4.4.1.20: leukotriene-C4 synthase
This is an abbreviated version!
For detailed information about leukotriene-C4 synthase, go to the full flat file.
Word Map on EC 4.4.1.20
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4.4.1.20
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asthma
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lta4
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cysteinyl
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5-lipoxygenase
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arachidonic
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eosinophil
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asthmatic
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flap
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bronchial
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eicosanoids
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aspirin
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cysteinyl-leukotrienes
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cys-lts
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cysltr1
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aspirin-induced
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bronchoconstriction
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5-lipoxygenase-activating
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aspirin-intolerant
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alox5ap
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montelukast
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1-chloro-2,4-dinitrobenzene
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mapeg
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aspirin-exacerbated
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rbl-1
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medicine
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bronchoconstrictors
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a23187-stimulated
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molecular biology
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drug development
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analysis
- 4.4.1.20
- asthma
- lta4
-
cysteinyl
-
5-lipoxygenase
-
arachidonic
-
eosinophil
-
asthmatic
- flap
- bronchial
-
eicosanoids
- aspirin
- cysteinyl-leukotrienes
-
cys-lts
-
cysltr1
-
aspirin-induced
-
bronchoconstriction
-
5-lipoxygenase-activating
-
aspirin-intolerant
-
alox5ap
- montelukast
- 1-chloro-2,4-dinitrobenzene
-
mapeg
-
aspirin-exacerbated
- rbl-1
- medicine
-
bronchoconstrictors
-
a23187-stimulated
- molecular biology
- drug development
- analysis
Reaction
Synonyms
(7E,9E,11Z,14Z)-(5S,6S)-5,6-epoxyicosa-7,9,11,14-tetraenoate:glutathione leukotriene-transferase (epoxide-ring-opening), EC 2.5.1.37, leukotriene A4:glutathione S-leukotrienyltransferase, leukotriene C4 synthase, leukotriene C4 synthetase, LT C4 synthase, LTC4 synthase, LTC4 synthetase, LTC4S, LTCS, synthase, leukotriene C4
ECTree
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analysis
drug development
medicine
molecular biology
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
analysis
cell-free and cell-based assay systems based on in situ-generated LTA4 that allow studying LTC4S activity and investigating LTC4S inhibitors
leukotrienes are an important therapeutic target in asthma and inflammatory diseases
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
aspirin induced urticaria aggregates in families inheriting the LTC4S -444C allele
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
medicine
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sodium nitroprusside inhibits leukotriene C4 synthase activity and dwonregulates the protein expression of the enzyme
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
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
medicine
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the C allele of the A-444C polymorphism is a risk factor for aspirin-induced urticaria in a Venezuelan population and may be a genetic marker for this phenotype. This single-nucleotide polymorphism is mainly associated with the cutaneous clinical pattern and with low skin response to histamine
medicine
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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
medicine
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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
medicine
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sodium nitroprusside inhibits leukotriene C4 synthase activity and dwonregulates the protein expression of the enzyme
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the third hydrophobic region, containing a putative transmembrane helix, acts as a nuclear envelope localization signal and is involved in the homooligomerization of LTC4S
molecular biology
TNF-alpha exposure downregulates the LTC4 synthase gene expression in monocytes/macrophages via a transcriptional mechanism
molecular biology
TNF-alpha exposure downregulates the LTC4 synthase gene expression in monocytes/macrophages via a transcriptional mechanism
molecular biology
transient transfection into human monocytic leukemia (THP-1), rat basophilic leukemia (RBL-1), and human embryonic kidney (HEK293/T) epithelial cells show that eGFP was expressed by cells which express leukotriene C4 synthase (RBL-1 and THP-1) but not by the leukotriene C4 synthase negative HEK293/T cells