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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
Chemical Compound Review

CHEBI:63989     (5Z,8Z,11Z,13E,15R)-15- hydroxyicosa-5,8,11...

Synonyms: CHEBI:104378, LMFA03060030, AC1NR1OH, 15R-HETE
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High impact information on LMFA03060030

  • In addition, aspirin-treated enterocytes generated 15R-HETE, a precursor of 15-epi-LXA4 biosynthesis, whose potent bioactions were mimicked by the stable analog 15R/S-methyl-LXA4 [1].
  • Remarkably, aspirin-treated COX-2 formed 15R-HETE with removal of the pro-S hydrogen at C-13 (3-9% retention of pro-S tritium label), the same stereoselectivity as in the formation of prostaglandins by native cyclooxygenase [2].
  • The acetylated COX-2 remains active, and upon cell activation, initiates the generation of 15R-HETE, a lipid substrate for 5-lipoxygenase (LOX) leading to the formation of 15-epi-LXA4 (also termed "aspirin-triggered lipoxin," or ATL) [3].

Biological context of LMFA03060030


Gene context of LMFA03060030

  • To understand the changes that lead to 15R-HETE synthesis in aspirin-treated COX-2, we employed pro-R- and pro-S-labeled [13-(3)H]arachidonic acids to investigate the selectivity of the initial hydrogen abstraction [2].


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