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p(HGNC:PTGS2)

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Entity

Name
PTGS2
Namespace
hgnc
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

Appears in Networks 5

albuquerque2009 v1.0.0

This file encodes the article Mammalian Nicotinic Acetylcholine Receptors: From Structure to Function by Albuquerque et al, 2009

Anatabine ameliorates experimental autoimmune thyroiditis. v1.0.0

Oxidative stress in health and disease: The therapeutic potential of Nrf2 activation v1.0.0

Phytochemicals as inhibitors of NF-κB for treatment of Alzheimer’s disease v1.0.0

Upstream regulators and downstream effectors of NF-κBinAlzheimer's disease v1.0.0

In-Edges 20

a(MESH:"Anti-Inflammatory Agents, Non-Steroidal") decreases act(p(HGNC:PTGS2)) View Subject | View Object

NSAIDs [e.g., drugs such as ibuprofen and NS398 (celecoxib or Celebrex)] antagonize to varying degrees two related cyclooxygenase (Cox) enzymes, Cox1 and Cox2 (also termed, prostaglandin-endoperoxide synthase 2), that are rate-limiting in converting arachidonic acid to prostaglandin H2, a precursor to many additional prostaglandins (for review, see Ref. 436). PubMed:19126755

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Text Location
Review

p(HGNC:CHRNA4) association p(HGNC:PTGS2) View Subject | View Object

A link between alpha4 nAChRs and Cox2 was suggested by the observation that interneurons in the hippocampus coexpress both proteins (165). A mechanistic connection was inferred when long-term treatment of aged animals with NS398 promoted retention of alpha4 nAChR expression in the brain, an effect that was antagonized by the coadministration of nicotine. PubMed:19126755

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Text Location
Review

a(CHEBI:Anatabine) decreases p(HGNC:PTGS2) View Subject | View Object

Anatabine suppressed in a dose- dependent manner the increase of iNOS and COX2 in- duced by interferon-g (Fig.4),confirming in vitro its antiinflammatory properties. The effect seen with inter- feron-g was also seen when macrophages were stimulated with lipopolysaccharide (Supplemental Fig. 1). PubMed:22807490

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p(HGNC:IFNG) increases p(HGNC:PTGS2) View Subject | View Object

Anatabine suppressed in a dose- dependent manner the increase of iNOS and COX2 in- duced by interferon-g (Fig.4),confirming in vitro its antiinflammatory properties. The effect seen with inter- feron-g was also seen when macrophages were stimulated with lipopolysaccharide (Supplemental Fig. 1). PubMed:22807490

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a(PUBCHEM:135316034) increases p(HGNC:PTGS2) View Subject | View Object

For example, 19 genes products have been associated with atherosclerosis and are up or down-regulated by Protandim. Of these 19 genes, the first 16 listed (84%) were regulated by Protandim in the opposing direction to that taken by the atherosclerosis disease process. The probable benefit of this effect of Protandim is further supported by the fact that of the 11 gene products currently being targeted by drug interventions (Table 1, in bold type), nine of them (Table 1, marked by asterisks) are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the therapeutic intervention. PubMed:22020111

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Annotations
MeSH
Atherosclerosis

a(PUBCHEM:135316034) increases p(HGNC:PTGS2) View Subject | View Object

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

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Annotations
MeSH
Alzheimer Disease

path(MESH:"Alzheimer Disease") increases p(HGNC:PTGS2) View Subject | View Object

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

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path(MESH:Atherosclerosis) increases p(HGNC:PTGS2) View Subject | View Object

For example, 19 genes products have been associated with atherosclerosis and are up or down-regulated by Protandim. Of these 19 genes, the first 16 listed (84%) were regulated by Protandim in the opposing direction to that taken by the atherosclerosis disease process. The probable benefit of this effect of Protandim is further supported by the fact that of the 11 gene products currently being targeted by drug interventions (Table 1, in bold type), nine of them (Table 1, marked by asterisks) are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the therapeutic intervention. PubMed:22020111

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a(CHEBI:"1,8-cineole") decreases p(HGNC:PTGS2) View Subject | View Object

Further-more, the expression of NOS-2, COX2 and NF-B was reduced by1,8-cineole [250]. PubMed:29179999

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a(CHEBI:curcumin) decreases p(HGNC:PTGS2) View Subject | View Object

Curcumin showed several anti-inflammatory characteristics. It deploys various cytokine-inhibitory, anti-inflammatory activities and decreases the expression levels of COX-2, LOX, and iNOS. Moreover, the expression of the pro-inflammatory cytokines, for instance, TNF-, IL-1, -2,-6, -8, and -12 and the neurotoxic factors were suppressed by curcumin in lipopolysaccharide (LPS)-stimulated monocytes and alveolar macrophages [103]. PubMed:29179999

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a(CHEBI:resveratrol) decreases p(HGNC:PTGS2) View Subject | View Object

Resveratrol crossed the blood-brain barrier (BBB) [111,112] and down-regulated several inflammatory biomarkers such as TNF-, COX2 and interleukins [113,114]. PubMed:29179999

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a(CHEBI:resveratrol) decreases p(HGNC:PTGS2) View Subject | View Object

It also lowered the expression of NO and iNOS, and prostaglandin E2 (PGE2) and COX2 in A-activated glial cells. All these effects were attributableto their suppression of nuclear NF-B translocation [116]. PubMed:29179999

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a(PUBCHEM:14193399) decreases p(HGNC:PTGS2) View Subject | View Object

Glaucocalyxin B, found in Rabdosia japonica, considerably atten-uated the expression of NO, TNF-, IL-1, COX-2 and iNOS in LPS-induced microglia cells [169–172]. Moreover, the activation of NF-B, p38 MAPK and ROS generation was interrupted by glauco- calyxin B in LPS-induced microglia cells [172]. PubMed:29179999

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Annotations
Cell Ontology (CL)
microglial cell

a(PUBCHEM:440312) decreases p(HGNC:PTGS2) View Subject | View Object

LPS-activated expression of pro-inflammatory and neurotoxic factors like NO, TNF-, PGE2, NO synthase and COX2 production and LOX activity were inhibited by dihydroasparagusic acid in microglia cells [243]. PubMed:29179999

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Annotations
Cell Ontology (CL)
microglial cell

a(PUBCHEM:44584733) decreases p(HGNC:PTGS2) View Subject | View Object

Punicalagin decreased the expression of COX2 and DNA binding of NF-B in human colon cancer cell line [126]. PubMed:29179999

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act(p(FPLX:NFkappaB)) regulates p(HGNC:PTGS2) View Subject | View Object

NF-B activation mediates the expression of the pro-oxidant NAPDH oxidase, cyclooxygenase 2 (COX2), interleukins and the antioxidant enzyme, superoxide dismutase (SOD) [78]. Additionally, NF-B activity is associated with the expression of BACE1 [79] and the activation of nucleotide-binding oligomerization domain-like receptor (NALP) 3 inflammosome [80]. PubMed:29179999

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a(CHEBI:"(+)-Tetrandrine") decreases p(HGNC:PTGS2) View Subject | View Object

Tetrandrine, is an herb-derived bisbenzylioquinoline alkaloid, may be a potent inhibitor of NF-κB activation and can inhibit the expression of iNOS and COX-2 which are involved in pro-inflammation. PubMed:27288790

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a(HBP:"amyloid-beta aggregates") association p(HGNC:PTGS2) View Subject | View Object

In addition, COX-2, mainly regulated by NF-κB, is notably upregulated in the brains of AD patients, which may be associated with the formation of Aβ plaque [65]. PubMed:27288790

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Annotations
MeSH
Brain

p(FPLX:NFkappaB) regulates p(HGNC:PTGS2) View Subject | View Object

In addition, COX-2, mainly regulated by NF-κB, is notably upregulated in the brains of AD patients, which may be associated with the formation of Aβ plaque [65]. PubMed:27288790

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path(MESH:"Alzheimer Disease") positiveCorrelation p(HGNC:PTGS2) View Subject | View Object

In addition, COX-2, mainly regulated by NF-κB, is notably upregulated in the brains of AD patients, which may be associated with the formation of Aβ plaque [65]. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Brain

Out-Edges 7

act(p(HGNC:PTGS2)) increases a(CHEBI:"prostaglandin H2") View Subject | View Object

NSAIDs [e.g., drugs such as ibuprofen and NS398 (celecoxib or Celebrex)] antagonize to varying degrees two related cyclooxygenase (Cox) enzymes, Cox1 and Cox2 (also termed, prostaglandin-endoperoxide synthase 2), that are rate-limiting in converting arachidonic acid to prostaglandin H2, a precursor to many additional prostaglandins (for review, see Ref. 436). PubMed:19126755

Appears in Networks:
Annotations
Text Location
Review

p(HGNC:PTGS2, loc(MESH:Neurons)) regulates path(MESH:"Neuronal Plasticity") View Subject | View Object

In the brain, however, Cox2 is constitutively expressed by neurons (212, 512), participates in modulating synaptic plasticity (53, 464), and conditionally can either inhibit or promote cell death (74, 85, 237, 322, 451). PubMed:19126755

Appears in Networks:
Annotations
MeSH
Brain
Text Location
Review

p(HGNC:PTGS2, loc(MESH:Neurons)) regulates bp(GO:"cell death") View Subject | View Object

In the brain, however, Cox2 is constitutively expressed by neurons (212, 512), participates in modulating synaptic plasticity (53, 464), and conditionally can either inhibit or promote cell death (74, 85, 237, 322, 451). PubMed:19126755

Appears in Networks:
Annotations
MeSH
Brain
Text Location
Review

p(HGNC:PTGS2) association p(HGNC:CHRNA4) View Subject | View Object

A link between alpha4 nAChRs and Cox2 was suggested by the observation that interneurons in the hippocampus coexpress both proteins (165). A mechanistic connection was inferred when long-term treatment of aged animals with NS398 promoted retention of alpha4 nAChR expression in the brain, an effect that was antagonized by the coadministration of nicotine. PubMed:19126755

Appears in Networks:
Annotations
Text Location
Review

p(HGNC:PTGS2) positiveCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

In addition, COX-2, mainly regulated by NF-κB, is notably upregulated in the brains of AD patients, which may be associated with the formation of Aβ plaque [65]. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Brain

p(HGNC:PTGS2) association a(HBP:"amyloid-beta aggregates") View Subject | View Object

In addition, COX-2, mainly regulated by NF-κB, is notably upregulated in the brains of AD patients, which may be associated with the formation of Aβ plaque [65]. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Brain

p(HGNC:PTGS2) increases path(MESH:Inflammation) View Subject | View Object

Tetrandrine, is an herb-derived bisbenzylioquinoline alkaloid, may be a potent inhibitor of NF-κB activation and can inhibit the expression of iNOS and COX-2 which are involved in pro-inflammation. PubMed:27288790

Appears in Networks:

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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.