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Literature summary for 1.1.1.141 extracted from

  • Yang, L.; Amann, J.M.; Kikuchi, T.; Porta, R.; Guix, M.; Gonzalez, A.; Park, K.H.; Billheimer, D.; Arteaga, C.L.; Tai, H.H.; DuBois, R.; Carbone, D.P.; Johnson, D.H.
    Inhibition of epidermal growth factor receptor signaling elevates 15-hydroxyprostaglandin dehydrogenase in non-small-cell lung cancer (2007), Cancer Res., 67, 5587-5593.
    View publication on PubMed
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Activating Compound

Activating Compound Comment Organism Structure
erlotinib epidermal growth factor receptor tyrosine kinase inhibitor, trreatment of cells increases the expression of the enzyme in a subset of non-small-cell lung cancer lines Homo sapiens

Application

Application Comment Organism
medicine in non-small-cell lung cancer cells, i.e. NSCLC cells, much lower expression of 15-hydroxyprostaglandin dehydrogenase in all histologic groups compared with healthy lung cell. Treatment with the epidermal growth factor receptor tyrosine kinase inhibitor erlotinib increases the expression of the enzyme in a subset of NSCLC lines Homo sapiens

Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
additional information Homo sapiens 15-hydroxyprostaglandin dehydrogenase may be repressed by an epigenetic mechanism involving histone deacetylation, resulting in increased prostaglandin E2 activity in tumors ?
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 ?

Organism

Organism UniProt Comment Textmining
Homo sapiens
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Source Tissue

Source Tissue Comment Organism Textmining
lung
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 Homo sapiens
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non-small cell lung cancer cell NSCLC cell, much lower expression of 15-hydroxyprostaglandin dehydrogenase in all NSCLC histologic groups compared with healthy lung cell. Treatment with the epidermal growth factor receptor tyrosine kinase inhibitor erlotinib increases the expression of the enzyme in a subset of NSCLC lines Homo sapiens
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Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
additional information 15-hydroxyprostaglandin dehydrogenase may be repressed by an epigenetic mechanism involving histone deacetylation, resulting in increased prostaglandin E2 activity in tumors Homo sapiens ?
-
 ?