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
Advanced search results
Engineering
Engineering on EC 4.4.1.20 - leukotriene-C4 synthase
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A444C
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the mutation is associated with the risk of ischemic cerebrovascular disease
A52S
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mutation increases the Km-value for the recombinant enzyme for glutathione
C56S
E4K
causes allergic diseases in patients such as bronchial asthma or allergic dermatitis
G1072A
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the mutation is associated with the risk of ischemic cerebrovascular disease
L121M
by site-directed mutagenesis to prepare the selenomethionine-substituted LTC4S, the mutant yeast clone is grown with selenomethionine, purified and crystallized similarly to the wild-type enzyme
LTCS(1-115)
C-terminally truncated protein, gives a bioluminescence resonance energy transfer signal when fused to Renilla luciferase
LTCS(1-24)
C-terminally truncated protein, gives no bioluminescence resonance energy transfer signal when fused to Renilla luciferase
LTCS(1-58)
C-terminally truncated protein, gives no bioluminescence resonance energy transfer signal when fused to Renilla luciferase
LTCS(1-88)
C-terminally truncated protein, gives a bioluminescence resonance energy transfer signal when fused to Renilla luciferase
LTCS(114-150)
N-terminally truncated protein, gives a bioluminescence resonance energy transfer signal when fused to Renilla luciferase
LTCS(23-115)
C- and N-terminally truncated protein, gives a bioluminescence resonance energy transfer signal when fused to Renilla luciferase
LTCS(23-150)
N-terminally truncated protein, gives a bioluminescence resonance energy transfer signal when fused to Renilla luciferase
LTCS(57-150)
N-terminally truncated protein, gives a bioluminescence resonance energy transfer signal when fused to Renilla luciferase
LTCS(87-150)
N-terminally truncated protein, gives a bioluminescence resonance energy transfer signal when fused to Renilla luciferase
N55A
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mutation increases the Km-value for the recombinant enzyme for glutathione
R104A
R104Q
substrate leukotriene A4, 2% of wild-type activity. No activity with substrate leukotriene A4 methyl ester
R31A
R31Q
R51I
R90A
substrate leukotriene A4, 6% of wild-type activity, substrate leukotriene A4 methyl ester, 21% ot wild-type activity
S36E
phosphomimetic mutant, displays about 20 % of wild-type activity. Mutant shows poor lipid substrate binding
V49F
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mutation increases the Km-value for the recombinant enzyme for glutathione
W116A
site-directed mutagenesis, altered kinetics compared to the wild-type enzyme
W116F
site-directed mutagenesis, the mutant shows a 3fold increased turnover of leukotriene A4 compared to the wild-type enzyme
Y59F
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mutation increases the Km-value for the recombinant enzyme for glutathione
Y93F
Y97F
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mutation increases the Km-value for the recombinant enzyme for glutathione
additional information
R104A
substrate leukotriene A4, 2% of wild-type activity. No activity with substrate leukotriene A4 methyl ester
R31A
substrate leukotriene A4, 6% of wild-type activity. No activity with substrate leukotriene A4 methyl ester
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mutation increases the Km-value for the recombinant enzyme for glutathione
Y93F
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activity of the mutant enzyme is less than 1% of the wild-type enzyme, shift in pH optimum of the residual activity to that of spontaneous conjugation
Y93F
reduces the enzyme activity to less than 1% of the wild-type enzyme, shift in the pH-optimum
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the LTC4S2 variant in LTC4 confers a 1.807fold increase in stroke when present at 2 copies, whereas the LTBR_2 variant in the LTB4R/LTB4R2 gene region confers a 1.671fold increase in stroke risk when present at 1 or more copies, LTBR_2 and LTBR_6, confer relative risks of 2.371 and 2.081 in cardioembolic stroke, variants in leukotriene C4 synthase confer a 1.5fold increase in risk of small vessel disease
additional information
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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