Affinage

PTGS2

Prostaglandin G/H synthase 2 · UniProt P35354

Round 2 corrected
Length
604 aa
Mass
69.0 kDa
Annotated
2026-04-28
130 papers in source corpus 35 papers cited in narrative 34 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

PTGS2 (COX-2) is an inducible bifunctional enzyme that catalyzes the committed step in prostanoid biosynthesis—converting arachidonic acid to PGH2 via sequential cyclooxygenase and peroxidase activities—and resides on the lumenal face of the endoplasmic reticulum and nuclear envelope (PMID:1380156, PMID:7947975, PMID:9545330). Transcriptional induction is driven by NF-κB, HIF1α, LRH-1, SMAD2/3, and CTCF/cohesin-dependent chromatin looping, while ATF3 acts as a transcriptional repressor; post-transcriptionally, miR-16 promotes ARE-mediated mRNA decay and AMPK stabilizes PTGS2 mRNA (PMID:25619459, PMID:25703332, PMID:15766526, PMID:31581537). Enzymatic output is amplified by iNOS-mediated S-nitrosylation and FYN-dependent Tyr446 phosphorylation, and aspirin acetylation redirects oxygenase stereospecificity to generate pro-resolution resolvin precursors from DHA (PMID:16373578, PMID:24970799, PMID:12391014). The PGE2 produced by PTGS2 drives diverse tissue-specific programs including intestinal epithelial repair downstream of TLR4, senescence surveillance via autocrine EP4 signaling, monocyte-to-MDSC differentiation, brown adipocyte recruitment in white fat, macrophage efferocytosis, and tumor immune evasion downstream of EPHA2-TGFβ (PMID:16952555, PMID:33730589, PMID:21972293, PMID:20448152, PMID:35017061, PMID:31162144).

Mechanistic history

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

    Cloning of human PTGS2 from endothelial cells and demonstration of cyclooxygenase activity in heterologous cells established it as a second, inducible prostaglandin H synthase isoform distinct from COX-1, answering whether a separate inducible cyclooxygenase gene exists in humans.

    Evidence Molecular cloning from HUVECs with functional expression in COS-7 cells; independently replicated with chromosomal mapping to 1q25

    PMID:1380156 PMID:8473346

    Open questions at the time
    • Crystal structure of human COX-2 not yet solved at this time
    • Substrate specificity differences versus COX-1 not yet characterized
    • In vivo physiological roles undefined
  2. 1994 High

    Determination of the PTGS2 gene structure revealed ARE-rich 3'-UTR elements and NF-κB/CRE promoter sites, explaining how COX-2 is both transcriptionally induced and post-transcriptionally labile; concurrent biochemical characterization of recombinant enzyme confirmed dual cyclooxygenase and peroxidase activities with self-inactivation kinetics.

    Evidence Genomic sequencing with FISH mapping; baculovirus-expressed purified enzyme with kinetic analysis

    PMID:7945196 PMID:7947975 PMID:8181472

    Open questions at the time
    • Identity of trans-acting factors for ARE-mediated decay unknown
    • Structural basis for NSAID selectivity not resolved
    • Post-translational regulatory mechanisms uncharacterized
  3. 1998 High

    Immunoelectron microscopy resolved the long-standing question of whether COX-1 and COX-2 occupy distinct compartments: both localize to the ER and nuclear envelope lumen, indicating their functional independence arises from differential expression rather than compartmentalization.

    Evidence Immunogold EM across monocytes, NIH 3T3, and HUVECs with subcellular fractionation and isozyme-selective inhibitor controls

    PMID:9545330

    Open questions at the time
    • Mechanism of preferential coupling to specific downstream synthases despite shared localization unclear
    • Whether nuclear envelope localization has distinct functional consequences unknown
  4. 1998 High

    Demonstration that COX-2-overexpressing tumor cells stimulate angiogenesis through prostaglandin production established COX-2 as a pro-tumorigenic enzyme, shifting the field beyond inflammation to cancer biology.

    Evidence Coculture angiogenesis assays with COX-2 overexpression and NS-398 inhibition in colon carcinoma and endothelial cells

    PMID:9630216

    Open questions at the time
    • Specific prostaglandin species mediating angiogenesis not fully defined
    • In vivo relevance to spontaneous tumor angiogenesis not yet shown
  5. 2002 High

    Discovery that aspirin-acetylated COX-2 retains oxygenase activity but with altered stereospecificity to produce 17R-HDHA (resolvin precursor) from DHA revealed an unexpected gain-of-function mechanism, redefining aspirin's anti-inflammatory action beyond simple enzyme inhibition.

    Evidence LC-MS lipidomic analysis of aspirin-treated recombinant COX-2 with cell-based validation in microglia and endothelial cells

    PMID:12391014

    Open questions at the time
    • Quantitative contribution of aspirin-triggered resolvins to clinical anti-inflammatory effects not established
    • Whether other COX-2 covalent modifications similarly redirect stereospecificity unknown
  6. 2005 High

    Two post-transcriptional and post-translational control layers were defined: miR-16 cooperates with tristetraprolin to degrade COX-2 mRNA via its ARE, and iNOS physically binds and S-nitrosylates COX-2 to enhance its catalytic activity, establishing that COX-2 output is regulated beyond transcription.

    Evidence miR-16 RNAi screen in Drosophila S2 validated in HeLa; iNOS–COX-2 Co-IP with S-nitrosylation assay and interaction disruption

    PMID:15766526 PMID:16373578

    Open questions at the time
    • S-nitrosylation site(s) on COX-2 not mapped
    • Whether miR-16 and S-nitrosylation operate simultaneously in the same cell types unclear
  7. 2006 High

    Genetic studies in TLR4-deficient mice placed PTGS2-derived PGE2 downstream of TLR4-MyD88 in intestinal epithelial repair, explaining how innate immune sensing drives mucosal homeostasis through prostanoid production.

    Evidence TLR4−/− mice with DSS colitis, MyD88 siRNA, BrdU/TUNEL assays, PGE2 rescue

    PMID:16952555

    Open questions at the time
    • EP receptor subtype mediating intestinal repair downstream of TLR4 not fully defined
    • Whether epithelial or stromal COX-2 is the principal source not resolved
  8. 2010 High

    COX-2 was identified as an effector of β-adrenergic signaling that drives brown adipocyte recruitment in white fat depots, and separately as a mechanoresponsive gene whose suppression by matrix stiffening removes the PGE2/EP2 brake on fibroblast activation, broadening COX-2 biology to metabolism and fibrosis.

    Evidence WAT-specific Cox-2 transgenic and knockout mice with metabolic phenotyping; tunable-stiffness polyacrylamide gels with PGE2/EP2 rescue in fibroblasts

    PMID:20448152 PMID:20733059

    Open questions at the time
    • Identity of the prostaglandin species mediating brown fat induction not fully resolved
    • In vivo relevance of matrix-stiffness–COX-2 axis in human fibrotic disease not confirmed
  9. 2011 High

    A COX-2/PGE2 autocrine feedback loop was shown to redirect monocyte differentiation toward immunosuppressive MDSCs via EP2/EP4, providing a mechanistic link between tumor-derived COX-2 activity and immune evasion.

    Evidence Monocyte differentiation assays with COX-2 inhibitors and EP2/EP4 antagonists; validated in ovarian cancer patient specimens

    PMID:21972293

    Open questions at the time
    • Whether this loop operates in all tumor types or is context-specific unclear
    • Downstream transcriptional program in MDSCs not fully mapped
  10. 2014 High

    FYN-mediated phosphorylation of COX-2 at Tyr446 was identified as a post-translational activating modification, establishing that kinase signaling directly modulates COX-2 enzymatic output independent of expression changes.

    Evidence Co-IP, in vitro kinase assay, phospho-mimetic and blocking mutants in prostate cancer cells

    PMID:24970799

    Open questions at the time
    • Whether Tyr446 phosphorylation occurs in non-cancer contexts unknown
    • Phosphatase(s) that reverse this modification not identified
  11. 2015 High

    Epigenetic and transcriptional silencing mechanisms were defined: DNA methylation at the PTGS2 CpG island disrupts CTCF/cohesin-mediated chromatin looping, while ATF3 directly represses the Ptgs2 promoter during inflammation resolution, establishing how PTGS2 is turned off.

    Evidence ChIP, 3C chromatin conformation capture, bisulfite sequencing, demethylation; Atf3−/− mice with peritonitis model and ChIP

    PMID:25619459 PMID:25703332

    Open questions at the time
    • Whether CTCF/cohesin and ATF3 mechanisms operate sequentially or independently unresolved
    • Writers responsible for PTGS2 CpG island methylation not identified
  12. 2019 High

    EPHA2-TGFβ signaling was placed upstream of PTGS2 in pancreatic cancer immune evasion, and AMPK-dependent mRNA stabilization was identified as a metabolic stress–responsive post-transcriptional mechanism, further expanding the repertoire of PTGS2 induction pathways.

    Evidence Epha2−/− and Ptgs2−/− mouse tumor models with immunotherapy; AMPK siRNA and activators with mRNA stability assays in astrocytes

    PMID:31162144 PMID:31581537

    Open questions at the time
    • AMPK-dependent stabilization mechanism (RNA-binding protein intermediary) not identified
    • Whether EPHA2-PTGS2 axis is specific to pancreatic cancer or generalizable unclear
  13. 2021 High

    COX-2 was shown to be essential for macrophage efferocytosis and subsequent pro-resolution reprogramming, and for shaping SASP composition during senescence surveillance via PGE2/EP4 autocrine signaling, revealing COX-2 as a gatekeeper of immune resolution programs.

    Evidence Macrophage-specific Cox2 KO with efferocytosis assays and LC-MS/MS lipidomics; RAS-induced senescence with Cox2 deletion and in vivo hepatocyte surveillance model

    PMID:33730589 PMID:35017061

    Open questions at the time
    • Molecular mechanism by which COX-2 loss impairs apoptotic cell binding not defined
    • Whether senescence surveillance role extends beyond hepatocytes unknown
  14. 2022 Medium

    Multiple transcriptional activators of PTGS2 were further defined: CTCF/PACERR/p300 complex in tumor-associated macrophages, DCLK1-phosphorylated Ku80 in colorectal cancer, HIF1α direct promoter binding in cardiac ischemia, and LRH-1 in beta cells, revealing tissue-specific transcriptional wiring converging on PTGS2.

    Evidence ChIP-seq, RNA pulldown, RIP for CTCF/PACERR; DCLK1 kinase assay with Co-IP; HIF1α ChIP in rat CME model; conditional beta-cell LRH-1 KO with EP receptor pharmacology

    PMID:35184402 PMID:35602948 PMID:35910805 PMID:36569299

    Open questions at the time
    • Whether PACERR lncRNA is required or modulatory for PTGS2 induction needs independent replication
    • DCLK1-Ku80-COX-2 axis demonstrated in single lab
    • HIF1α-PTGS2-ferroptosis link requires human validation
  15. 2024 High

    An endothelial-specific suppressive pathway was delineated: ROBO4 recruits TRAF7 to ubiquitinate IQGAP1, preventing sustained RAC1 activation and thereby suppressing PTGS2 expression, with Robo4-deficient mice exhibiting exacerbated inflammatory disease.

    Evidence Co-IP of ROBO4-IQGAP1-TRAF7, ubiquitination assay, RAC1 activation assay, Robo4−/− mice with arthritis/edema/pain models

    PMID:38762541

    Open questions at the time
    • Whether ROBO4-TRAF7 axis operates in non-endothelial cell types unknown
    • Direct ligand triggering ROBO4 to suppress COX-2 not defined

Open questions

Synthesis pass · forward-looking unresolved questions
  • Unresolved questions include: the structural basis for how S-nitrosylation and Tyr446 phosphorylation individually and combinatorially alter COX-2 catalytic geometry; the mechanism by which COX-2 preferentially couples to mPGES-1 despite shared ER localization with COX-1; and whether COX-2's roles in efferocytosis, senescence surveillance, and brown fat recruitment depend on the same or distinct prostaglandin products.
  • No crystal structure of S-nitrosylated or Tyr446-phosphorylated COX-2
  • Prostaglandin species specificity for individual tissue-level functions not resolved
  • Mechanistic basis for preferential COX-2–mPGES-1 coupling still debated

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016491 oxidoreductase activity 4 GO:0009975 cyclase activity 2
Localization
GO:0005635 nuclear envelope 1 GO:0005783 endoplasmic reticulum 1
Pathway
R-HSA-162582 Signal Transduction 6 R-HSA-168256 Immune System 6 R-HSA-1430728 Metabolism 5 R-HSA-1643685 Disease 4
Partners
ATF3CTCFFYNIQGAP1NOS2TRAF7XRCC5

Evidence

Reading pass · 34 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1992 Human COX-2 (PTGS2) was cloned from umbilical vein endothelial cells; its cDNA encodes a 604-amino-acid polypeptide 61% identical to COX-1, and expression of the open reading frame in COS-7 cells confers cyclooxygenase activity, demonstrating it is a functional prostaglandin H synthase. COX-2 mRNA was preferentially induced by PMA and LPS in endothelial cells and monocytes. Molecular cloning, in vitro translation, heterologous expression in COS-7 cells with enzymatic activity assay Proceedings of the National Academy of Sciences of the United States of America High 1380156
1993 Human PHS II (PTGS2) was independently cloned from an endothelial cell cDNA library; the protein shares 61% identity with PHS I, maps to chromosome 1 (distinct from PHS I on chromosome 9), and its mRNA is induced by TNF, PMA, LPS, and IL-1 in endothelial cells, with induction correlating with increased prostacyclin biosynthesis. Cycloheximide induced mRNA without activity increase, confirming translation is required for functional enzyme. Molecular cloning, chromosomal mapping (Southern analysis), mRNA induction assays, prostacyclin biosynthesis measurement The Journal of biological chemistry High 8473346
1994 Structure of the human COX-2 gene (PTGS2) was determined: 10 exons spanning ~8.3 kb, mapped to chromosome 1q25.2-q25.3 (distinct from PTGS1 at 9q32-q33.3). The 5'-flanking region contains a TATA box and regulatory elements including NF-κB, CRE, AP-2, SP1, and Ets-1 sites. The large 3'-UTR exon contains 22 copies of the AUUUA mRNA instability element, indicating post-transcriptional regulation. Genomic library screening, DNA sequencing, primer extension, fluorescence in situ hybridization (FISH) European journal of biochemistry / The Biochemical journal High 7945196 8181472
1994 Recombinant human PTGS2 (PGHS-2) expressed in a baculovirus system possesses both cyclooxygenase and peroxidase activities, has high affinity for arachidonate as substrate, and undergoes self-inactivation during catalysis. The enzyme is glycosylated with heterogeneous glycosylation, and certain NSAIDs selectively inhibit PGHS-2 over PGHS-1. Baculovirus expression, enzyme purification, kinetic assays (cyclooxygenase and peroxidase activities), SDS-PAGE, N-terminal sequencing Biochimica et biophysica acta High 7947975
1994 COX-2 protein is constitutively expressed at a basal level in granulomatous tissue during the chronic phase of murine inflammation, and COX-2 protein rises progressively during inflammation peaking at day 14, while COX-1 protein remains unaltered throughout—establishing distinct regulatory behavior for the two isoforms in vivo. Western blot, enzymatic activity assay in murine air-pouch granuloma model Proceedings of the National Academy of Sciences of the United States of America High 7510883
1998 PTGS2 (COX-2) subcellular localization was determined by immunoelectron microscopy: both PGHS-1 and PGHS-2 reside on the lumenal surfaces of the endoplasmic reticulum and nuclear envelope (inner and outer nuclear membranes) in human monocytes, NIH 3T3 cells, and HUVECs. Subcellular fractionation and isozyme-specific inhibitor studies confirm similar distribution and product profiles, indicating independent functioning is not attributable to different subcellular compartments. Immunoelectron microscopy, subcellular fractionation, Western blotting, isozyme-selective inhibitor product analysis The Journal of biological chemistry High 9545330
1998 COX-2-overexpressing colon carcinoma cells stimulate endothelial cell migration and tube formation (angiogenesis) through production of prostaglandins and proangiogenic factors; selective COX-2 inhibitor NS-398 blocks this effect. COX-1 in endothelial cells also regulates angiogenesis independently, as shown by COX-1 antisense inhibition of tube formation, establishing a dual-mechanism model for cyclooxygenase regulation of tumor angiogenesis. In vitro coculture angiogenesis assay, COX-2 overexpression, NS-398 inhibition, neutralizing antibodies to angiogenic factors, COX-1 antisense oligonucleotides Cell High 9630216
1997 In adult human kidney, COX-2 immunoreactivity localizes to endothelial and smooth muscle cells of arteries and veins and to intraglomerular podocytes (not macula densa, unlike rat), suggesting a primary role in regulation of renal perfusion and glomerular hemodynamics. In fetal kidney, COX-2 appears in podocytes only at the end-stage of renal development. Immunohistology, in situ mRNA hybridization with digoxigenin-labeled riboprobes The American journal of physiology High 9140046
2002 Aspirin acetylates COX-2, switching its oxygenation of DHA from 13-HDHA to 17R-HDHA; human COX-2 converts DHA to 13-hydroxy-DHA which is redirected by aspirin-acetylation to 17R-HDHA, the precursor of anti-inflammatory resolvins. This demonstrates that aspirin-acetylated COX-2 retains oxygenase activity but with altered stereospecificity, enabling biosynthesis of pro-resolution lipid mediators. Lipidomic analysis (LC-MS), in vitro enzyme assays with aspirin-treated human COX-2, isotope labeling, cell-based experiments with human microglial and endothelial cells The Journal of experimental medicine High 12391014
2002 A common COX-2 promoter variant (-765G>C) significantly reduces promoter activity (~28-31% lower) in human lung fibroblasts basally and in serum-stimulated conditions. Carriers of the -765C allele show lower post-operative CRP elevation after coronary bypass surgery, linking reduced PTGS2 promoter activity to attenuated acute-phase inflammatory response in vivo. Reporter gene assay, PCR-based variant screening, clinical association study with plasma CRP measurement Arteriosclerosis, thrombosis, and vascular biology High 12377741
2003 Membrane-bound prostaglandin E synthase-2 (mPGES-2), while constitutively expressed, promotes PGE2 production via both COX-1 and COX-2 with modest COX-2 preference, in contrast to mPGES-1 which preferentially couples to COX-2. This establishes that PTGS2 (COX-2) can functionally couple with multiple downstream prostaglandin synthases. Cell-based overexpression, isozyme-selective inhibitor studies, PGE2 measurement by immunoassay, subcellular fractionation The Journal of biological chemistry High 12835322
2005 Inducible nitric oxide synthase (iNOS) physically binds to COX-2 (PTGS2) and S-nitrosylates it, enhancing COX-2 catalytic activity. Selectively disrupting the iNOS–COX-2 binding interaction prevents NO-mediated activation of COX-2, establishing a direct protein–protein interaction that amplifies inflammatory signaling. Co-immunoprecipitation, S-nitrosylation assay, selective disruption of protein-protein interaction, in vitro activity assay Science High 16373578
2005 miR-16, containing a sequence complementary to the AU-rich element (ARE) in the COX-2 3'-UTR, is required for ARE-mediated mRNA turnover of COX-2 mRNA. miR-16 works in concert with the ARE-binding protein tristetraprolin (TTP) through association with Ago/eiF2C family members to target ARE-containing mRNAs for degradation, establishing a microRNA-dependent mechanism for post-transcriptional regulation of PTGS2. RNAi screen in Drosophila S2 cells, siRNA knockdown in HeLa cells, mRNA stability assays, sequence-specificity controls Cell High 15766526
2006 TLR4 signaling via MyD88 is required for optimal Cox-2 expression in intestinal epithelial cells; LPS-mediated PGE2 production is blocked by Cox-2 inhibition or siRNA against MyD88. TLR4-deficient mice show reduced proliferation and increased apoptosis after DSS injury, which is rescued by exogenous PGE2, establishing that PTGS2-derived PGE2 downstream of TLR4 is essential for intestinal epithelial repair, potentially through transactivation of the EGF receptor. Reporter luciferase assay, siRNA knockdown, immunohistochemistry, Western blotting, BrdU/TUNEL assays in TLR4-/- mice, PGE2 rescue experiments Gastroenterology High 16952555
2007 COX-2 (PTGS2), together with epiregulin and matrix metalloproteinases 1 and 2, facilitates assembly of new tumor blood vessels, release of tumor cells into circulation, and breaching of lung capillaries to seed pulmonary metastasis from breast cancer cells. Genetic and pharmacological approaches in human breast cancer cells and xenograft models established COX2 as a mediator of vascular remodeling co-opted for lung metastasis. Genetic perturbation (shRNA knockdown), pharmacological inhibition, xenograft mouse models, in vitro vascular permeability and angiogenesis assays Nature High 17429393
2010 COX-2 is a downstream effector of β-adrenergic signaling in white adipose tissue (WAT) and is required for induction of brown adipose tissue (BAT) in WAT depots. Prostaglandins produced by COX-2 shift differentiation of mesenchymal progenitors toward a brown adipocyte phenotype. COX-2 overexpression in WAT induced de novo BAT recruitment, increased systemic energy expenditure, and protected mice against diet-induced obesity. Cox-2 transgenic mouse model (WAT-specific overexpression), Cox-2 genetic deletion, mesenchymal progenitor differentiation assays, metabolic phenotyping Science High 20448152
2010 Increasing matrix stiffness across the pathophysiological range strongly suppresses fibroblast COX-2 expression and PGE2 synthesis. Exogenous PGE2 or EP2 receptor agonist completely counteracts the proliferative and matrix-synthetic effects of increased stiffness, establishing an autocrine feedback loop in which COX-2-derived PGE2 maintains fibroblast quiescence and its suppression by matrix stiffening amplifies progressive fibrosis. Polyacrylamide gel matrix stiffness manipulation, COX-2 mRNA/protein measurement, PGE2 ELISA, pharmacological rescue with exogenous PGE2/EP2 agonist, proliferation and collagen synthesis assays The Journal of cell biology High 20733059
2011 A positive feedback loop between PGE2 and COX-2 redirects monocyte differentiation from CD1a+ dendritic cells to CD14+CD33+CD34+ myeloid-derived suppressor cells (MDSCs). Exogenous PGE2 or diverse COX-2 activators (LPS, IL-1β, IFNγ) induce COX-2 expression and endogenous PGE2 production, driving MDSC-associated suppressive factors. Disruption of COX2-PGE2 feedback using COX2 inhibitors or EP2/EP4 antagonists suppresses MDSC function. Monocyte differentiation assays, flow cytometry, pharmacological inhibition (COX2 inhibitors, EP2/EP4 antagonists), ovarian cancer patient samples Blood High 21972293
2014 The non-receptor tyrosine kinase FYN physically interacts with COX-2 (PTGS2) and phosphorylates it at Tyr446; a phospho-mimetic mutation at Tyr446 promotes COX-2 activity, while a phosphorylation-blocking mutation prevents FYN-mediated activity increase, establishing post-translational regulation of COX-2 enzymatic activity by tyrosine phosphorylation independent of changes in protein expression. Co-immunoprecipitation, in vitro kinase assay, site-directed mutagenesis (phospho-mimetic and blocking mutants), COX-2 activity assays in prostate cancer cells Oncotarget High 24970799
2015 DNA methylation at the PTGS2 CpG island disrupts CTCF/cohesin complex binding, abrogating chromatin loop formation at the PTGS2 locus and reducing enrichment of positive elongation factor b at the transcriptional start site, thereby downregulating PTGS2 expression. Demethylation restores CTCF/cohesin binding and chromatin looping, re-activating PTGS2 transcription. Chromatin immunoprecipitation (ChIP), chromatin conformation capture (3C), bisulfite sequencing, demethylation treatment, CTCF/cohesin knockdown Oncogene High 25703332
2015 Ku80 binds the COX-2 (PTGS2) gene promoter and upregulates COX-2 expression in lung cancer cells; the transcriptional co-activator CBP interacts with Ku80 and acetylates it, promoting COX-2 promoter activation. Ku80 knockdown suppresses COX-2 expression, inhibits ERK phosphorylation, and impairs tumor growth in vivo. Streptavidin-agarose promoter pulldown with proteomics, Co-IP, siRNA knockdown, reporter assays, xenograft mouse model Oncotarget Medium 25797267
2015 The transcription factor ATF3 negatively regulates Ptgs2 expression by binding to the Ptgs2 promoter in activated macrophages. In Atf3-/- mice, peritoneal macrophages show higher Ptgs2 expression and prostaglandin production after zymosan stimulation, and acute peritonitis shows increased leukocyte accumulation and PGE2/PGD2 levels, establishing ATF3 as a transcriptional repressor that terminates Ptgs2 expression during acute inflammation. Chromatin immunoprecipitation (ChIP), Atf3-/- mouse model, RT-PCR, ELISA for prostaglandins, peritonitis model Prostaglandins & other lipid mediators High 25619459
2019 EPHA2 signaling through TGFβ promotes PTGS2 expression in pancreatic tumor cells; Epha2 or Ptgs2 deletion each reverses T cell exclusion from the tumor microenvironment and sensitizes tumors to immunotherapy, placing PTGS2 downstream of EPHA2-TGFβ in a pathway that drives immunosuppression. Genetic deletion (Epha2-/- and Ptgs2-/- mouse models), pharmacological PTGS2 inhibition, tumor immunophenotyping, immunotherapy response assays The Journal of clinical investigation High 31162144
2019 Cisplatin induces PTGS2 expression through ROS/NF-κB pathway; PTGS2 then mediates resistance to apoptosis via PGE2/EP4/MAPKs (ERK1/2, P38) axis, upregulating BCL2. Inhibition of PTGS2 by celecoxib augments cisplatin cytotoxicity in resistant gastric cancer cells and xenografts through suppression of PTGS2 and BCL2. Western blotting, ROS measurement, NF-κB pathway inhibitors, PGE2/EP4 axis interrogation, xenograft mouse model, clinical specimen correlation The international journal of biochemistry & cell biology Medium 31518663
2019 Inhibition of mitochondrial oxidative phosphorylation activates AMPK, which stabilizes Ptgs2 mRNA post-transcriptionally in astrocytes, leading to increased COX-2 protein and enhanced eicosanoid secretion (PGE2, PGF2α, 6-keto-PGF1α). AMPK silencing prevents Ptgs2 upregulation by mitochondrial inhibitors, while AMPK activators recapitulate Ptgs2 mRNA stabilization. Mitochondrial inhibitors, AMPK siRNA knockdown, AMPK activators, mRNA stability assay, LC/MS eicosanoid profiling Cells Medium 31581537
2021 Macrophage COX-2 is required for efferocytosis (phagocytosis of apoptotic neutrophils) and efferocytosis-dependent macrophage reprogramming. Loss of Cox2 impairs macrophage binding capacity for apoptotic cells, dysregulates polarization, and inhibits production of pro-resolution eicosanoids (PGI2, PGE2, lipoxin A4, 15d-PGJ2). COX2-competent efferocytic macrophages induce intestinal epithelial organoid restitution and repair. Macrophage-specific Cox2 knockout, pharmacological COX2 inhibition, efferocytosis assays with apoptotic neutrophils and synthetic targets, LC-MS/MS eicosanoid lipidomics, intestinal organoid co-culture Cellular and molecular gastroenterology and hepatology High 35017061
2021 During RAS-induced senescence, COX2 regulates SASP composition through an autocrine feedback loop: COX2-derived PGE2 binds EP4 to modulate expression of multiple inflammatory SASP components including CXCL1. In vivo, Cox2 is required for hepatocyte senescence surveillance, NK/T cell-mediated clearance of senescent cells, and tumor suppression; loss of Cox2 enriches immunosuppressive immature myeloid cells and Treg lymphocytes in the intrahepatic immune microenvironment. RAS-induced senescence model, Cox2 genetic deletion, in vivo hepatocyte senescence model, immune cell profiling, SASP cytokine measurement, PGE2/EP4 pathway pharmacology Cell reports High 33730589
2022 The transcription factor CTCF, together with the lncRNA PACERR, recruits the histone acetyltransferase p300 to the promoter regions of PTGS2, enhancing histone acetylation and increasing PTGS2 transcription in tumor-associated macrophages. This CTCF/PACERR/p300 complex promotes M2-like macrophage polarization in pancreatic ductal adenocarcinoma. RNA-seq, ATAC-seq, ChIP-seq, RNA immunoprecipitation, RNA pulldown, CTCF/PACERR knockdown with lentivirus, in vitro and in vivo functional assays Clinical and translational medicine Medium 35184402
2022 DCLK1 kinase binds and phosphorylates XRCC5 (Ku80), which then transcriptionally activates COX-2 (PTGS2) expression and enhances PGE2 production, generating an inflammatory tumor microenvironment that promotes colorectal cancer aggressiveness and stemness. Proteomics, Co-IP, in vitro kinase assay, DCLK1 kinase inhibition in CRC mouse models, gene expression analysis Theranostics Medium 35910805
2024 Endothelial ROBO4 suppresses PTGS2/COX-2 expression by interacting with IQGAP1 and the ubiquitin E3 ligase TRAF7; ROBO4 enhances TRAF7-mediated ubiquitination of IQGAP1, inhibiting prolonged RAC1 activation and thereby decreasing PTGS2 expression in inflammatory endothelial cells. Robo4-deficient mice show exacerbated PTGS2-associated inflammatory diseases (arthritis, edema, pain). RNA-seq, Co-IP (ROBO4-IQGAP1-TRAF7 interaction), ubiquitination assay, RAC1 activation assay, Robo4-/- mouse model with inflammatory disease phenotyping Communications biology High 38762541
2016 A small but significant amount of COX-2 protein and mRNA is constitutively expressed in human platelets; the COX1/COX2 mRNA ratio in platelets is ~370:1 and protein ratio ~17:1. COX-2 is also present in platelet-derived microparticles, suggesting a role for platelet COX-2 in physiological and pathological processes including thrombosis. Quantitative RT-PCR, immunostaining, Western blotting of isolated platelets and platelet-derived microparticles Platelets Medium 27534811
2022 The transcription factor HIF1α binds to the promoter of Ptgs2 and upregulates its expression; atorvastatin inhibits the HIF1α/Ptgs2 axis, attenuating Ptgs2-mediated ferroptosis and inflammation following coronary microembolization in rats, as confirmed by chromatin immunoprecipitation demonstrating direct HIF1α binding to the Ptgs2 promoter. Chromatin immunoprecipitation (ChIP), Ptgs2 silencing, rat CME model, ferroptosis marker quantification (MDA, GSH, Fe2+), cardiac function assessment Frontiers in pharmacology Medium 36569299
2016 Activin A upregulates PTGS2 expression and increases PGE2 production in human granulosa-lutein cells via an ACVR1B-mediated SMAD2/3-SMAD4 signaling pathway, as demonstrated by TGF-β/activin receptor inhibition and SMAD-specific siRNA knockdown. Receptor inhibitor (SB431542), siRNA knockdown of SMADs, PTGS2 mRNA/protein measurement, PGE2 ELISA in primary and immortalized human granulosa-lutein cells Reproduction Medium 27624482
2022 LRH-1/NR5A2 regulates PTGS2/COX-2 expression in pancreatic beta cells; LRH-1 ablation blunts Ptgs2 induction by the LRH-1 agonist BL001. Ptgs2 inactivation reduces PGE2 levels and abrogates BL001-mediated islet survival (increased cytochrome c release and cleaved PARP). The PTGER1 receptor antagonist negates BL001-mediated islet survival, defining the LRH-1/PTGS2/PGE2/PTGER1 signaling axis as a beta cell survival pathway. Conditional beta-cell-specific LRH-1 knockout, Ptgs2 inactivation, PGE2 measurement, cytochrome c release and PARP cleavage assays, EP receptor pharmacology iScience Medium 35602948

Source papers

Stage 0 corpus · 130 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1998 Cyclooxygenase regulates angiogenesis induced by colon cancer cells. Cell 2060 9630216
2002 Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proceedings of the National Academy of Sciences of the United States of America 1479 12477932
1992 Human cyclooxygenase-2 cDNA. Proceedings of the National Academy of Sciences of the United States of America 1379 1380156
2002 Resolvins: a family of bioactive products of omega-3 fatty acid transformation circuits initiated by aspirin treatment that counter proinflammation signals. The Journal of experimental medicine 1306 12391014
2017 Architecture of the human interactome defines protein communities and disease networks. Nature 1085 28514442
1994 Inducible isoforms of cyclooxygenase and nitric-oxide synthase in inflammation. Proceedings of the National Academy of Sciences of the United States of America 917 7510883
1999 COX-2 inhibitors. Lancet (London, England) 823 9929039
2021 Dual proteome-scale networks reveal cell-specific remodeling of the human interactome. Cell 705 33961781
2005 Involvement of microRNA in AU-rich element-mediated mRNA instability. Cell 690 15766526
1993 Molecular cloning of human prostaglandin endoperoxide synthase type II and demonstration of expression in response to cytokines. The Journal of biological chemistry 663 8473346
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
2010 Feedback amplification of fibrosis through matrix stiffening and COX-2 suppression. The Journal of cell biology 654 20733059
1973 Detection and isolation of an endoperoxide intermediate in prostaglandin biosynthesis. Proceedings of the National Academy of Sciences of the United States of America 644 4514999
2007 Mediators of vascular remodelling co-opted for sequential steps in lung metastasis. Nature 554 17429393
2004 The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC). Genome research 438 15489334
2005 Inducible nitric oxide synthase binds, S-nitrosylates, and activates cyclooxygenase-2. Science (New York, N.Y.) 429 16373578
1994 Structure of the human cyclo-oxygenase-2 gene. The Biochemical journal 426 7945196
2011 Positive feedback between PGE2 and COX2 redirects the differentiation of human dendritic cells toward stable myeloid-derived suppressor cells. Blood 425 21972293
2005 Diversification of transcriptional modulation: large-scale identification and characterization of putative alternative promoters of human genes. Genome research 409 16344560
1996 Normalization and subtraction: two approaches to facilitate gene discovery. Genome research 401 8889548
2018 DNA Repair Network Analysis Reveals Shieldin as a Key Regulator of NHEJ and PARP Inhibitor Sensitivity. Cell 379 29656893
2010 Cyclooxygenase-2 controls energy homeostasis in mice by de novo recruitment of brown adipocytes. Science (New York, N.Y.) 373 20448152
2006 Cox-2 is regulated by Toll-like receptor-4 (TLR4) signaling: Role in proliferation and apoptosis in the intestine. Gastroenterology 367 16952555
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