| + |
5-benzoyl-2,3-dihydro-1H-pyrrolizine-1-carboxylic acid | down-regulates activity 
chemical inhibition
|
PTGS2 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258324 |
|
|
in vitro |
|
| pmid |
sentence |
| 22091869 |
Here we report the application of STD-NMR to characterize the binding of the anti-inflammatory drugs ibuprofen, diclofenac, and ketorolac to COX-1 and COX-2. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
PTGS2 | up-regulates 
|
Inflammation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-262509 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 32995789 |
Given our finding that COX-2 signaling does not regulate viral entry or replication, the role of COX-2 induction upon SARS-CoV-2 infection remains an area for future investigation. Rather than directly affecting viral entry or replication, COX-2 induction may regulate the severe lung inflammation and injury seen in COVID-19 patients (35, 36), though it is unclear whether COX-2 would be beneficial, neutral, or detrimental to disease. COX-2 could enhance lung injury in COVID-19, as PGE2 has been reported to induce IL-1β and exacerbate lung injury in bone marrow transplant mice |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | SARS-CoV INFLAMMATORY RESPONSE |
| + |
PTGS2 | up-regulates 
chemical modification
|
prostaglandin F2alpha |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-113291 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11751058 |
Cox catalyzes two enzymatic activities;namely, the conversion of aa to the hydroperoxy endoperoxide pgg2, followed by its subsequent reduction to the labile product pgh2. Pgh2_ is the common substrate for a number of different cell-specific synthases, which convert pgh2_ to the individual pgs or tx, including pge2, pgi2_ (prostacyclin), pgd2, pgf2alfa, and txa2. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255359 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20219869 |
NSAIDs are strong inhibitors of cycloxygenases (COX), and thereby impair the metabolism of arachidonic acid that is necessary for the synthesis of prostaglandins |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
ibuprofen | down-regulates activity
chemical inhibition
|
PTGS2 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258325 |
|
|
in vitro |
|
| pmid |
sentence |
| 22091869 |
Here we report the application of STD-NMR to characterize the binding of the anti-inflammatory drugs ibuprofen, diclofenac, and ketorolac to COX-1 and COX-2. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258604 |
|
|
in vitro |
|
| pmid |
sentence |
| 9057869 |
Naproxen had similar activity against both COX-1 and COX-2 enzymes (IC50s of 3.2 and 2.5 μM, respectively), whereas ibuprofen was approximately 100-fold more potent for COX-2 (IC50 = 0.1 μM) than for COX-1 (IC50 = 11 μM), and indomethacin was about 50-fold more potent for COX-1 (IC50 = 0.012 μM) than for COX-2 (IC50 = 0.56 μM). |
|
| Publications: |
2 |
Organism: |
In Vitro |
| + |
NFATC2 | up-regulates quantity by expression
transcriptional regulation
|
PTGS2 |
0.385 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-264025 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21871017 |
NFAT induces the transcription of the COX2 (cyclo-oxygenase-2) gene incancer cells thereby enhancing invasive migration |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
|
PTGS2 |
0.378 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260262 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17705188 |
Inflammatory stimuli can activate IkappaB kinase (IKK) signalsome and subsequently the nuclear factor kappa B (NF-kappaB), which influences gene expression of cyclooxygenase-2 (Cox-2) along with other transcription factors. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, SARS-CoV INFLAMMATORY RESPONSE |
| + |
PTGS2 | up-regulates
chemical modification
|
prostaglandin D2 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-113282 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11751058 |
Cox catalyzes two enzymatic activities;namely, the conversion of aa to the hydroperoxy endoperoxide pgg2, followed by its subsequent reduction to the labile product pgh2. Pgh2_ is the common substrate for a number of different cell-specific synthases, which convert pgh2_ to the individual pgs or tx, including pge2, pgi2_ (prostacyclin), pgd2, pgf2alfa, and txa2 |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
suprofen | down-regulates activity
chemical inhibition
|
PTGS2 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-257808 |
|
|
Homo sapiens |
PC-3 Cell |
| pmid |
sentence |
| 18667313 |
Profens, that is, Ketoprofen 1, Suprofen 2 (Fig. 1), were chosen because of their interesting inhibitory activity against cyclooxygenase and of their different selectivity versus the two isoforms COX-1/COX-2. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
acetylsalicylic acid | down-regulates
chemical inhibition
|
PTGS2 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-114380 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11809688 |
Nsaids inhibit cyclooxygenase (cox) isozymes, which are responsible for the committed step in prostaglandin biosynthesis, and this has been considered the primary mechanism by which nsaids exert their antitumorigenic effects. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
oxaprozin | down-regulates activity
chemical inhibition
|
PTGS2 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258930 |
|
|
Homo sapiens |
Blood Platelet, Synovial Cell |
| pmid |
sentence |
| 9650852 |
We used human platelets cyclooxygenase-1 and interleukin-1beta-stimulated human synovial cell cyclooxygenase-2 for measuring cyclooxygenase selectivity. The presence of the enzymes was confirmed by immunoblotting and immunoprecipitation analysis, and by the reverse transcriptase-polymerase chain reaction. Mean IC50 values (microM) for human platelet cyclooxygenase-1 and interleukin-1beta-stimulated human synovial cell cyclooxygenase-2 and cyclooxygenase-1/-2 IC50 ratio of various NSAIDs were as follows: aspirin, 3.2, 26, 0.12; diclofenac, 0.037, 0.00097, 38; etodolac, 122, 0.68, 179; ibuprofen, 3.0, 3.5, 0.86; indomethacin, 0.013, 0.044, 0.30; loxoprofen (active metabolite), 0.38, 0.12, 3.2; NS-398, 12, 0.0095, 1263; oxaprozin, 2.2, 36, 0.061; zaltoprofen, 1.3, 0.34, 3.8; respectively. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
indometacin | down-regulates activity
chemical inhibition
|
PTGS2 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258606 |
|
|
in vitro |
|
| pmid |
sentence |
| 9057869 |
Naproxen had similar activity against both COX-1 and COX-2 enzymes (IC50s of 3.2 and 2.5 μM, respectively), whereas ibuprofen was approximately 100-fold more potent for COX-2 (IC50 = 0.1 μM) than for COX-1 (IC50 = 11 μM), and indomethacin was about 50-fold more potent for COX-1 (IC50 = 0.012 μM) than for COX-2 (IC50 = 0.56 μM). |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261089 |
|
|
Rattus norvegicus |
|
| pmid |
sentence |
| 15770365 |
Indomethacin, a nonselective cyclooxygenase inhibitor, may prevent AAA formation by inhibiting cyclooxygenase-2 (COX-2) activity. |
|
| Publications: |
2 |
Organism: |
In Vitro, Rattus Norvegicus |
| Tissue: |
Aorta |
| + |
PTGS2 | up-regulates quantity
chemical modification
|
prostaglandin E2(1-) |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255684 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16540375 |
Arachidonic acid is transformed into PGE2 via cyclooxygenase (COX) enzymes and terminal prostaglandin E synthases (PGES) |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML |
| + |
AML1-ETO | up-regulates quantity by expression
transcriptional regulation
|
PTGS2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255683 |
|
|
Mus musculus |
Bone Marrow Cell |
| pmid |
sentence |
| 23645839 |
AML1-ETO (AE) is an oncogene that plays an important role in inducing self-renewal of hematopoietic stem/progenitor cells (HSPCs), leading to the development of leukemia stem cells. Here, we show that AE also induces expression of the Cox-2 gene and activates β-catenin in mouse bone marrow cells. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML |
| + |
PTGS2 | up-regulates
|
MYOD1 |
0.269 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256214 |
|
|
Homo sapiens |
Skeletal Muscle |
| pmid |
sentence |
| 20219869 |
Furthermore, COX-2 inhibition reduced MyoD expression in regenerating muscle, suggesting a role for COX-2 in modulating muscle differentiation, as well as growth |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PTGS2 | up-regulates quantity
chemical modification
|
prostaglandin G2(1-) |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269770 |
|
|
in vitro |
|
| pmid |
sentence |
| 7592599 |
[14C]Arachidonate metabolism by oPGHS-1 and hPGHS-2 was examined in reactions with a series of GSP/Cox ratios (Fig. 3). The principal metabolite for both isoforms was the endoperoxide PGH2, with lesser amounts of PGF2a, PGE2, PGD2, |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
SRF | up-regulates
|
PTGS2 |
0.256 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255965 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22225874 |
Srf within myofibers modulates Il6 and Cox2/Il4 expressions and, therefore, exerts a paracrine control of satellite cell proliferation and fusion, respectively, which in turn support skeletal muscle hypertrophy. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NFATC1 | up-regulates quantity by expression
transcriptional regulation
|
PTGS2 |
0.326 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-264026 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21871017 |
NFAT induces the transcription of the COX2 (cyclo-oxygenase-2) gene incancer cells thereby enhancing invasive migration |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PTGS2 | up-regulates
|
IL4 |
0.464 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255967 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22225874 |
Cox2 Is a Direct Srf Target Gene and Controls Il4 Expression |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ketoprofen | down-regulates activity
chemical inhibition
|
PTGS2 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-257811 |
|
|
Homo sapiens |
PC-3 Cell |
| pmid |
sentence |
| 18667313 |
Profens, that is, Ketoprofen 1, Suprofen 2 (Fig. 1), were chosen because of their interesting inhibitory activity against cyclooxygenase and of their different selectivity versus the two isoforms COX-1/COX-2. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NFATC3 | up-regulates quantity by expression
transcriptional regulation
|
PTGS2 |
0.285 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-264028 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21871017 |
NFAT induces the transcription of the COX2 (cyclo-oxygenase-2) gene incancer cells thereby enhancing invasive migration |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
celecoxib | down-regulates
chemical inhibition
|
PTGS2 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-190928 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PTGS2 | up-regulates
chemical modification
|
Prostacycline |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-113300 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11751058 |
Cox catalyzes two enzymatic activities;namely, the conversion of aa to the hydroperoxy endoperoxide pgg2, followed by its subsequent reduction to the labile product pgh2. Pgh2_ is the common substrate for a number of different cell-specific synthases, which convert pgh2_ to the individual pgs or tx, including pge2, pgi2_ (prostacyclin), pgd2, pgf2alfa, and txa2 |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
Pravadoline | down-regulates
chemical inhibition
|
PTGS2 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-206322 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
S | up-regulates activity
transcriptional regulation
|
PTGS2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-262315 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17267381 |
Spike protein of SARS‐CoV activated COX‐2 expression in a protein concentration‐dependent manner |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | SARS-CoV INFLAMMATORY RESPONSE |
| + |
N | up-regulates activity
transcriptional regulation
|
PTGS2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-262314 |
|
|
Homo sapiens |
HEK-293T Cell |
| pmid |
sentence |
| 16546436 |
SARS-CoV N protein activates COX-2 promoter and induces COX-2 protein expression |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | SARS-CoV INFLAMMATORY RESPONSE |
| + |
naproxen | down-regulates activity
chemical inhibition
|
PTGS2 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258602 |
|
|
in vitro |
|
| pmid |
sentence |
| 9057869 |
Naproxen had similar activity against both COX-1 and COX-2 enzymes (IC50s of 3.2 and 2.5 μM, respectively), whereas ibuprofen was approximately 100-fold more potent for COX-2 (IC50 = 0.1 μM) than for COX-1 (IC50 = 11 μM), and indomethacin was about 50-fold more potent for COX-1 (IC50 = 0.012 μM) than for COX-2 (IC50 = 0.56 μM). |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
PTGS2 | down-regulates 
|
GSK3B |
0.424 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-141783 |
|
|
Homo sapiens |
Colonic Cancer Cell |
| pmid |
sentence |
| 16293724 |
We show that pge2 stimulates colon cancer cell growth through its heterotrimeric guanine nucleotide-binding protein (g protein)coupled receptor, ep2, by a signaling route that involves the activation of phosphoinositide 3-kinase and the protein kinase akt by free g protein bg subunits and the direct association of the g protein as subunit with the regulator of g protein signaling (rgs) domain of axin. This leads to the inactivation and release of glycogen synthase kinase 3b from its complex with axin, thereby relieving the inhibitory phosphorylation of b-catenin and activating its signaling pathway. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia |
| + |
PTGS2 | up-regulates quantity
chemical modification
|
prostaglandin H2(1-) |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269776 |
|
|
in vitro |
|
| pmid |
sentence |
| 7592599 |
[14C]Arachidonate metabolism by oPGHS-1 and hPGHS-2 was examined in reactions with a series of GSP/Cox ratios (Fig. 3). The principal metabolite for both isoforms was the endoperoxide PGH2, with lesser amounts of PGF2a, PGE2, PGD2, |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
piroxicam | down-regulates activity
chemical inhibition
|
PTGS2 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258608 |
|
|
in vitro |
|
| pmid |
sentence |
| 9083488 |
Meloxicam (5),an NSAID in the enol−carboxamide class, was developed on the basis of its antiinflammatory activity and relative safety in animal models. This favorable therapeutic index has been confirmed in clinical trials. In subsequent studies we and others discovered that it possessed a selectivity profile for COX-2 superior to several other marketed NSAIDs.1 A comparison of 5 with piroxicam (6) revealed different inhibitory profiles for the two enzymes |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
meloxicam | down-regulates activity
chemical inhibition
|
PTGS2 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258609 |
|
|
in vitro |
|
| pmid |
sentence |
| 9083488 |
Meloxicam (5),an NSAID in the enol−carboxamide class, was developed on the basis of its antiinflammatory activity and relative safety in animal models. This favorable therapeutic index has been confirmed in clinical trials. In subsequent studies we and others discovered that it possessed a selectivity profile for COX-2 superior to several other marketed NSAIDs.1 A comparison of 5 with piroxicam (6) revealed different inhibitory profiles for the two enzymes |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
NFATC4 | up-regulates quantity by expression
transcriptional regulation
|
PTGS2 |
0.288 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-264027 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21871017 |
NFAT induces the transcription of the COX2 (cyclo-oxygenase-2) gene incancer cells thereby enhancing invasive migration |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
paracetamol | down-regulates activity
chemical inhibition
|
PTGS2 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-257757 |
|
|
Homo sapiens |
Monocyte |
| pmid |
sentence |
| 17884974 |
Acetaminophen (paracetamol) is a selective cyclooxygenase-2 inhibitor in man |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PTGS2 | down-regulates quantity
chemical modification
|
episterol ester |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-264270 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19126760 |
After biosynthesis, 2-AG is partially degraded by postsynaptic COX-2, and partly released to the extracellular space.  |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
IRX1 | up-regulates quantity by expression
transcriptional regulation
|
PTGS2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261662 |
|
|
Homo sapiens |
SGC-7901 Cell |
| pmid |
sentence |
| 20440264 |
We identified a number of target genes by global microarray analysis after IRX1 transfection combined with real-time PCR and chromatin immunoprecipitation assay.| Upregulation of PTGS2, ANPEP, KDR, UGT8, INHBA, ERMAP, RALGPS1 and SPON1 was confirmed. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
arachidonic acid | up-regulates
|
PTGS2 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255394 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15878913 |
AA increases PC-3 prostate tumor cell growth, total DNA content and endogenous PGE 2 levels via induction of c-fos , cPLA 2 and cox-2 mRNA transcription. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
3.0
PTGS2
- 
- 