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albuquerque2009 v1.0.0

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

In-Edges 5

a(MESH:"Anti-Inflammatory Agents, Non-Steroidal") decreases act(p(HGNC:PTGS1)) 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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a(PUBCHEM:135316034) decreases p(HGNC:PTGS1) 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

a(PUBCHEM:135316034) decreases p(HGNC:PTGS1) 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

path(MESH:"Alzheimer Disease") increases p(HGNC:PTGS1) 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

path(MESH:Atherosclerosis) increases p(HGNC:PTGS1) 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

Out-Edges 1

act(p(HGNC:PTGS1)) 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

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BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

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.