by carboxyl-terminal proteolytic truncation of cell surface RAGE (not by alternative splicing as in humans), is glycosylated, contains disulfide bonds, and binds heparin, which may mediate its distribution in the extracellular matrix and on cell surfaces. Purification, biochemical characterization (glycosylation analysis, disulfide pattern determination, heparin-binding assay) The Journal of biological chemistry Medium 15381690
2011 The solution structure of human sRAGE was determined by synchrotron small-angle X-ray scattering; the monomer adopts a J-like shape, and the homodimer is formed through association of the two N-terminal (V) domains, yielding an elongated structure. Oligomerization is concentration-dependent and is also mediated by Ca²⁺ ions. Small-angle X-ray scattering (SAXS) structure determination; concentration-dependent oligomerization assays The Journal of biological chemistry High 21865159
2005 Activation of AGER (RAGE) by its ligand S100B on human pancreatic islets induces PTGS2 (COX-2) expression and prostaglandin E2 production via protein kinase C and oxidative stress signaling pathways. RT-PCR, Western blot, PGE2 enzyme immunoassay; pharmacological inhibition of PKC and oxidant stress pathways in human islets treated with S100b Diabetologia Medium 16341840
2010 sRAGE directly binds human monocytes and monocyte-derived macrophages, promoting their survival and differentiation to macrophages, and activates the Akt, Erk, and NF-κB intracellular signaling pathways in these cells. sRAGE also induces monocyte and neutrophil migration and pro-inflammatory cytokine/chemokine production in vitro. Direct binding assay (sRAGE binding to cells), in vitro migration assay, cytokine/chemokine measurement, Western blot for Akt/Erk/NF-κB activation, intratracheal administration in vivo Journal of immunology Medium 20574008
2012 AGER promotes pancreatic tumorigenesis by mediating autophagic flux that supports IL-6-induced phosphorylation of STAT3 and its mitochondrial localization, thereby increasing ATP availability and cellular proliferation. Targeted ablation of AGER in a KRAS-driven murine model diminishes autophagic flux and attenuates development of early pancreatic intraepithelial neoplasia (PanIN) lesions. A positive feedback loop exists between autophagy activation and the IL6-pSTAT3 pathway downstream of AGER. Genetic knockout (Ager-/-) in KRAS-driven mouse model, autophagic flux assays, IL-6/pSTAT3 immunoblotting, mitochondrial fractionation, ATP measurement, cell proliferation assay Autophagy High 22722139
2016 AGER activates the hexosamine biosynthetic pathway, leading to enhanced O-GlcNAcylation of c-Jun at Ser73, increasing c-Jun activity and stability. c-Jun in turn enhances AGER transcription, establishing a positive autoregulatory feedback loop that promotes hepatocellular carcinoma tumorigenesis under high-glucose conditions. AGER overexpression/knockdown in HCC cells, O-GlcNAcylation analysis, site-directed mutagenesis (Ser73), ChIP/transcriptional reporter assays, cell proliferation assays Diabetes Medium 26825459
2016 The rs2070600 (Gly82Ser) AGER variant functionally reduces sRAGE production: airway epithelial cells overexpressing the RAGE-Ser82 variant produce lower sRAGE levels upon HMGB1 stimulation compared to cells overexpressing the RAGE-Gly82 variant, demonstrating a functional role of this SNP in modulating sRAGE generation. Transfection of BEAS2B-R1 cells with Gly82 or Ser82 RAGE variants, HMGB1 stimulation, sRAGE ELISA; RNA-Seq for transcript identification; clinical cohort for association PloS one Medium 27755550
2017 AGER deletion (Ager-/-) in diabetic mice restores adaptive inflammation after hindlimb ischemia by increasing circulating Ly6Chi monocytes and augmenting macrophage infiltration into ischemic muscle, thereby rescuing angiogenesis and blood flow recovery. In vitro, Ager deletion in macrophages reverses the high-glucose-induced shift from tissue-repair to tissue-damage inflammatory gene expression and restores macrophage-endothelial cell interactions. Genetic knockout (Ager-/-), transgenic Glo1 overexpression, femoral artery ligation model, flow cytometry, immunofluorescence, in vitro macrophage/endothelial co-culture assays Arteriosclerosis, thrombosis, and vascular biology High 28642238
2017 sRAGE prevents neutrophilic asthma by blocking HMGB1/RAGE signaling in airway CD11c+ dendritic cells, inhibiting RAGE and IL-23 expression, suppressing Th17 polarization, and reducing neutrophilic inflammation. Adoptive transfer of rHMGB1-activated DCs restored airway inflammation; transfer of DCs activated with rHMGB1 plus sRAGE significantly reduced it. Murine neutrophilic asthma model, intratracheal sRAGE administration, adoptive DC transfer, in vitro Th17 polarization assay, flow cytometry, cytokine ELISA Scientific reports Medium 29079726
2018 sRAGE attenuates angiotensin II-induced cardiomyocyte hypertrophy by downregulating RAGE and AT1R expression, reducing HMGB1 and IL-1β secretion, and inhibiting PKC, ERK1/2, NF-κB, and NLRP3 inflammasome activation. RAGE thus drives cardiac hypertrophy through PKC-ERK1/2 and NF-κB-NLRP3-IL-1β pathway activation. Western blot, fluorescence microscopy (ROS, phospho-p65), ELISA (HMGB1, IL-1β) in H9C2 cells treated with Ang II ± sRAGE Inflammation research Medium 29796842
2019 AGER is required for caspase-11 inflammasome activation in macrophages: AGER-mediated lipid peroxidation via arachidonate 5-lipoxygenase (ALOX5) enables nDAMP-induced caspase-11 activation, gasdermin D cleavage, IL-1β maturation, and pyroptosis. Global (Ager-/-) or myeloid-specific AGER deletion protects mice from LPS-induced septic death. Genetic knockout (global and myeloid-conditional Ager-/-), pharmacological inhibition of AGER-ALOX5 pathway, caspase-11/gasdermin D cleavage assays, LDH release, IL-1β ELISA, in vivo LPS sepsis model Frontiers in immunology High 31440260
2021 DCN (decorin) released during ferroptosis binds to AGER on macrophages, triggering NF-κB-dependent production of pro-inflammatory cytokines. Pharmacological and genetic inhibition of the DCN-AGER axis protects against ferroptotic death-related acute pancreatitis and limits tumor-protective immune responses. Co-immunoprecipitation/binding assay (DCN-AGER), genetic AGER knockout, pharmacological inhibition, in vivo pancreatitis model, cytokine measurement Autophagy High 34964698
2021 HMGB1 released by alkaliptotic cancer cells binds AGER on macrophages and activates the STING1 pathway to produce pro-inflammatory cytokines (TNF and IL-6). Genetic or pharmacological inhibition of the HMGB1-AGER-STING1 pathway limits cytokine production during alkaliptosis. Genetic knockdown/knockout of HMGB1, AGER, and STING1; cytokine ELISA; co-culture of alkaliptotic cancer cells with macrophages Biochemical and biophysical research communications Medium 33992959
2021 YAP participates with the transcription factors KLF5, NFIB, and NKX2-1 to regulate AGER expression in alveolar epithelial cells. YAP activation increased AT1 cell numbers and AGER expression; YAP deletion increased AT2 cell gene expression. Motif enrichment and chromatin accessibility analysis identified the transcriptional network. Transgenic mouse models (YAP activation and deletion), ATAC-seq, transcriptomic analysis, motif enrichment iScience Medium 34466790
2018 AGER expression in alveolar type 1 (AT1) cells is high in adult lung; the Ager-CreERT2 allele enables lineage labeling and selective killing of AT1 cells. When ~50% of AT1 cells are killed, SFTPC+ AT2 cells proliferate and upregulate Ager expression during repair, establishing AGER as a marker and functional indicator of AT1 cell identity and repair capacity. Ager-CreERT2 knock-in mouse generation, tamoxifen-induced lineage tracing, Rosa26-DTA AT1 cell ablation, immunofluorescence, cell proliferation quantification American journal of respiratory cell and molecular biology Medium 30011373
2024 Extracellular NCOA4 (secreted by activated macrophages via ATG5/MCOLN1-dependent lysosomal exocytosis, or passively released during GSDMD-mediated pyroptosis) binds AGER (not TLR4) on macrophages and activates NF-κB by promoting NFKBIA degradation, driving septic inflammation and death. Neutralizing antibodies against NCOA4 or AGER delay septic death and reduce organ damage in mouse models. Co-IP (NCOA4-AGER interaction), genetic knockout (Ager-/-, ATG5, MCOLN1, GSDMD), monoclonal antibody neutralization, in vivo endotoxemia and polymicrobial sepsis models, NF-κB/NFKBIA Western blot Autophagy High 38916095
2025 AGER mediates resistance to the KRAS-G12D inhibitor MRTX1133 in pancreatic cancer by upregulating macropinocytosis through its interaction with the formin protein DIAPH1, driving RAC1-dependent macropinosome formation, serum albumin internalization, amino acid generation, and glutathione synthesis that inhibits apoptosis. Co-IP (AGER-DIAPH1 interaction), RAC1 activity assay, macropinocytosis assay, patient-derived xenograft, orthotopic and genetically engineered mouse models, pharmacological inhibitors (RAGE299, EIPA) Science translational medicine High 39879317
2019 miR-182-5p directly targets AGER as a downstream effector in NSCLC cells, and AGER loss mediates NF-κB pathway suppression; LINC00173 acts as a competing endogenous RNA to sequester miR-182-5p and restore AGER expression. Alteration of AGER expression or NF-κB inhibition partially counteracts the proliferation/migration phenotype induced by miR-182-5p. Luciferase reporter assay (AGER as direct miR-182-5p target), siRNA/overexpression, functional assays (proliferation, migration, apoptosis), NF-κB inhibition American journal of translational research Medium 31396332
2018 The AGEs/AGER axis induces ROS generation and apoptosis in adipose tissue-derived stem cells (ADSCs); miR-5591-5p directly targets AGER and suppresses AGEs/AGER-mediated ROS generation and apoptosis via the JNK signaling pathway. siRNA knockdown of AGER, miR-5591-5p overexpression/inhibition, ROS measurement, apoptosis assay, JNK signaling Western blot, in vivo diabetic wound repair model Cell death & disease Medium 29752466
2012 In the AGER -429T/C promoter polymorphism, the minor C allele is associated with increased AGER promoter activity (measured by luciferase assay), demonstrating a functional effect of this SNP on RAGE expression levels. Luciferase reporter assay of AGER -429T vs. -429C promoter constructs in BEAS-2B cells PloS one Medium 22860029
2020 AGER overexpression in NSCLC H1299 cells decreases cell viability, proliferation, migration, and invasion, and increases apoptosis with upregulation of Bax and downregulation of Bcl-2; AGER knockdown has the opposite effects. Lentiviral overexpression and siRNA knockdown, MTT assay, flow cytometry, wound-healing assay, Transwell invasion assay, Western blot (Bax, Bcl-2) Molecular medicine reports Medium 32468030
2018 AGER promotes proliferation, migration, and inhibits apoptosis of cervical squamous cancer cells; AGER protein localizes primarily in the cytoplasm and cytomembrane of these cells. siRNA-mediated AGER blockade suppresses proliferation and migration and stimulates apoptosis. siRNA knockdown, AGER overexpression, immunofluorescence localization, MTT proliferation assay, migration assay, flow cytometry Bioscience reports Medium 29298878
2022 Cadmium activates AGER-mediated inflammatory signaling via the AGER/PKC/p65 pathway in pancreatic β-cells. Ferroptosis inhibitor Fer-1 antagonizes cadmium-induced AGER-mediated immune activation, placing AGER downstream of ferroptotic lipid peroxidation in the inflammatory cascade. Transcriptomic analysis, ferroptosis marker assays (GSH, GPX4, lipid peroxidation, mitochondrial ultrastructure), AGER/PKC/p65 pathway Western blot, Fer-1 pharmacological inhibition in MIN6 cells and mice The Science of the total environment Medium 35931150

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2004 Purification and characterization of mouse soluble receptor for advanced glycation end products (sRAGE). The Journal of biological chemistry 184 15381690
2017 AGEs, RAGEs and s-RAGE; friend or foe for cancer. Seminars in cancer biology 157 28712719
2013 sRAGE and risk of diabetes, cardiovascular disease, and death. Diabetes 147 23396398
2013 Systemic soluble receptor for advanced glycation endproducts is a biomarker of emphysema and associated with AGER genetic variants in patients with chronic obstructive pulmonary disease. American journal of respiratory and critical care medicine 130 23947473
2021 DCN released from ferroptotic cells ignites AGER-dependent immune responses. Autophagy 109 34964698
2021 The use of the soluble receptor for advanced glycation-end products (sRAGE) as a potential biomarker of disease risk and adverse outcomes. Redox biology 106 33839083
2010 Soluble form of a receptor for advanced glycation end products (sRAGE) as a biomarker. Frontiers in bioscience (Elite edition) 102 20515790
2018 Plasma sRAGE is independently associated with increased mortality in ARDS: a meta-analysis of individual patient data. Intensive care medicine 100 30051136
2007 Receptor for advanced glycation end products (RAGE)--soluble form (sRAGE) and gene polymorphisms in patients with breast cancer. Cancer investigation 97 18058469
2007 Serum levels of soluble form of receptor for advanced glycation end products (sRAGE) are positively associated with circulating AGEs and soluble form of VCAM-1 in patients with type 2 diabetes. Microvascular research 85 18474381
2012 AGER/RAGE-mediated autophagy promotes pancreatic tumorigenesis and bioenergetics through the IL6-pSTAT3 pathway. Autophagy 83 22722139
2015 Circulating soluble receptor for advanced glycation end products (sRAGE) as a biomarker of emphysema and the RAGE axis in the lung. American journal of respiratory and critical care medicine 76 26132989
2008 Association between LTA, TNF and AGER polymorphisms and late diabetic complications. PloS one 76 18575614
2007 Kinetics, role and therapeutic implications of endogenous soluble form of receptor for advanced glycation end products (sRAGE) in diabetes. Current drug targets 76 17979674
2019 Pathological Implications of Receptor for Advanced Glycation End-Product (AGER) Gene Polymorphism. Disease markers 72 30863465
2009 Receptor for advanced glycation end-products (RAGE) and soluble RAGE (sRAGE): cardiovascular implications. Diabetes & vascular disease research 66 19156622
2018 Serum levels of advanced glycation end-products (AGEs) and the decoy soluble receptor for AGEs (sRAGE) can identify non-alcoholic fatty liver disease in age-, sex- and BMI-matched normo-glycemic adults. Metabolism: clinical and experimental 65 29409822
2018 Is there any evidence that AGE/sRAGE is a universal biomarker/risk marker for diseases? Molecular and cellular biochemistry 65 29961210
2010 sRAGE induces human monocyte survival and differentiation. Journal of immunology (Baltimore, Md. : 1950) 65 20574008
2021 Soluble receptor for advanced glycation end products (sRAGE) as a biomarker of COVID-19 disease severity and indicator of the need for mechanical ventilation, ARDS and mortality. Annals of intensive care 63 33751264
2020 Plasma sRAGE Acts as a Genetically Regulated Causal Intermediate in Sepsis-associated Acute Respiratory Distress Syndrome. American journal of respiratory and critical care medicine 62 31487195
2022 Cadmium induces ferroptosis mediated inflammation by activating Gpx4/Ager/p65 axis in pancreatic β-cells. The Science of the total environment 60 35931150
2013 Circulating nucleosomes and immunogenic cell death markers HMGB1, sRAGE and DNAse in patients with advanced pancreatic cancer undergoing chemotherapy. International journal of cancer 58 23729200
2016 High Glucose Stimulates Tumorigenesis in Hepatocellular Carcinoma Cells Through AGER-Dependent O-GlcNAcylation of c-Jun. Diabetes 56 26825459
2014 Novel CoQ10 antidiabetic mechanisms underlie its positive effect: modulation of insulin and adiponectine receptors, Tyrosine kinase, PI3K, glucose transporters, sRAGE and visfatin in insulin resistant/diabetic rats. PloS one 56 24586567
2008 Soluble receptor for advanced glycation end products (sRAGE) and endogenous secretory RAGE (esRAGE) in amniotic fluid: modulation by infection and inflammation. Journal of perinatal medicine 54 18593373
2017 sRAGE alleviates neutrophilic asthma by blocking HMGB1/RAGE signalling in airway dendritic cells. Scientific reports 50 29079726
2012 Plasma sRAGE enables prediction of acute lung injury after cardiac surgery in children. Critical care (London, England) 50 22616947
2019 Prebiotic supplementation modulates advanced glycation end-products (AGEs), soluble receptor for AGEs (sRAGE), and cardiometabolic risk factors through improving metabolic endotoxemia: a randomized-controlled clinical trial. European journal of nutrition 47 31728681
2010 Soluble receptor for advanced glycation end-products (sRAGE) and polymorphisms of RAGE and glyoxalase I genes in patients with pancreas cancer. Clinical biochemistry 47 20398646
2021 Soluble receptor for advanced glycation end products (sRAGE) as a biomarker of COPD. Respiratory research 46 33906653
2021 YAP regulates alveolar epithelial cell differentiation and AGER via NFIB/KLF5/NKX2-1. iScience 46 34466790
2013 Follicular fluid soluble receptor for advanced glycation end-products (sRAGE): a potential indicator of ovarian reserve. The Journal of clinical endocrinology and metabolism 46 24276462
2018 sRAGE attenuates angiotensin II-induced cardiomyocyte hypertrophy by inhibiting RAGE-NFκB-NLRP3 activation. Inflammation research : official journal of the European Histamine Research Society ... [et al.] 44 29796842
2019 AGER-Mediated Lipid Peroxidation Drives Caspase-11 Inflammasome Activation in Sepsis. Frontiers in immunology 42 31440260
2017 Cross-sectional Analysis of AGE-CML, sRAGE, and esRAGE with Diabetes and Cardiometabolic Risk Factors in a Community-Based Cohort. Clinical chemistry 42 28280052
2005 Increased expression of cyclooxygenase-2 in human pancreatic islets treated with high glucose or ligands of the advanced glycation endproduct-specific receptor (AGER), and in islets from diabetic mice. Diabetologia 42 16341840
2019 Diminished LINC00173 expression induced miR-182-5p accumulation promotes cell proliferation, migration and apoptosis inhibition via AGER/NF-κB pathway in non-small-cell lung cancer. American journal of translational research 41 31396332
2019 CRISPR/Cas9 Edited sRAGE-MSCs Protect Neuronal Death in Parkinson’s Disease Model. International journal of stem cells 39 30836725
2012 AGER -429T/C is associated with an increased lung disease severity in cystic fibrosis. PloS one 38 22860029
2017 Ager Deletion Enhances Ischemic Muscle Inflammation, Angiogenesis, and Blood Flow Recovery in Diabetic Mice. Arteriosclerosis, thrombosis, and vascular biology 37 28642238
2016 AGEs/sRAGE, a novel risk factor in the pathogenesis of end-stage renal disease. Molecular and cellular biochemistry 36 27714575
2011 Solution structure of the soluble receptor for advanced glycation end products (sRAGE). The Journal of biological chemistry 36 21865159
2016 The Ser82 RAGE Variant Affects Lung Function and Serum RAGE in Smokers and sRAGE Production In Vitro. PloS one 35 27755550
2012 Elevated serum levels of AGEs, sRAGE, and pentosidine in Tunisian patients with severity of diabetic retinopathy. Microvascular research 35 22835520
2017 Long non-coding RNA AGER-1 functionally upregulates the innate immunity gene AGER and approximates its anti-tumor effect in lung cancer. Molecular carcinogenesis 34 29068471
2018 Ager-CreERT2: A New Genetic Tool for Studying Lung Alveolar Development, Homeostasis, and Repair. American journal of respiratory cell and molecular biology 33 30011373
2018 miR-5591-5p regulates the effect of ADSCs in repairing diabetic wound via targeting AGEs/AGER/JNK signaling axis. Cell death & disease 32 29752466
2017 AGER gene polymorphisms and soluble receptor for advanced glycation end product in patients with idiopathic pulmonary fibrosis. Respirology (Carlton, Vic.) 32 28198072
2006 Expression and purification of the soluble isoform of human receptor for advanced glycation end products (sRAGE) from Pichia pastoris. Biochemical and biophysical research communications 32 16806067
2021 The HMGB1-AGER-STING1 pathway mediates the sterile inflammatory response to alkaliptosis. Biochemical and biophysical research communications 29 33992959
2020 The role of soluble receptor for advanced glycation end-products (sRAGE) in the general population and patients with diabetes mellitus with a focus on renal function and overall outcome. Critical reviews in clinical laboratory sciences 29 32669010
2013 High-mobility group box-1 (HMGB-1) and serum soluble receptor for advanced glycation end products (sRAGE) in children affected by vernal keratoconjunctivitis. Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology 29 24236762
2010 Soluble receptor for advanced glycation end products (sRAGE) in plasma and synovial fluid is inversely associated with disease severity of knee osteoarthritis. Clinical biochemistry 28 20627100
2017 Effect of RAGE gene polymorphisms and circulating sRAGE levels on susceptibility to gastric cancer: a case-control study. Cancer cell international 27 28184178
2017 Protection against RAGE-mediated neuronal cell death by sRAGE-secreting human mesenchymal stem cells in 5xFAD transgenic mouse model. Brain, behavior, and immunity 26 28760504
2015 Protective effect of sRAGE on fetal development in pregnant rats with gestational diabetes mellitus. Cell biochemistry and biophysics 26 25205260
2025 AGER-dependent macropinocytosis drives resistance to KRAS-G12D-targeted therapy in advanced pancreatic cancer. Science translational medicine 25 39879317
2017 sRAGE prolonged stem cell survival and suppressed RAGE-related inflammatory cell and T lymphocyte accumulations in an Alzheimer's disease model. Biochemical and biophysical research communications 25 29127006
2019 The soluble receptor for advanced glycation end-products (sRAGE) has a dual phase-dependent association with residual cardiovascular risk after an acute coronary event. Atherosclerosis 24 31181415
2018 Therapeutic effects of recombinant human S100A6 and soluble receptor for advanced glycation end products(sRAGE) on CCl4-induced liver fibrosis in mice. European journal of pharmacology 23 29800549
2016 Decreased levels of sRAGE in follicular fluid from patients with PCOS. Reproduction (Cambridge, England) 23 27965400
2020 Serum levels of advanced glycation end products (AGEs) are increased and their soluble receptor (sRAGE) reduced in Hashimoto's thyroiditis. Journal of endocrinological investigation 22 32232775
2020 Effect of AGER on the biological behavior of non‑small cell lung cancer H1299 cells. Molecular medicine reports 22 32468030
2019 AGER expression and alternative splicing in bronchial biopsies of smokers and never smokers. Respiratory research 22 30971245
2012 Intrafollicular soluble receptor for advanced glycation end products (sRAGE) and embryo quality in assisted reproduction. Reproductive biomedicine online 22 23182743
2024 Extracellular NCOA4 is a mediator of septic death by activating the AGER-NFKB pathway. Autophagy 21 38916095
2013 Plasma sRAGE and N-(carboxymethyl) lysine in patients with CHF and/or COPD. European journal of clinical investigation 21 23590548
2009 Association between serum levels of the soluble receptor (sRAGE) for advanced glycation endproducts (AGEs) and their receptor (RAGE) in peripheral blood mononuclear cells of children with type 1 diabetes mellitus. Journal of pediatric endocrinology & metabolism : JPEM 21 20020577
2021 Advanced Glycation End-Products (AGEs) and Their Soluble Receptor (sRAGE) in Women Suffering from Systemic Lupus Erythematosus (SLE). Cells 20 34944030
2017 Associations between Soluble Receptor for Advanced Glycation End Products (sRAGE) and S100A12 (EN-RAGE) with Mortality in Long-term Hemodialysis Patients. Journal of Korean medical science 20 27914132
2021 AGEs and sRAGE Variations at Different Timepoints in Patients with Chronic Kidney Disease. Antioxidants (Basel, Switzerland) 19 34943097
2019 Divergent Changes in Plasma AGEs and sRAGE Isoforms Following an Overnight Fast in T1DM. Nutrients 19 30781793
2008 Soluble RAGE, diabetic nephropathy and genetic variability in the AGER gene. Archives of physiology and biochemistry 19 18615900
2019 Obesity and Comorbidity: Could Simultaneous Targeting of esRAGE and sRAGE Be the Panacea? Frontiers in physiology 18 31293451
2018 Metabolic Derangements Contribute to Reduced sRAGE Isoforms in Subjects with Alzheimer's Disease. Mediators of inflammation 18 29681765
2014 Circulating concentrations of soluble receptor for AGE are associated with age and AGER gene polymorphisms in children with newly diagnosed type 1 diabetes. Diabetes care 18 24742661
2014 Changes of HMGB1 and sRAGE during the recovery of COPD exacerbation. Journal of thoracic disease 18 24976997
2014 [Receptor of advanced glycation endproducts RAGE/AGER: an integrative view for clinical applications]. Annales de biologie clinique 18 25486663
2011 Clinical significance of serum sRAGE and esRAGE in women with normal pregnancy and preeclampsia. Journal of perinatal medicine 18 21767223
2020 Long non-coding RNA AGER-1 inhibits colorectal cancer progression through sponging miR-182. The International journal of biological markers 17 32031046
2020 The Gly82Ser mutation in AGER contributes to pathogenesis of pulmonary fibrosis in combined pulmonary fibrosis and emphysema (CPFE) in Japanese patients. Scientific reports 17 32732977
2019 Serum Soluble Receptor for AGE (sRAGE) Levels Are Associated With Unhealthy Lifestyle and Nonalcoholic Fatty Liver Disease. Clinical and translational gastroenterology 17 31082855
2014 Advanced glycation end products (AGEs) and the soluble receptor for AGE (sRAGE) in patients with type 1 diabetes and coeliac disease. Nutrition, metabolism, and cardiovascular diseases : NMCD 17 25467215
2011 sRAGE in diabetic and non-diabetic critically ill patients: effects of intensive insulin therapy. Critical care (London, England) 17 21871056
2018 AGER promotes proliferation and migration in cervical cancer. Bioscience reports 16 29298878
2013 Association of four genetic polymorphisms of AGER and its circulating forms with coronary artery disease: a meta-analysis. PloS one 16 23894685
2022 Association of soluble receptor for advanced glycation end-products (sRAGE) serum on COVID-19 severity: A cross-sectional study. Annals of medicine and surgery (2012) 15 35127073
2020 Study of sRAGE, HMGB1, AGE, and S100A8/A9 Concentrations in Plasma and in Serum-Extracted Extracellular Vesicles of Pregnant Women With Preterm Premature Rupture of Membranes. Frontiers in physiology 15 32655405
2020 Soluble Receptor for Advanced Glycation End-products (sRAGE) and Colorectal Cancer Risk: A Case-Control Study Nested within a European Prospective Cohort. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology 15 33082206
2015 Dynamic changes in sRAGE levels and relationship with cardiac function in STEMI patients. Clinical biochemistry 15 25562186
2023 The Potential Influence of Advanced Glycation End Products and (s)RAGE in Rheumatic Diseases. International journal of molecular sciences 14 36769213
2022 Carbocysteine Modifies Circulating miR-21, IL-8, sRAGE, and fAGEs Levels in Mild Acute Exacerbated COPD Patients: A Pilot Study. Pharmaceuticals (Basel, Switzerland) 14 35215330
2019 Evaluation of the AGE/sRAGE Axis in Patients with Multiple Myeloma. Antioxidants (Basel, Switzerland) 14 30836666
2017 S100A8/A9 and sRAGE kinetic after polytrauma; an explorative observational study. Scandinavian journal of trauma, resuscitation and emergency medicine 14 29178941
2015 AGER genetic polymorphisms increase risks of breast and lung cancers. Genetics and molecular research : GMR 14 26782423
2014 Serum sRAGE as a potential biomarker for pediatric bronchiolitis: a pilot study. Lung 14 25355250
2021 An Integrative Genomic Strategy Identifies sRAGE as a Causal and Protective Biomarker of Lung Function. Chest 13 34237330
2020 Elevated plasma sRAGE and IGFBP7 in heart failure decrease after heart transplantation in association with haemodynamics. ESC heart failure 12 32548968
2016 Genetically lowered concentrations of circulating sRAGE might cause an increased risk of cancer: Meta-analysis using Mendelian randomization. The Journal of international medical research 12 26857858

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