1.17.4.5: vitamin-K-epoxide reductase (warfarin-insensitive)
This is an abbreviated version!
For detailed information about vitamin-K-epoxide reductase (warfarin-insensitive), go to the full flat file.
Word Map on EC 1.17.4.5
-
1.17.4.5
-
anticoagulant
-
coagulation
-
k-dependent
-
carboxylase
-
non-hepatic
-
4-hydroxycoumarins
-
dosing
-
warfarin-resistant
-
vkorc1
-
2,3-epoxide
-
clotting
-
s-warfarin
-
pharmacogenetic
-
dithiothreitol-dependent
-
scottish
-
rodenticide
- 1.17.4.5
-
anticoagulant
-
coagulation
-
k-dependent
- carboxylase
-
non-hepatic
- 4-hydroxycoumarins
-
dosing
-
warfarin-resistant
- vkorc1
- 2,3-epoxide
-
clotting
-
s-warfarin
-
pharmacogenetic
-
dithiothreitol-dependent
-
scottish
-
rodenticide
Reaction
Synonyms
EC 1.1.4.2, non-VKOR, reductase, vitamin K epoxide (warfarin-insensitive), vitamin K 2,3 epoxide reductase, vitamin K epoxide reductase, vitamin K epoxide reductase (warfarin-insensitive), vitamin K epoxide reductase-like1, vitamin KO reductase, VKOR, VKOR-like1, VKORC1L1, VKORL1
ECTree
Advanced search results
General Information
General Information on EC 1.17.4.5 - vitamin-K-epoxide reductase (warfarin-insensitive)
Please wait a moment until all data is loaded. This message will disappear when all data is loaded.
evolution
VKORL1, EC 1.1.4.2, is more highly conserved among vertebrates than its evolutionary relative VKOR, EC 1.1.4.1. The human paralogous proteins are 42-60% identical
physiological function
vitamin K dependent oxidative protection is independent of VKOR inhibition by warfarin and GGCX inhibition by 2-chloro-vitamin K1, which indicates that vitamin K plays potential physiological roles outside of the realm of carboxylation. The hVKORL1 turnover rate for vitamin K 2,3-epoxide reductase activity is significantly slower than for hVKOR, EC 1.1.4.1. the physiological role for VKORL1 reduction of vitamin K 2,3-epoxide is minimal
additional information
-
conserved loop cysteines in VKOR are not required for active site regeneration after each cycle of oxidation. Missense mutations identified in the VKOR coding region, especially hotspot mutation at position 139, lead to a VKOR molecule more resistant to warfarin inhibition, thus requiring higher therapeutic warfarin doses