Figure 1
Figure 1. Vitamin K cycle. Vitamin K hydroquinone (KH2) is oxidized to vitamin K epoxide (KO) by the vitamin K-dependent γ-glutamyl carboxylase (GGCX) with concomitant carboxylation of glutamic acid to γ-carboxyglutamic acid (GLA) in PT and other vitamin K–dependent proteins. VKOR uses electrons from a thioredoxin-like protein dithiol to reduce vitamin K epoxide to vitamin K quinone (K) and then vitamin K hydroquinone to complete the vitamin K cycle. VKOR is sensitive to inhibition by warfarin, brodifacoum, and other vitamin K antagonists. A NADPH-dependent pathway catalyzed by NQO1 and related enzymes may help to rescue blood coagulation after coumarin poisoning. NAD(P)+, NAD phosphate.

Vitamin K cycle. Vitamin K hydroquinone (KH2) is oxidized to vitamin K epoxide (KO) by the vitamin K-dependent γ-glutamyl carboxylase (GGCX) with concomitant carboxylation of glutamic acid to γ-carboxyglutamic acid (GLA) in PT and other vitamin K–dependent proteins. VKOR uses electrons from a thioredoxin-like protein dithiol to reduce vitamin K epoxide to vitamin K quinone (K) and then vitamin K hydroquinone to complete the vitamin K cycle. VKOR is sensitive to inhibition by warfarin, brodifacoum, and other vitamin K antagonists. A NADPH-dependent pathway catalyzed by NQO1 and related enzymes may help to rescue blood coagulation after coumarin poisoning. NAD(P)+, NAD phosphate.

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