EC Number   |
Application |
Reference |
|---|
    4.4.1.20 | analysis |
although structural differences near the active site and along the C-terminal alpha-helix V suggest that the mouse and human enzymes may function differently in vivo, the mouse enzyme is a useful tool in pharmacological research and drug development |
730788 |
| 4.4.1.20 | analysis |
cell-free and cell-based assay systems based on in situ-generated LTA4 that allow studying LTC4S activity and investigating LTC4S inhibitors |
747181 |
| 4.4.1.20 | drug development |
although structural differences near the active site and along the C-terminal alpha-helix V suggest that the mouse and human enzymes may function differently in vivo, the mouse enzyme is a useful tool in pharmacological research and drug development |
730788 |
| 4.4.1.20 | drug development |
leukotrienes are an important therapeutic target in asthma and inflammatory diseases |
665848 |
| 4.4.1.20 | medicine |
(-1072)GNA and (-444)ANC promoter polymorphisms of LTC4 synthase influence risk of transient ischemic attack and ischemic stroke, but not risk of ischemic heart disease/coronary atherosclerosis, asthma, or chronic obstructive pulmonary disease in a Danish population. The (-1072)A allele has a frequency of 0.07 while the (-444)C allele has a frequency of 0.29. The (-1072)A and (-444)C alleles are on different haplotypes, thus one polymorphism cannot tag the other. Genetically altered leukotriene C4 synthase activity may play a role in thrombi formation rather than the development of atherosclerosis |
709560 |
| 4.4.1.20 | medicine |
aspirin desensitization may provide effective therapy for aspirin-exacerbated respiratory disease, at least in part, through mitigation of STAT6 expression, thereby downregulating LTC4S pathways |
708859 |
| 4.4.1.20 | medicine |
aspirin induced urticaria aggregates in families inheriting the LTC4S -444C allele |
678958 |
| 4.4.1.20 | medicine |
damaged or inflamed bronchial epithelium may synthesize leukotrienes that contribute directly to bronchoconstriction and leucocytosis in airway inflammation, LTC4 synthase is constitutively expressed in primary bronchial epithelial cells and in the 16-HBE 14o-cell line |
679295 |
| 4.4.1.20 | medicine |
mRNA levels for the three key enzymes/proteins in the biosynthesis of cysteinyl-leukotrienes, 5-lipoxygenase, 5-LO-activating protein, and LTC4 synthase, are significantly increased in the wall of human abdominal aortic aneurysm. Immunohistochemical staining reveals focal expression of 5-lipoxygenase, 5-LO-activating protein, and LTC4 synthase proteins in the media and adventitia, localized in areas rich in inflammatory cells, including macrophages, neutrophils, and mast cells. Challenge of abdominal aortic aneurysm wall tissue with exogenous LTD4 increases the release of matrix metalloproteinases 2 and 9, and selective inhibition of the CysLT1 receptor by montelukast blocks this effect |
716764 |
| 4.4.1.20 | medicine |
resequencing the gene coding for leukotriene C4 synthase in an population with extreme risk of venous thromboembolism, ischemic stroke and myocardial infarction, among more than 1500 individuals, reveals 17 unknown mutations, of which four are likely to change protein function, i.e. 211G>A, with minor allele frequency, IVS3 + 1G>A, 374G>A and 451_453+10del. Age and sex adjusted odds ratios for venous thromboembolism are 2.0 for IVS3+1G>A heterozygotes versus wild-type, and 1.9 for any mutation heterozygote versus wild-type. Corresponding values are 2.0 and 1.5 for ischemic stroke, and 1.0 and 1.2 for myocardial infarction |
716061 |
