HCSGD entry for PTGS2
1. General information
Official gene symbol | PTGS2 |
---|---|
Entrez ID | 5743 |
Gene full name | prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase) |
Other gene symbols | COX-2 COX2 GRIPGHS PGG/HS PGHS-2 PHS-2 hCox-2 |
Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
---|---|---|---|
GO:0001516 | Prostaglandin biosynthetic process | ISS NAS | biological_process |
GO:0001525 | Angiogenesis | IEA | biological_process |
GO:0004601 | Peroxidase activity | NAS | molecular_function |
GO:0004666 | Prostaglandin-endoperoxide synthase activity | IDA | molecular_function |
GO:0005634 | Nucleus | ISS | cellular_component |
GO:0005737 | Cytoplasm | IDA ISS | cellular_component |
GO:0005789 | Endoplasmic reticulum membrane | TAS | cellular_component |
GO:0006693 | Prostaglandin metabolic process | TAS | biological_process |
GO:0006928 | Cellular component movement | TAS | biological_process |
GO:0006954 | Inflammatory response | IEA | biological_process |
GO:0006979 | Response to oxidative stress | IEA | biological_process |
GO:0007566 | Embryo implantation | IEA | biological_process |
GO:0007612 | Learning | IEA | biological_process |
GO:0007613 | Memory | IEA | biological_process |
GO:0008217 | Regulation of blood pressure | ISS | biological_process |
GO:0008285 | Negative regulation of cell proliferation | IEA | biological_process |
GO:0008289 | Lipid binding | IEA | molecular_function |
GO:0009750 | Response to fructose | IEA | biological_process |
GO:0010042 | Response to manganese ion | IEA | biological_process |
GO:0010226 | Response to lithium ion | IEA | biological_process |
GO:0010575 | Positive regulation vascular endothelial growth factor production | ISS | biological_process |
GO:0019233 | Sensory perception of pain | IEA | biological_process |
GO:0019369 | Arachidonic acid metabolic process | TAS | biological_process |
GO:0019371 | Cyclooxygenase pathway | IDA TAS | biological_process |
GO:0019372 | Lipoxygenase pathway | TAS | biological_process |
GO:0019899 | Enzyme binding | IPI | molecular_function |
GO:0020037 | Heme binding | ISS | molecular_function |
GO:0030282 | Bone mineralization | IEA | biological_process |
GO:0030728 | Ovulation | IEA | biological_process |
GO:0031394 | Positive regulation of prostaglandin biosynthetic process | NAS | biological_process |
GO:0031622 | Positive regulation of fever generation | ISS | biological_process |
GO:0031915 | Positive regulation of synaptic plasticity | IEA | biological_process |
GO:0032227 | Negative regulation of synaptic transmission, dopaminergic | IEA | biological_process |
GO:0032355 | Response to estradiol | IEA | biological_process |
GO:0032496 | Response to lipopolysaccharide | IEA | biological_process |
GO:0033280 | Response to vitamin D | IEA | biological_process |
GO:0034612 | Response to tumor necrosis factor | IEA | biological_process |
GO:0034644 | Cellular response to UV | IEA | biological_process |
GO:0035633 | Maintenance of blood-brain barrier | IEA | biological_process |
GO:0042346 | Positive regulation of NF-kappaB import into nucleus | IEA | biological_process |
GO:0042493 | Response to drug | IEA | biological_process |
GO:0042640 | Anagen | IEA | biological_process |
GO:0042803 | Protein homodimerization activity | IEA | molecular_function |
GO:0043005 | Neuron projection | IDA | cellular_component |
GO:0043065 | Positive regulation of apoptotic process | IEA | biological_process |
GO:0043234 | Protein complex | IEA | cellular_component |
GO:0044281 | Small molecule metabolic process | TAS | biological_process |
GO:0045429 | Positive regulation of nitric oxide biosynthetic process | ISS | biological_process |
GO:0045786 | Negative regulation of cell cycle | IEA | biological_process |
GO:0045907 | Positive regulation of vasoconstriction | IEA | biological_process |
GO:0045986 | Negative regulation of smooth muscle contraction | IEA | biological_process |
GO:0045987 | Positive regulation of smooth muscle contraction | IEA | biological_process |
GO:0046697 | Decidualization | IEA | biological_process |
GO:0046872 | Metal ion binding | IEA | molecular_function |
GO:0048661 | Positive regulation of smooth muscle cell proliferation | IEA | biological_process |
GO:0050473 | Arachidonate 15-lipoxygenase activity | TAS | molecular_function |
GO:0050727 | Regulation of inflammatory response | NAS | biological_process |
GO:0050873 | Brown fat cell differentiation | IEA | biological_process |
GO:0051384 | Response to glucocorticoid | IEA | biological_process |
GO:0051926 | Negative regulation of calcium ion transport | IEA | biological_process |
GO:0051968 | Positive regulation of synaptic transmission, glutamatergic | IEA | biological_process |
GO:0070542 | Response to fatty acid | IEA | biological_process |
GO:0071260 | Cellular response to mechanical stimulus | IEA | biological_process |
GO:0071318 | Cellular response to ATP | IEA | biological_process |
GO:0071456 | Cellular response to hypoxia | IEP | biological_process |
GO:0071636 | Positive regulation of transforming growth factor beta production | ISS | biological_process |
GO:0090050 | Positive regulation of cell migration involved in sprouting angiogenesis | ISS | biological_process |
GO:0090271 | Positive regulation of fibroblast growth factor production | ISS | biological_process |
GO:0090336 | Positive regulation of brown fat cell differentiation | ISS | biological_process |
GO:0090362 | Positive regulation of platelet-derived growth factor production | ISS | biological_process |
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4. Expression levels in datasets
- Meta-analysis result
p-value up | p-value down | FDR up | FDR down |
---|---|---|---|
0.0000455302 | 0.0155563276 | 0.0188203125 | 0.2446159619 |
- Individual experiment result
( "-" represent NA in the specific microarray platform )
( "-" represent NA in the specific microarray platform )
Data source | Up or down | Log fold change |
---|---|---|
GSE11954 | Down | -0.3621480588 |
GSE13712_SHEAR | Down | -0.6044554365 |
GSE13712_STATIC | Up | 0.7019809237 |
GSE19018 | Down | -1.0177360707 |
GSE19899_A1 | Up | 4.9397001503 |
GSE19899_A2 | Up | 5.3374156105 |
PubMed_21979375_A1 | Up | 8.0314030249 |
PubMed_21979375_A2 | Up | 7.9162606842 |
GSE35957 | Down | -2.2168772999 |
GSE36640 | Down | -1.6095494044 |
GSE54402 | Up | 0.9242470919 |
GSE9593 | Down | -1.1565242119 |
GSE43922 | Up | 4.3831444811 |
GSE24585 | Up | 0.4764688236 |
GSE37065 | Up | 1.7597580477 |
GSE28863_A1 | Down | -0.0401968243 |
GSE28863_A2 | Up | 1.7974249766 |
GSE28863_A3 | Down | -1.1764554504 |
GSE28863_A4 | Down | -0.2685555081 |
GSE48662 | Down | -0.3743800284 |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
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- Drugs
Not regulated by drugs
- MicroRNAs
- mirTarBase
- mirTarBase
MiRNA_name | mirBase ID | miRTarBase ID | Experiment | Support type | References (Pubmed ID) |
---|---|---|---|---|---|
hsa-miR-137 | MIMAT0000429 | MIRT006329 | Luciferase reporter assay//Western blot | Functional MTI | 22406049 |
hsa-miR-16-5p | MIMAT0000069 | MIRT001426 | pSILAC//Proteomics;Other | Functional MTI (Weak) | 18668040 |
hsa-miR-16-5p | MIMAT0000069 | MIRT001426 | Luciferase reporter assay | Functional MTI | 23226427 |
hsa-let-7b-5p | MIMAT0000063 | MIRT001603 | pSILAC//Proteomics;Other | Functional MTI (Weak) | 18668040 |
hsa-miR-101-3p | MIMAT0000099 | MIRT004297 | qRT-PCR//Luciferase reporter assay//Western blot | Functional MTI | 19133256 |
hsa-miR-101-3p | MIMAT0000099 | MIRT004297 | qRT-PCR | Functional MTI (Weak) | 20712078 |
hsa-miR-101-3p | MIMAT0000099 | MIRT004297 | qRT-PCR//Western blot | Functional MTI | 23013439 |
hsa-miR-26b-5p | MIMAT0000083 | MIRT004659 | Luciferase reporter assay//Western blot//Reporter assay | Functional MTI | 20100477 |
hsa-miR-335-5p | MIMAT0000765 | MIRT017755 | Microarray | Functional MTI (Weak) | 18185580 |
hsa-miR-132-3p | MIMAT0000426 | MIRT021768 | Microarray | Functional MTI (Weak) | 17612493 |
hsa-miR-128-3p | MIMAT0000424 | MIRT021956 | Microarray | Functional MTI (Weak) | 17612493 |
hsa-miR-124-3p | MIMAT0000422 | MIRT022542 | Microarray | Functional MTI (Weak) | 18668037 |
hsa-miR-181a-5p | MIMAT0000256 | MIRT025094 | Microarray | Functional MTI (Weak) | 17612493 |
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- mirRecord
- mirRecord
MicroRNA name | mirBase ID | Target site number | MiRNA mature ID | Test method inter | MiRNA regulation site | Reporter target site | Pubmed ID |
---|---|---|---|---|---|---|---|
hsa-miR-101-3p | MIMAT0000099 | 1 | hsa-miR-101 | {Western blot} | {overexpression by mature miRNA transfection} | 19133256 |
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6. Text-mining results about the gene
Gene occurances in abstracts of cellular senescence-associated articles: 10 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
---|---|
26190312 | Morphologic changes, phospho-p38 MAPK (P-p38) activation, development of senescence, and induction of uterotonins (COX-2 expression) were quantified using light microscopy, Western blot, senescence-associated beta-galactosidase (SA beta-gal) staining, and qRT-PCR, respectively, after 48 and 72 hr of exposure |
26190312 | COX-2 expression was higher after 72 hr of treatment with PBDE-99 |
25090227 | A p38 MAPK-mediated alteration of COX-2/PGE2 regulates immunomodulatory properties in human mesenchymal stem cell aging |
25090227 | Among the anti-inflammatory cytokines, the production of prostaglandin E2 (PGE2) and the expression of its primary enzyme, cyclooxygenase-2 (COX-2), were profoundly increased by pre-stimulation with interferon gamma (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha), and this response was significantly decreased with consecutive passages |
25090227 | In conclusion, our data indicate that the immunomodulatory ability of hMSCs gradually declines with consecutive passages via a p38-mediated alteration of COX-2 and PGE2 levels |
24046862 | Here, we investigated the mechanism by which the COX-2/PGE2 axis induces senescence |
24046862 | We therefore investigated the role of PGE2 by invalidating the PGE2 synthases downstream of COX-2, or the specific PGE2 receptors, or by applying PGE2 or specific agonists or antagonists |
24046862 | Taken together, these results suggest that COX-2 contributes to the establishment and maintenance of senescence of normal human fibroblasts via an independent-ROS and a dependent-PGE2/EPs intracrine pathway |
23853351 | The innate immunity genes, such as highly expressed anti-inflammatory +896 G KIR4 allele, CCR5Delta32 variant, -765 C Cox-2 allele, -1708 G and 21 C 5-Lox alleles are detected in centenarians |
22563892 | NO and COX-2, in addition to activation of SIRT1, play a critical role in the inhibition of senescence induction in human endothelial cells by RWE |
19449178 | Increases in CTS-induced osteopontin (OPN) synthesis, cyclooxygenase-2 (Cox-2) mRNA expression, and nitric oxide (NO) production by osteoblasts did not change at the third and fifth passages |
18848576 | Selective COX-2 inhibitors modulate cellular senescence in human dermal fibroblasts in a catalytic activity-independent manner |
18848576 | It has been recently proposed that pro-inflammatory genes such as cyclooxygenase-2 (COX-2) play a key role in the aging process |
18848576 | We therefore examined the effect of COX-2 inhibitors on aging in the cellular senescence model of human dermal fibroblasts (HDFs) |
18848576 | The senescence-regulating effect of selective COX-2 inhibitors had no correlation with cellular reactive oxygen species levels, NF-kappaB activities or protein levels of p53 and p21 |
18848576 | We instead found that selective COX-2 inhibitors regulate caveolin-1 expression at transcriptional levels, which was closely associated with the inhibitors' effect on the senescence |
16672767 | In attempts to define the molecular events associated with the age-dependent changes in cAMP profiles, we determined the protein kinase A (PKA) activity, phosphorylation of cAMP-response element binding protein (CREB), and the protein expression of CRE-regulatory genes, c-fos and COX-2 in young and senescent HDFs |
16672767 | In senescent cells, after LPA treatment, the expression of c-fos and COX-2 decreased initially, followed by an increase |
16672767 | In young HDFs, CREB phosphorylation decreased following LPA treatment, and both c-fos and COX-2 protein levels increased rapidly |
15130753 | Selective COX-2 inhibitor, NS-398, inhibits the replicative senescence of cultured dermal fibroblasts |
15130753 | Cyclooxygenase 2 (COX-2) is known to be increased in aged cells |
15130753 | Recent studies suggest that the increased expression of COX-2 may be involved in the pathogenesis of age-associated diseases such as rheumatoid arthritis and cancer |
15130753 | Using the replicative senescence model of dermal fibroblasts, we demonstrated the increased expression of COX-2 and increased PGE(2) levels associated with replicative senescence |
9722719 | According to RT-PCR analysis, gene expression of COX-2, IL-1 beta, IL-6, and tissue type (t) PA was higher in old cells than in young cells |
9722719 | Cyclic tension force to HPLF also stimulated phenotypic and gene expression of IL-1 beta, PGE2 (COX-2 gene) and tPA |
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