Affinage

AGER

Advanced glycosylation end product-specific receptor · UniProt Q15109

Round 2 corrected
Length
404 aa
Mass
42.8 kDa
Annotated
2026-04-28
130 papers in source corpus 33 papers cited in narrative 33 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

AGER (RAGE) is a multiligand pattern-recognition receptor of the immunoglobulin superfamily that transduces danger signals from advanced glycation end products (AGEs), HMGB1, S100/calgranulins, amyloid-β, complement C1q, decorin, and extracellular RNA into NF-κB, MAPK, Rac1/Cdc42, and CaMKII signaling cascades, thereby orchestrating inflammatory, neurodegenerative, and metabolic responses (PMID:1378843, PMID:8751438, PMID:10399917, PMID:22386596, PMID:27798148, PMID:34964698). Ligand engagement at the extracellular V-type Ig domain requires an intact 43-residue cytoplasmic tail, which bifurcates signaling: Ras-dependent NF-κB activation versus Rac1/Cdc42-dependent cytoskeletal remodeling and neurite outgrowth; additionally, RAGE undergoes ligand-independent transactivation through preformed heterocomplexes with AT1R and β1AR (PMID:10391939, PMID:30530993, PMID:26966719). Soluble decoy isoforms arise by ADAM10-mediated ectodomain shedding (cRAGE) or alternative splicing (esRAGE) and competitively antagonize RAGE signaling, while RAGE dimerization—stabilized by transmembrane cysteines C259/C301—is required for full signaling activity (PMID:18603587, PMID:12495433, PMID:28108276). Intracellularly, RAGE engages DIAPH1 to activate RAC1-dependent macropinocytosis, conferring amino acid scavenging and therapy resistance in pancreatic cancer (PMID:39879317).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 1992 High

    Establishing that a novel immunoglobulin-superfamily receptor specifically binds AGEs answered the fundamental question of how cells sense glycation damage, founding the RAGE field.

    Evidence cDNA cloning from bovine lung, recombinant expression in HEK293 cells with radioligand binding (Kd ~100 nM) and antibody blockade

    PMID:1378843

    Open questions at the time
    • No downstream signaling pathway yet identified
    • Endogenous ligand specificity beyond AGE-albumin unknown
    • Physiological relevance in vivo not demonstrated
  2. 1996 High

    Identification of amyloid-β as a second RAGE ligand on neurons and microglia recast RAGE from a metabolic receptor to a broader pattern-recognition receptor implicated in neurodegeneration.

    Evidence Direct RAGE–Aβ binding assays, antibody blockade, cell-based neurotoxicity assays, immunohistochemistry in Alzheimer's disease brain

    PMID:8751438

    Open questions at the time
    • Structural basis of Aβ–RAGE interaction undefined
    • In vivo causality in AD not yet tested with genetic tools
  3. 1997 High

    Discovery of NF-κB-responsive elements in the RAGE promoter established a positive-feedback transcriptional loop whereby RAGE-driven NF-κB amplifies RAGE expression itself.

    Evidence Deletion-reporter constructs, DNase I footprinting, EMSA, and site-directed mutagenesis in vascular cells

    PMID:9195959

    Open questions at the time
    • Whether other transcription factors cooperate at the RAGE promoter remained unknown
    • Epigenetic regulation not addressed
  4. 1998 High

    Demonstration that soluble RAGE (sRAGE) administration suppressed diabetic atherosclerosis independent of glycemia proved in vivo causal relevance and introduced the decoy-receptor therapeutic concept.

    Evidence Pharmacological sRAGE in streptozotocin-diabetic ApoE-KO mice with lesion quantification

    PMID:9734395

    Open questions at the time
    • sRAGE source (shedding vs. splice variant) not yet distinguished
    • Whether sRAGE blocks all RAGE ligands equally was untested
  5. 1999 High

    S100/calgranulin family members were identified as proinflammatory RAGE ligands, and the cytoplasmic domain was shown to bifurcate signaling into Ras→NF-κB versus Rac1/Cdc42→cytoskeletal remodeling branches, defining RAGE as a multi-pathway signaling hub.

    Evidence Receptor binding assays, in vivo DTH/colitis blockade models, dominant-negative GTPase epistasis with domain-deletion mutants in neuroblastoma cells

    PMID:10391939 PMID:10399917 PMID:10531386

    Open questions at the time
    • Direct cytoplasmic interactors mediating Ras or Rac activation unknown
    • Whether CML is the sole AGE species relevant in vivo undetermined
  6. 2003 High

    Parallel discoveries that RAGE mediates Aβ transcytosis across the blood–brain barrier and that alternative splicing produces secreted esRAGE as an endogenous decoy defined two critical functional dimensions: RAGE as a transporter of pathogenic cargo and endogenous soluble isoforms as built-in negative regulators.

    Evidence In vivo BBB transport assays in APPsw mice with RAGE blockade; RT-PCR cloning of splice variants with ERK/VEGF pathway assays in COS-7 and endothelial cells

    PMID:12495433 PMID:12808450

    Open questions at the time
    • Structural difference between esRAGE and later-discovered cRAGE unresolved
    • Quantitative contribution of each sRAGE species in vivo unknown
  7. 2005 High

    Establishing that HMGB1–RAGE signaling in dendritic cells drives maturation and T cell polarization positioned RAGE as a key innate-to-adaptive immune bridge.

    Evidence RAGE−/− DCs, neutralizing antibodies, DC maturation markers by FACS, IL-12 production, T cell proliferation assays

    PMID:15944249

    Open questions at the time
    • Whether RAGE cooperates with TLR4 for HMGB1 sensing on DCs not fully resolved
    • Relevance to human DC biology not confirmed
  8. 2007 High

    Crystallographic and biophysical analysis of multimeric S100B–RAGE V-domain interaction revealed that RAGE activation involves receptor oligomerization driven by multivalent ligand assemblies.

    Evidence 1.9 Å X-ray crystal structure of S100B, SPR, analytical ultracentrifugation showing tetrameric S100B binds two RAGE molecules

    PMID:17660747

    Open questions at the time
    • Full-length RAGE oligomeric structure unresolved
    • Whether all RAGE ligands promote similar receptor clustering untested
  9. 2008 High

    Three convergent advances resolved RAGE's injury-sensing role and its regulation: HMGB1–RAGE on macrophages mediates post-ischemic neuroinflammation (with cell-type specificity via bone marrow chimeras), ADAM10 was identified as the sheddase generating circulating cRAGE, and RAGE/Rac1/Cdc42 drives neuronal differentiation.

    Evidence MCAO ischemia model with bone marrow chimeras; ADAM10-KO MEFs and protease inhibitor screening; RNAi in P19 cells and primary neurons with constitutively active Rac1/Cdc42 rescue

    PMID:18058943 PMID:18603587 PMID:19005067

    Open questions at the time
    • Whether ADAM10 shedding is regulated by all RAGE ligands not tested
    • Downstream adaptor linking RAGE cytoplasmic tail to Rac1 still unidentified
  10. 2012 High

    Identification of C1q as a RAGE ligand (forming a ternary complex with Mac-1) and development of the V-domain inhibitor FPS-ZM1 provided a new innate immune axis and a pharmacological proof-of-concept tool.

    Evidence SPR binding (Kd ~5.6 µM), pull-down of RAGE–Mac-1 complex; FPS-ZM1 multi-readout analysis in aged APPsw mice

    PMID:22386596 PMID:22406537

    Open questions at the time
    • Structural basis of RAGE–Mac-1 cooperation unknown
    • FPS-ZM1 selectivity profile across all RAGE ligands incomplete
  11. 2015 High

    Discovery that AT1R transactivates RAGE independently of RAGE ligands via a preformed receptor heterocomplex revealed a ligand-independent mode of RAGE signaling that selectively drives NF-κB inflammation downstream of Ang II.

    Evidence Co-IP of AT1R–RAGE complex, RAGE-KO and ectodomain-deletion mouse models, rescue with WT vs. S391A mutant RAGE peptide in Ager/ApoE-KO atherosclerosis model

    PMID:30530993

    Open questions at the time
    • Whether other GPCRs transactivate RAGE untested beyond β1AR
    • Structural interface of AT1R–RAGE heterocomplex undefined
  12. 2016 High

    Three studies expanded RAGE's signaling repertoire: β1AR–RAGE heterocomplexes drive CaMKII-dependent cardiomyocyte death; RAGE acts as a co-receptor delivering RNA to endosomal TLR7/8/13; and RAGE feeds a hexosamine/O-GlcNAcylation/c-Jun positive feedback loop in HCC.

    Evidence Co-IP of β1AR–RAGE, double KO epistasis, CaMKII activity; RNA binding/uptake assays with RAGE KO/overexpression in TLR reporter systems; O-GlcNAc mass spectrometry and c-Jun S73 mutagenesis with AGER promoter reporter

    PMID:26825459 PMID:26966719 PMID:27798148

    Open questions at the time
    • Whether RAGE–nucleic acid sensing extends to dsDNA innate pathways beyond TLR9 not settled
    • Structural basis of β1AR–RAGE interaction undefined
  13. 2017 High

    Identification of C259 and C301 as dimerization-critical cysteines modified by H2S (S-sulfhydration) established the molecular basis for RAGE oligomeric assembly and introduced a redox-based regulatory mechanism controlling receptor surface stability.

    Evidence Split-GFP dimerization assay, C259S/C301S mutagenesis, tag-switch S-sulfhydration detection, cycloheximide chase for half-life

    PMID:28108276

    Open questions at the time
    • Whether endogenous H2S levels regulate RAGE dimerization in vivo unproven
    • Role of other cysteine residues untested
  14. 2021 High

    Decorin released from ferroptotic cells was identified as a novel RAGE ligand on macrophages, linking ferroptosis to NF-κB-dependent sterile inflammation; separately, HMGB1–RAGE was shown to activate STING1 during alkaliptosis.

    Evidence Co-IP of DCN–AGER, AGER KO macrophages, NF-κB reporter, acute pancreatitis model; FANCD2 genetic perturbation, AGER KO macrophages, STING1/TBK1/IRF3 pathway readout

    PMID:33992959 PMID:34964698

    Open questions at the time
    • Whether decorin–RAGE axis operates during physiological wound healing unknown
    • STING1 activation mechanism downstream of RAGE unclear
  15. 2025 High

    RAGE was shown to drive macropinocytosis via DIAPH1→RAC1 to scavenge amino acids for glutathione synthesis, conferring resistance to KRAS-G12D inhibitor MRTX1133 in pancreatic cancer—identifying the first direct cytoplasmic adaptor (DIAPH1) for RAGE.

    Evidence Co-IP of AGER–DIAPH1, RAC1 activity assay, fluorescent albumin uptake, GSH measurement, patient-derived xenografts, orthotopic and genetically engineered mouse PDAC models

    PMID:39879317

    Open questions at the time
    • Whether DIAPH1 is the universal cytoplasmic adaptor for all RAGE signaling arms is untested
    • Structural basis of AGER–DIAPH1 interaction unresolved
    • Whether RAGE-driven macropinocytosis occurs in non-cancer contexts unknown

Open questions

Synthesis pass · forward-looking unresolved questions
  • A full-length RAGE signaling complex structure—including the cytoplasmic tail bound to DIAPH1 and/or other adaptors—has not been solved; how a single 43-residue cytoplasmic tail activates at least four distinct downstream cascades (NF-κB, Rac1/Cdc42, CaMKII, STING1) remains the central unresolved question.
  • No atomic-resolution structure of full-length RAGE or RAGE–adaptor complex
  • Mechanism of pathway selectivity by a short cytoplasmic tail undefined
  • Relative physiological importance of >8 different ligands unranked

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060089 molecular transducer activity 7 GO:0038024 cargo receptor activity 2 GO:0140299 molecular sensor activity 2 GO:0098631 cell adhesion mediator activity 1
Localization
GO:0005886 plasma membrane 7 GO:0005576 extracellular region 3 GO:0005768 endosome 1
Pathway
R-HSA-162582 Signal Transduction 6 R-HSA-168256 Immune System 6 R-HSA-1643685 Disease 5 R-HSA-5357801 Programmed Cell Death 3 R-HSA-9612973 Autophagy 2
Partners
ADAM10ADRB1AGTR1CDC42DIAPH1HMGB1ITGAMRAC1
Complex memberships
AT1R–RAGE heterocomplexRAGE–DIAPH1 complexRAGE–Mac-1 (CD11b/CD18) complexβ1AR–RAGE heterocomplex

Evidence

Reading pass · 33 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1992 RAGE was cloned from a bovine lung cDNA library and identified as a ~35-kDa cell-surface receptor for advanced glycation end products (AGEs). The protein is a member of the immunoglobulin superfamily with an extracellular domain of 332 aa, a single transmembrane domain of 19 aa, and a 43-aa cytoplasmic tail. Expression of RAGE cDNA in HEK293 cells conferred saturable, antibody-blockable binding of 125I-AGE-albumin (Kd ~100 nM), establishing RAGE as a functional AGE receptor. cDNA cloning, recombinant expression in HEK293 cells, radioligand binding assay, Western blot The Journal of Biological Chemistry High 1378843
1996 RAGE was identified as a neuronal cell-surface receptor for amyloid-β (Aβ) peptide. RAGE expression was found elevated in Alzheimer's disease brain. RAGE–Aβ interaction on neurons and microglia mediated Aβ-induced oxidant stress and neurotoxicity, establishing a direct mechanistic link between RAGE ligation and neurodegeneration. Binding assays with recombinant RAGE and Aβ peptide, cell-based neurotoxicity assays, immunohistochemistry of AD brain, antibody blockade experiments Nature High 8751438
1997 The RAGE gene promoter contains functional NF-κB binding sites. Deletion analysis and DNase I footprinting/EMSA identified two active NF-κB-like sites (sites 1 and 2) in the −1543/−587 region that drive basal and LPS-stimulated RAGE expression in endothelial and smooth muscle cells. Simultaneous mutation of both sites markedly reduced promoter activity, establishing NF-κB-dependent transcriptional autoregulation of RAGE. 5′-deletion luciferase reporter constructs, DNase I footprinting, electrophoretic mobility shift assay (EMSA), transient transfection in vascular endothelial and smooth muscle cells The Journal of Biological Chemistry High 9195959
1998 Administration of the soluble extracellular domain of RAGE (sRAGE) completely suppressed accelerated atherosclerosis in diabetic apolipoprotein E-deficient mice in a glycemia- and lipid-independent manner, demonstrating that AGE–RAGE interaction is causally required for diabetic macrovascular disease and that sRAGE acts as a decoy receptor to block this pathway. In vivo mouse model (streptozotocin-diabetic ApoE-KO mice), pharmacological sRAGE administration, atherosclerotic lesion quantification Nature Medicine High 9734395
1999 RAGE was identified as a central cell-surface receptor for S100/calgranulin polypeptides (EN-RAGE and related family members). Engagement of S100/calgranulins by RAGE on endothelium, mononuclear phagocytes, and lymphocytes triggered cellular activation and generation of proinflammatory mediators. Blockade of EN-RAGE/RAGE signaling suppressed delayed-type hypersensitivity and inflammatory colitis in murine models, defining a novel RAGE-dependent proinflammatory axis. Receptor binding assays, cell activation assays, in vivo murine models (DTH, colitis) with antibody blockade and soluble RAGE Cell High 10399917
1999 RAGE-mediated neurite outgrowth (induced by amphoterin/HMGB1) and NF-κB activation use distinct intracellular signaling pathways both requiring the RAGE cytoplasmic domain. Neurite outgrowth is blocked by dominant-negative Rac and Cdc42 (but not Ras), whereas NF-κB activation is blocked by dominant-negative Ras (but not Rac/Cdc42). Deletion of the cytoplasmic domain of RAGE abolished both responses. Transfection of RAGE constructs (full-length and cytoplasmic domain deletion mutants) into neuroblastoma cells, dominant-negative GTPase overexpression, NF-κB reporter assays, neurite outgrowth assays on amphoterin-coated substrates The Journal of Biological Chemistry High 10391939
1999 CML (Nε-carboxymethyllysine) adducts of proteins are direct RAGE ligands. CML-modified proteins engage cellular RAGE and activate NF-κB signaling and downstream gene expression in vascular cells, identifying a specific AGE molecular species responsible for RAGE-mediated vascular and inflammatory complications. Cell-based RAGE binding assays with CML-modified proteins, NF-κB activation assays, gene expression analysis The Journal of Biological Chemistry High 10531386
2000 S100B and S100A1 activate RAGE in concert with amphoterin to induce neurite outgrowth and NF-κB activation. Nanomolar S100B promotes RAGE-dependent cell survival via upregulation of anti-apoptotic Bcl-2, whereas micromolar S100B induces RAGE-dependent apoptosis. Both trophic and toxic effects require full-length RAGE with an intact cytoplasmic domain. Transfection of full-length vs. cytoplasmic domain deletion RAGE mutants, cell survival/apoptosis assays, Bcl-2 immunoblotting, neurite outgrowth assays, NF-κB reporter assays The Journal of Biological Chemistry High 11007787
2002 RAGE is expressed on human peritoneal mesothelial cells (HPMC). AGE binding to RAGE (specifically CML-albumin) stimulates VCAM-1 (but not ICAM-1) overexpression and enhances leukocyte adhesion. Both anti-RAGE antibody and recombinant RAGE (acting as decoy) blocked the CML-albumin-induced VCAM-1 upregulation, establishing a direct AGE–RAGE–VCAM-1 signaling axis in mesothelial inflammation. FACS detection of RAGE on HPMC, RT-PCR, radiometric VCAM-1/ICAM-1 expression assay, antibody and decoy receptor blockade, videomicroscopy of leukocyte adhesion Kidney International Medium 11786095
2002 The G82S polymorphism in the RAGE ligand-binding domain amplifies the inflammatory response. Cells bearing the RAGE 82S allele displayed enhanced binding of S100/calgranulins and greater cytokine/MMP generation compared to 82G allele cells. In vivo, blockade of RAGE suppressed clinical and histologic arthritis and reduced TNF-α, IL-6, and MMPs 3, 9, and 13 in affected tissues in a collagen-induced arthritis model. Cell-based binding assays with allelic RAGE variants, cytokine/MMP production assays, in vivo murine collagen-induced arthritis model with RAGE blockade, human case-control genetic association Genes and Immunity High 12070776
2003 RAGE expressed on brain endothelial cells mediates transcytosis of circulating Aβ peptides across the blood-brain barrier (BBB) into brain parenchyma and drives expression of proinflammatory cytokines and endothelin-1 (causing vasoconstriction). Inhibition of RAGE–ligand interaction at the BBB suppressed Aβ accumulation in brain parenchyma in APPsw transgenic mice. Systemic Aβ infusion in mice, transgenic mouse models, pharmacological RAGE blockade, BBB transport assays, cerebral blood flow measurements, ET-1 and cytokine quantification Nature Medicine High 12808450
2003 Novel splice variants of RAGE lacking either the N-terminal V-type Ig domain (N-truncated, membrane-bound) or the C-terminal transmembrane domain (C-truncated/endogenous secretory RAGE, esRAGE) are expressed in vascular endothelial cells and pericytes. The C-truncated (esRAGE) isoform is secreted, binds AGEs via its intact V-domain, and completely abolished AGE-induced ERK phosphorylation and VEGF induction, identifying esRAGE as an endogenous cytoprotective decoy receptor. N-truncated RAGE lacks ligand-binding capacity. RT-PCR cloning of splice variants, COS-7 transfection, AGE-affinity column binding, secretion assays, ERK phosphorylation assays, VEGF quantification, endothelial cord formation assay The Biochemical Journal High 12495433
2005 Dendritic cells (DCs) actively release HMGB1 upon activation, and this secreted HMGB1 signals through RAGE on DCs to drive their maturation (CD80/CD83/CD86 upregulation, IL-12 production) and to sustain T cell clonal expansion, survival, and polarization. Using RAGE−/− cells and neutralizing antibodies, RAGE was demonstrated to be required for the HMGB1 effect on DCs, acting through downstream MAPK and NF-κB activation. RAGE−/− cells, neutralizing antibodies to RAGE and HMGB1, DC maturation marker FACS, IL-12 ELISA, T cell proliferation and polarization assays, MAPK/NF-κB signaling assays Journal of Immunology High 15944249
2007 The X-ray crystal structure of Ca2+-loaded S100B at 1.9 Å resolution revealed an octameric architecture (four homodimers arranged as two tetramers). Tetrameric S100B binds RAGE with higher affinity than dimeric S100B and, by AUC, binds two RAGE molecules via the V-domain. Tetrameric S100B caused stronger cell growth activation and survival than the dimer, suggesting RAGE activation involves receptor dimerization/oligomerization driven by multimeric S100B. X-ray crystallography (1.9 Å), size-exclusion chromatography of brain extracts, purification of S100B oligomers from E. coli, surface plasmon resonance binding studies, analytical ultracentrifugation, cell growth/survival assays The EMBO Journal High 17660747
2008 RAGE functions as a sensor of necrotic cell death in ischemic brain injury. HMGB1 released from ischemic tissue engages RAGE on (micro)glial cells to mediate neurotoxicity. RAGE deficiency or soluble RAGE reduced infarct size. Chimeric mouse experiments transplanting RAGE−/− bone marrow into wild-type recipients showed that RAGE deficiency specifically in bone marrow-derived macrophages significantly reduced infarct size, positioning macrophage RAGE as a critical effector of HMGB1-mediated post-ischemic inflammation. Mouse cerebral ischemia model (MCAO), RAGE−/− mice, soluble RAGE administration, anti-HMGB1 antibody, HMGB1 box A antagonist, bone marrow chimera experiments, infarct volume quantification, in vitro (micro)glial neurotoxicity assay The Journal of Neuroscience High 19005067
2008 Most circulating soluble RAGE in human blood is produced by proteolytic ectodomain shedding (cleaved RAGE, cRAGE) rather than by the alternative splice variant esRAGE. Screening of chemical inhibitors and genetically modified MEFs identified ADAM10 as the responsible sheddase. HMGB1 ligand binding promotes RAGE shedding by ADAM10, and cRAGE acts as a decoy receptor. Anti-esRAGE vs. pan-sRAGE antibody comparison, transfection of full-length RAGE cDNA, ADAM10-deficient MEFs, chemical protease inhibitor panel, HMGB1 stimulation shedding assay FASEB Journal High 18603587
2008 RAGE mediates neuronal differentiation and neurite outgrowth in P19 embryonic carcinoma stem cells. RAGE knockdown by RNAi blocked retinoic acid-induced neuronal differentiation, inhibited NF-κB nuclear translocation, and strongly suppressed neurite outgrowth. In primary cerebellar granule neurons, RAGE KD inhibited neurite outgrowth through the Rac1/Cdc42 GTPase pathway; constitutively active Rac1/Cdc42 rescued neurite outgrowth in RAGE-deficient neurons. RNAi knockdown in P19 cells and primary cerebellar granule neurons, NF-κB nuclear translocation assay, dominant-negative and constitutively active Rac1/Cdc42 overexpression, neurite outgrowth quantification Journal of Neuroscience Research High 18058943
2011 RAGE is a positive regulator of autophagy and a negative regulator of apoptosis during oxidative stress in pancreatic cancer cells. RAGE upregulation via NF-κB decreases ROS-induced oxidative injury; suppression of RAGE increases sensitivity to oxidative stress-induced cell death, positioning RAGE as a switch between autophagy-mediated survival and apoptosis. RAGE knockdown and overexpression in pancreatic cancer cells, ROS measurement, autophagy flux assay, apoptosis assays (flow cytometry), NF-κB reporter assay Autophagy Medium 21317562
2012 RAGE is a native receptor for the globular domain of complement component C1q. Direct C1q–RAGE interaction was demonstrated by surface plasmon resonance (Kd ~5.6 µM) and ELISA-like multivalent binding assay. Pull-down experiments indicated RAGE forms a complex with Mac-1 (CD11b/CD18) to enhance C1q binding affinity. Antibodies to RAGE or Mac-1 inhibited C1q-induced U937 cell adhesion and phagocytosis. Surface plasmon resonance, ELISA-based binding assay, pull-down (RAGE–Mac-1 complex), cell adhesion assay, phagocytosis assay with antibody blockade Cellular Immunology High 22386596
2012 FPS-ZM1, a high-affinity small-molecule RAGE inhibitor targeting the V-domain, blocked Aβ binding to RAGE, inhibited RAGE-mediated Aβ transcytosis across the BBB into brain, suppressed β-secretase activity and Aβ production in brain, reduced microglial neuroinflammation, and normalized cognitive performance and cerebral blood flow in aged APPsw transgenic mice. In vitro RAGE–Aβ binding assay, RAGE-expressing cell stress assays, in vivo aged APPsw/0 transgenic mice, BBB transport assay, β-secretase activity assay, Aβ ELISA, Morris water maze, cerebral blood flow measurement The Journal of Clinical Investigation High 22406537
2015 RAGE undergoes ligand-independent transactivation by the type 1 angiotensin II receptor (AT1R). AT1R and RAGE form a preformed heteromeric complex at the cell surface. Ang II stimulation of AT1R triggers transactivation of the RAGE cytosolic tail, driving NF-κB-dependent proinflammatory gene expression independently of RAGE ligand binding or the RAGE ectodomain. Deletion or inhibition of RAGE selectively attenuated AT1R-driven proinflammatory signaling without affecting canonical Gq signaling. A mutant RAGE peptide (S391A-RAGE362-404) inhibited transactivation and attenuated Ang II-dependent inflammation and atherogenesis in vivo. Co-immunoprecipitation of AT1R–RAGE complex, RAGE-KO and ectodomain-deletion mouse models, NF-κB reporter assay, Ager/Apoe-KO mouse atherosclerosis model, rescue with WT vs. mutant RAGE peptide, atherosclerotic lesion quantification The Journal of Clinical Investigation High 30530993
2016 RAGE and the β1-adrenergic receptor (β1AR) physically interact to form a receptor complex that activates CaMKII, causing cardiomyocyte death and maladaptive remodeling. RAGE deficiency or inhibition blocks β1AR-mediated myocardial injury; β1AR ablation abolishes RAGE-induced detrimental effects. The convergence point of both receptors is CaMKII activation. Co-immunoprecipitation of β1AR–RAGE complex, RAGE-KO and β1AR-KO mice, cardiomyocyte death assays, CaMKII activity assay, cardiac remodeling histology, pharmacological RAGE and β1AR inhibitors JCI Insight High 26966719
2016 RAGE binds RNA molecules in a sequence-independent manner and facilitates RNA uptake into endosomes, enhancing ssRNA sensing by TLR7, TLR8, and TLR13. Gain- and loss-of-function studies established RAGE as an integral co-receptor of the endosomal nucleic acid-sensing system, extending its previously described role for DNA/TLR9 to all ssRNA-sensing TLRs. RNA–RAGE binding assays, cellular RNA uptake assays (fluorescent RNA), gain-of-function (RAGE overexpression) and loss-of-function (RAGE KO) in TLR reporter systems, TLR7/8/13 activation assays Journal of Immunology High 27798148
2016 AGER activates a hexosamine biosynthetic pathway in hepatocellular carcinoma cells under high-glucose conditions, leading to enhanced O-GlcNAcylation of c-Jun at Ser73, which increases c-Jun activity and stability. c-Jun in turn transcriptionally upregulates AGER, establishing a positive autoregulatory feedback loop that drives diabetic HCC tumorigenesis. AGER knockdown/overexpression in HCC cells, O-GlcNAcylation mass spectrometry and western blot, site-directed mutagenesis of c-Jun Ser73, luciferase reporter for AGER promoter, co-immunoprecipitation Diabetes High 26825459
2017 RAGE deficiency (Ager KO) in diabetic mice restored adaptive inflammation after hindlimb ischemia, increased circulating Ly6Chi monocytes and macrophage infiltration into ischemic muscle, and rescued angiogenesis and blood flow recovery. In vitro, Ager deletion in macrophages reversed high-glucose-mediated skewing toward tissue-damage gene expression and restored macrophage–endothelial cell interactions, placing AGER as a suppressor of adaptive inflammation in diabetic peripheral vascular disease. Ager-KO and Glo1-transgenic diabetic mice, femoral artery ligation, laser Doppler blood flow, immunohistochemistry for angiogenesis markers and macrophage content, Ly6Chi monocyte FACS, macrophage-endothelial co-culture assays, gene expression profiling Arteriosclerosis, Thrombosis, and Vascular Biology High 28642238
2017 Hydrogen sulfide (H2S) reduces RAGE toxicity by inhibiting RAGE dimerization and impairing its membrane stability. H2S (via NaHS) attenuated Aβ1-42- and AGE-induced cell injury. NaHS reduced H2O2-enhanced RAGE dimerization (shown by split-GFP complementation and Western blot) and decreased membrane RAGE expression. S-sulfhydration assay identified C259/C301 as the residues directly modified by H2S; mutation of these sites (C259S/C310S double mutant) mimicked H2S effects and caused ER retention, reduced membrane expression, and shortened half-life of RAGE. Split-GFP complementation dimerization assay, Western blot, immunofluorescence, cycloheximide chase, ubiquitination assay, tag-switch S-sulfhydration assay, site-directed mutagenesis (C259S/C310S) Free Radical Biology & Medicine High 28108276
2018 RAGE modulates autophagy in hepatocellular carcinoma (HCC) cells to promote proliferation and sorafenib resistance. RAGE deficiency activated AMPK/mTOR signaling and induced autophagy, which improved sorafenib response. HMGB1 and S100A4 ligands positively upregulated RAGE expression, indicating a ligand-driven autocrine amplification loop in HCC. RAGE knockdown and overexpression in HCC cell lines, AMPK/mTOR pathway assays, autophagy flux assays, sorafenib cytotoxicity assays, HMGB1/S100A4 ligand stimulation experiments Cell Death & Disease Medium 29445087
2018 miR-5591-5p directly targets AGER mRNA (3′UTR), suppressing AGER expression. AGEs downregulate miR-5591-5p in adipose-derived stem cells (ADSCs), activating the AGE/AGER/JNK signaling axis to induce ROS generation and apoptosis. miR-5591-5p overexpression blocked this axis, promoted ADSC survival, and enhanced cutaneous wound repair in vivo. miRNA mimic/inhibitor transfection, luciferase 3′UTR reporter assay for AGER targeting, AGER siRNA, ROS assay, JNK phosphorylation assay, apoptosis flow cytometry, in vivo diabetic wound healing model Cell Death & Disease Medium 29752466
2021 Decorin (DCN), a proteoglycan released by ferroptotic cells via secretory autophagy and lysosomal exocytosis, binds to AGER on macrophages to trigger NF-κB-dependent pro-inflammatory cytokine production. Pharmacological and genetic inhibition of the DCN–AGER axis protected against ferroptotic death-related acute pancreatitis and limited tumor-protective immune responses to ferroptotic cancer cells. Cell death assays (ferroptosis induction), DCN release quantification, Co-IP of DCN–AGER interaction, AGER KO macrophages, NF-κB reporter, in vivo acute pancreatitis model, tumor immunization experiments Autophagy High 34964698
2021 During alkaliptosis (intracellular alkalization-driven cell death), HMGB1 is released from the nucleus to the extracellular space via a FANCD2-dependent (not ATM-mediated) DNA damage signaling pathway. Released HMGB1 binds AGER on macrophages and then activates the STING1 pathway to produce pro-inflammatory cytokines (TNF, IL-6). Inhibition of the HMGB1–AGER–STING1 pathway limits cytokine production during alkaliptosis. HMGB1 nuclear-to-cytoplasmic translocation assay, FANCD2/ATM genetic perturbation, AGER KO macrophages, STING1 pathway readout (IRF3/TBK1 phosphorylation), cytokine ELISA Biochemical and Biophysical Research Communications Medium 33992959
2021 YAP participates in a transcriptional network with KLF5, NFIB, and NKX2-1 to regulate AGER expression in alveolar epithelial cells. YAP activation increased AT1 cell numbers and enhanced DNA accessibility at AGER promoter regions; YAP deletion increased AT2 markers. Chromatin accessibility (ATAC-seq) and motif enrichment analysis identified the transcription factor network controlling AGER during alveolar differentiation. Transgenic YAP activation/deletion mouse models, ATAC-seq, transcription factor motif enrichment, RNA-seq, immunostaining for AT1/AT2 markers iScience Medium 34466790
2022 Cadmium (Cd) induces ferroptosis in pancreatic β-cells, and ferroptosis inhibitor Fer-1 antagonized Cd-induced AGER-mediated inflammation. Cd exposure decreased Gpx4 expression (enabling ferroptosis) and activated the AGER/PKC/p65 (NF-κB) inflammatory axis. The Gpx4/AGER/p65 pathway was identified as a novel mechanistic axis linking ferroptotic cell death to pancreatic inflammation and β-cell dysfunction. Transcriptomic analysis (RNA-seq) of Cd-treated MIN6 cells, GSH/lipid peroxidation assays, Gpx4 knockdown/inhibition, ferroptosis inhibitor (Fer-1), AGER expression analysis, PKC/NF-κB pathway assays, in vivo Cd-exposed mouse model The Science of the Total Environment Medium 35931150
2025 AGER mediates resistance to KRAS-G12D inhibitor MRTX1133 in pancreatic ductal adenocarcinoma by driving macropinocytosis. AGER interacts with DIAPH1 (diaphanous-related formin 1), which activates RAC1-dependent macropinosome formation, enabling internalization of serum albumin and generation of amino acids used for glutathione synthesis and apoptosis resistance. Combination of MRTX1133 with AGER–DIAPH1 complex inhibitor (RAGE299) or macropinocytosis inhibitor (EIPA) was effective in patient-derived xenografts, orthotopic, and genetically engineered mouse models. This combination also induced HMGB1 release and CD8+ T cell antitumor responses. AGER overexpression/knockdown in PDAC cells, Co-IP of AGER–DIAPH1 complex, RAC1 activity assay, macropinocytosis assay (fluorescent albumin uptake), glutathione measurement, patient-derived xenografts, orthotopic mouse models, genetically engineered mouse PDAC models, CD8+ T cell immune response assays Science Translational Medicine High 39879317

Source papers

Stage 0 corpus · 130 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1996 RAGE and amyloid-beta peptide neurotoxicity in Alzheimer's disease. Nature 1759 8751438
2019 Blood-Brain Barrier: From Physiology to Disease and Back. Physiological reviews 1645 30280653
1999 RAGE mediates a novel proinflammatory axis: a central cell surface receptor for S100/calgranulin polypeptides. Cell 1613 10399917
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