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EC Number General Information Commentary Reference
Show all pathways known for 3.4.19.14Display the word mapDisplay the reaction diagram Show all sequences 3.4.19.14malfunction disruption of gamma-glutamyl leukotrienase (GGL) results in disruption of leukotriene D4 synthesis in vivo and attenuation of the acute inflammatory response. In spleen and uterus, deletion of GGL alone abolishes more than 90% of leukotriene D4 synthesis activity. Mice deficient in both gamma-glutamyl transpeptidase (GGT) and GGL have a phenotype similar to the GGT-deficient mice, but about 70% of these mice die before 4 weeks of age, at least 2 months earlier than mice deficient only in GGT. GGL-deficient mice show an attenuation in neutrophil recruitment but not of plasma protein influx 718108
Show all pathways known for 3.4.19.14Display the word mapDisplay the reaction diagram Show all sequences 3.4.19.14malfunction gamma-glutamyl leukotrienase-deficient mice show leukotriene C4 accumulation and significantly more airway hyperreponsiveness than wild-type mice in the experimental asthma 717066
Show all pathways known for 3.4.19.14Display the word mapDisplay the reaction diagram Show all sequences 3.4.19.14physiological function in vivo gamma-glutamyl leukotrienase, and notgamma-glutamyl transpeptidase, is primarily responsible for conversion of leukotriene C4 to leukotriene D4. The enzyme plays an important role in inflammatory processes 717066
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