ライフサイエンスコーパス: vitamin K

1 ylloquinone, the primary circulating form of vitamin K.

2 ificantly increased serum levels of oxidized vitamin K.

3 dustrial pollutant and the metabolic role of vitamin K.

4 ted the theory against published evidence on vitamin K.

5 physiological function other than recycling vitamin K.

6 lation at the physiological concentration of vitamin K.

7 olecule with a chemical structure similar to vitamin K.

8 rm the naphthoquinone ring of phylloquinone (vitamin K(1) ).

9 y acids, trans fatty acids, total fiber, and vitamins K(1), B(6), B(12), and E) were categorized into

10 , its regeneration is necessary and involves vitamin K 2,3-epoxide reductase (VKOR) activity.

11 using the "classical" dithiothreitol-driven vitamin K 2,3-epoxide reductase (VKOR) assay has not ref

12 h the p.Arg98Trp mutation results in reduced vitamin K 2,3-epoxide reductase activity, the molecular

13 Vitamin K 2,3-epoxide reductase complex subunit 1 (VKORC

14 Since the discovery of warfarin-sensitive vitamin K 2,3-epoxide reductase complex subunit 1 (VKORC

15 VKORC1 catalyzes the reduction of vitamin K 2,3-epoxide to vitamin K and to vitamin K hydr

16 patients and results in high serum levels of vitamin K 2,3-epoxide, suggesting that supplemented vita

17 were generated per glucose via a diaphorase-vitamin K(3) electron shuttle system at the anode).

18 s (antithrombin dabigatran etexilate or anti-vitamin K acenocoumarol) was started 2 days before inocu

19 s that mediate electron transport, including Vitamin K and Coenzyme Q.

20 es the reduction of vitamin K 2,3-epoxide to vitamin K and to vitamin K hydroquinone, the latter requ

21 e nutrients, including magnesium, potassium, vitamin K, and antioxidant and anti-inflammatory phytonu

22 uding tocopherol [vitamin E], phylloquinone [vitamin K] and plastoquinone) metabolism and contain a l

23 al Direct Factor Xa Inhibition Compared with Vitamin K Antagonism for Prevention of Stroke and Emboli

24 al Direct Factor Xa Inhibition Compared with Vitamin K Antagonism for Prevention of Stroke and Emboli

25 l, Direct Factor Xa Inhibition Compared With Vitamin K Antagonism for Prevention of Stroke and Emboli

26 al Direct Factor Xa Inhibition Compared with Vitamin K Antagonism for Prevention of Stroke and Emboli

27 l, Direct Factor Xa Inhibition Compared With Vitamin K Antagonism for Prevention of Stroke and Emboli

28 l, direct factor Xa inhibition Compared with vitamin K antagonism for prevention of stroke and Emboli

29 l, Direct Factor Xa Inhibition Compared With Vitamin K Antagonism for Prevention of Stroke and Emboli

30 l, direct factor Xa inhibition Compared with vitamin K antagonism for prevention of stroke and Emboli

31 l, Direct Factor Xa Inhibition Compared With Vitamin K Antagonism for Prevention of Stroke and Emboli

32 al Direct Factor Xa Inhibition Compared With Vitamin K Antagonism for Prevention of Stroke and Emboli

33 al Direct Factor Xa Inhibition Compared With Vitamin K Antagonism for Prevention of Stroke and Emboli

34 l, Direct Factor Xa Inhibition Compared With Vitamin K Antagonism for Prevention of Stroke and Emboli

35 Vitamin K antagonist (eg, warfarin) use is nowadays chal

36 of 301 patients allocated to enoxaparin and vitamin K antagonist (hazard ratio [HR] 0.67, 95% CI 0.3

37 2), or standard therapy with a dose-adjusted vitamin K antagonist (once daily) plus DAPT for 1, 6, or

38 ment with low-molecular-weight heparin and a vitamin K antagonist (RR, 0.67; 95% CI, 0.37-1.20; I2 =

39 and safety of adding antiplatelet therapy to vitamin K antagonist (VKA) in atrial fibrillation patent

40 Compared with vitamin K antagonist (VKA) in prevalent AF, VKA plus ant

41 ine, 37,539 patients (52%) were treated with vitamin K antagonist (VKA) monotherapy, 25,458 (35%) wit

42 The safety and effectiveness of non-vitamin K antagonist (VKA) oral anticoagulants, dabigatr

43 ry stenting traditionally are treated with a vitamin K antagonist (VKA) plus dual antiplatelet therap

44 Managing vitamin K antagonist (VKA) therapy is challenging in chi

45 omen treated with any of the following: 1) a vitamin K antagonist (VKA) throughout pregnancy; 2) low-

46 e increased risk of bleeding associated with vitamin K antagonist (VKA) treatment was particularly ev

47 s quality of anticoagulation control amongst vitamin K antagonist (VKA) users.

48 treatment regimen: triple therapy (TT) with vitamin K antagonist (VKA)+aspirin+clopidogrel, VKA+anti

49 Use of low-dose aspirin, clopidogrel, a vitamin K antagonist (VKA), a direct oral anticoagulant,

50 Rapid reversal of vitamin K antagonist (VKA)-induced anticoagulation is of

51 l anticoagulant (NOAC) who transitioned to a vitamin K antagonist (VKA).

52 (RFA) in comparison with uninterrupted oral vitamin K antagonist administration.

53 (1) ablation was performed under therapeutic vitamin K antagonist and heparin to maintain activated c

54 well-controlled vitamin K antagonists or non-vitamin K antagonist anticoagulants.

55 may at least not be worse than that of major vitamin K antagonist bleeding, and probably better.

56 ere 1.84% (95% CrI, 1.33%-2.51%) for the UFH-vitamin K antagonist combination and 1.30% (95% CrI, 1.0

57 However, findings suggest that the UFH-vitamin K antagonist combination is associated with the

58 bination, a treatment strategy using the UFH-vitamin K antagonist combination was associated with an

59 Compared with the LMWH-vitamin K antagonist combination, a treatment strategy u

60 h a lower risk of bleeding than was the LMWH-vitamin K antagonist combination, with a lower proportio

61 nd 0.89% (95% CrI, 0.66%-1.16%) for the LMWH-vitamin K antagonist combination.

62 nd 1.30% (95% CrI, 1.02%-1.62%) for the LMWH-vitamin K antagonist combination.

63 enous thromboembolism compared with the LMWH-vitamin K antagonist combination.

64 with enoxaparin followed by an adjusted-dose vitamin K antagonist for 3, 6, or 12 months.

65 If transition from rivaroxaban to vitamin K antagonist is needed, timely monitoring and ca

66 tion of an OAC with warfarin sodium or a non-vitamin K antagonist OAC.

67 44 (59.8%) were treated with warfarin or non-vitamin K antagonist OACs.

68 09 (61.8%) were treated with warfarin or non-vitamin K antagonist OACs.

69 predictive ability for bleeding, whether on vitamin K antagonist or not (c-statistic approximately 0

70 ence regarding ICH related to the use of non-vitamin K antagonist oral anticoagulant (NOAC) agents.

71 to determine if they are candidates for non-vitamin K antagonist oral anticoagulant (NOAC) therapy.

72 ticoagulation, either with warfarin or a non-vitamin K antagonist oral anticoagulant (NOAC), is indic

73 of rt-PA in patients who are receiving a non-vitamin K antagonist oral anticoagulant (NOAC).

74 It is unclear whether the non-vitamin K antagonist oral anticoagulant agents rivaroxab

75 In comparing the 2 non-vitamin K antagonist oral anticoagulant agents with each

76 Non-vitamin K antagonist oral anticoagulant drugs have recen

77 icular thrombus plus the availability of non-vitamin K antagonist oral anticoagulant drugs may lead t

78 Non-vitamin K antagonist oral anticoagulant-associated ICH h

79 The non-vitamin K antagonist oral anticoagulants (NOACs) apixaba

80 Current guidelines recommend non-vitamin K antagonist oral anticoagulants (NOACs) as the

81 Although non-vitamin K antagonist oral anticoagulants (NOACs) do not

82 farin) use is nowadays challenged by the non-vitamin K antagonist oral anticoagulants (NOACs) for str

83 These novel non-vitamin K antagonist oral anticoagulants (NOACs) have be

84 The use of non-vitamin K antagonist oral anticoagulants (NOACs) instead

85 Dose reduction of non-vitamin K antagonist oral anticoagulants (NOACs) is indi

86 NR] >/=2) and 8290 (8.8%) were receiving non-vitamin K antagonist oral anticoagulants (NOACs) precedi

87 There are now 4 new non-vitamin K antagonist oral anticoagulants (NOACs) that ar

88 Phase III trials comparing non-vitamin K antagonist oral anticoagulants (NOACs) with wa

89 Of patients given OAC, 17.2% received non-vitamin K antagonist oral anticoagulants (NOACs).

90 Non-vitamin K antagonist oral anticoagulants are expensive a

91 Specific reversal agents for non-vitamin K antagonist oral anticoagulants are lacking.

92 Whether the use of non-vitamin K antagonist oral anticoagulants could lower the

93 s enrolled in phase 3 clinical trials of non-vitamin K antagonist oral anticoagulants in prevention o

94 Low-thromboembolic-risk and/or non-vitamin K antagonist patient groups were used for compar

95 umber of patients managed with uninterrupted vitamin K antagonist phenprocoumon (international normal

96 nt bleeding than was standard therapy with a vitamin K antagonist plus DAPT for 1, 6, or 12 months.

97 t of stents, standard anticoagulation with a vitamin K antagonist plus dual antiplatelet therapy (DAP

98 concentrate (4F-PCC) with plasma for urgent vitamin K antagonist reversal.

99 e taking vitamin K antagonists require rapid vitamin K antagonist reversal.

100 OAC in AF patients, but with low quality of vitamin K antagonist therapy and insufficient adherence

101 Long-term vitamin K antagonist therapy can be complicated by unsta

102 alternative to plasma for urgent reversal of vitamin K antagonist therapy in major bleeding events, a

103 d-dose idraparinux with adjustable-dose oral vitamin K antagonist therapy in patients with AF.

104 tion in rivaroxaban participants switched to vitamin K antagonist therapy.

105 Results from this trial suggest that during vitamin K antagonist treatment INR monitoring could be r

106 Vitamin K antagonist use in the first trimester compared

107 nd it was amplified by diabetes and previous vitamin K antagonist use.

108 better efficacy and safety compared with the vitamin K antagonist warfarin for preventing strokes or

109 At the EOS visit, open-label vitamin K antagonist was recommended, and the internatio

110 initially for 6 uninterrupted months with a vitamin K antagonist were randomized and followed up bet

111 , usually overlapping with and followed by a vitamin K antagonist) for at least 3 months.

112 ompared with treatment with enoxaparin and a vitamin K antagonist, although there was no difference b

113 agulant followed by long-term therapy with a vitamin K antagonist, many clinical questions remain una

114 Vitamin K antagonist-treated patients receiving periproc

115 nsitioned from blinded therapy to open-label vitamin K antagonist.

116 tients Who Have Failed or Are Unsuitable for Vitamin-K Antagonist Treatment (AVERROES) trial and othe

117 r stroke, relative risk of stroke, and prior vitamin-K antagonist use in the life-time model.

118 Warfarin, a vitamin K "antagonist" used clinically for the preventio

119 including 907 patients with AF treated with vitamin K antagonists (3,865 patient-years), to assess C

120 difference was identified between NOACs and vitamin K antagonists (RR, 0.84; 95% CI, 0.59-1.19; I2 =

121 Overall, 43,299 AF patients initiating vitamin K antagonists (VKA) (42%), dabigatran (29%), riv

122 Vitamin K antagonists (VKA) have long been the default d

123 acy and bleeding outcomes in comparison with vitamin K antagonists (VKA) in elderly participants (age

124 rivaroxaban or apixaban or dabigatran versus vitamin K antagonists (VKA) in patients with venous thro

125 Vitamin K antagonists (VKA) use is challenging because o

126 Thromboprophylaxis can be obtained with vitamin K antagonists (VKA, eg, warfarin) or a non-VKA o

127 t strategies for intracerebral hemorrhage on vitamin K antagonists (VKA-ICH).

128 ality in intracranial haemorrhage related to vitamin K antagonists (VKA-ICH).

129 aban) are effective and safe alternatives to vitamin K antagonists (VKAs) and low-molecular-weight he

130 erm (>/=3 months) vs short-term therapy with vitamin K antagonists (VKAs) associated with differences

131 the efficacy and safety of the NOACs versus vitamin K antagonists (VKAs) for atrial fibrillation and

132 Vitamin K antagonists (VKAs) have been the standard of c

133 onist oral anticoagulants (NOACs) instead of vitamin K antagonists (VKAs) in patients with atrial fib

134 Bleeding risk with vitamin K antagonists (VKAs) is closely related to the q

135 Women receiving vitamin K antagonists (VKAs) require adequate contracept

136 ared a direct oral anticoagulant (DOAC) with vitamin K antagonists (VKAs).

137 e these drugs have several benefits over the vitamin K antagonists (VKAs).

138 Oral anticoagulants (both vitamin K antagonists [VKAs] and non-VKA oral anticoagul

139 vidence for adding aspirin to the regimen of vitamin K antagonists and clopidogrel seems to be weaken

140 t anticoagulation with specific guidance for vitamin K antagonists and direct-acting oral anticoagula

141 These drugs, which could replace vitamin K antagonists and heparins in many patients, are

142 aban, provide potential advantages over oral vitamin K antagonists and subcutaneous low-molecular-wei

143 ecular-weight heparin (LMWH) along with with vitamin K antagonists and the benefits and proven safety

144 sceptibility of some extrahepatic tissues to vitamin K antagonists and the lack of effects of vitamin

145 Vitamin K antagonists are also inhibitors of VKORC1L1, b

146 Vitamin K antagonists are commonly used by clinicians to

147 Vitamin K antagonists are highly effective in preventing

148 For example, vitamin K antagonists are the most efficacious for preve

149 Vitamin K antagonists are widely used as treatment of ve

150 anticoagulant therapy and have replaced the vitamin K antagonists as the preferred treatment for man

151 icoagulants, such as edoxaban, compared with vitamin K antagonists during extended therapy for venous

152 ving heparin bridging during interruption of vitamin K antagonists for elective procedures.

153 ew oral anticoagulants are poised to replace vitamin K antagonists for many patients with atrial fibr

154 NOACs) have been proposed as alternatives to vitamin K antagonists for the prevention of stroke and s

155 But vitamin K antagonists have limitations, including causin

156 ized, controlled trials comparing NOACs with vitamin K antagonists in patients with atrial fibrillati

157 risk in atrial fibrillation (AF) using oral vitamin K antagonists is closely related to bleeding ris

158 n vitro prediction of the in vivo potency of vitamin K antagonists is complicated by the complex mult

159 ndent proteins in patients not maintained on vitamin K antagonists is most commonly associated with p

160 vascular and renovascular calcification, and vitamin K antagonists may be associated with a decreased

161 min K antagonists and the lack of effects of vitamin K antagonists on the functionality of the vitami

162 ncreased risk of stroke with well-controlled vitamin K antagonists or non-vitamin K antagonist antico

163 OAC use, whether as well controlled vitamin K antagonists or nonvitamin K antagonists oral a

164 acteristics and natural history of acute non-vitamin K antagonists oral anticoagulants (NOAC)-associa

165 Anticoagulation with vitamin K antagonists reduces major thromboembolic compl

166 rial fibrillation, oral anticoagulation with vitamin K antagonists reduces the risk of stroke by more

167 nts experiencing major bleeding while taking vitamin K antagonists require rapid vitamin K antagonist

168 zyme appears to be 50-fold more resistant to vitamin K antagonists than VKORC1.

169 Until recently, vitamin K antagonists were the only available oral antic

170 For these reasons, we anticipate that the vitamin K antagonists will continue to be important anti

171 Although the use of oral anticoagulants (vitamin K antagonists) has been abandoned in primary car

172 scade either by an indirect mechanism (e.g., vitamin K antagonists) or by a direct one (e.g., the nov

173 py (low-molecular-weight heparin followed by vitamin K antagonists).

174 2) describe the advantages of the DOACs over vitamin K antagonists, (3) summarize the experience with

175 x concentrate in the nonemergent reversal of vitamin K antagonists, and limiting routine computed tom

176 lines recommended the use of triple therapy (vitamin K antagonists, aspirin, and clopidogrel) for the

177 vidually, NOACs were at least noninferior to vitamin K antagonists, but a clear superiority in overal

178 ACs were pooled to perform a comparison with vitamin K antagonists, calculating pooled relative risks

179 amiliarity with the dosing and monitoring of vitamin K antagonists, clinicians are accustomed to usin

180 Recent data suggest that BPVT responds to vitamin K antagonists, emphasizing the need for reliable

181 tcome measure was the use of anticoagulants (vitamin K antagonists, factor Xa inhibitors, and direct

182 roxaban compared with enoxaparin followed by vitamin K antagonists, in the subgroup of patients with

183 anticoagulants, with options including LMWH, vitamin K antagonists, or direct factor Xa or direct fac

184 Vitamin K antagonists, such as warfarin, are underused a

185 Vitamin K antagonists, such as warfarin, have been the m

186 nd clinical outcomes between NOAC-ICH versus vitamin K antagonists-ICH (VKA-ICH).

187 ng that has hindered usage and acceptance of vitamin K antagonists.

188 re can predict the patient's suitability for vitamin K antagonists.

189 n confined to long-term anticoagulation with vitamin K antagonists.

190 n inhibitors may represent an alternative to vitamin K antagonists.

191 and more particularly its susceptibility to vitamin K antagonists.

192 th an overall clinical benefit compared with vitamin K antagonists.

193 bolic events in patients receiving long-term vitamin K antagonists.

194 nts to have greater benefits than risks over vitamin K antagonists.

195 coagulated with a combination of aspirin and vitamin K antagonists.

196 (NOACs) that are attractive alternatives to vitamin K antagonists.

197 need to reverse the anticoagulant effect of vitamin K antagonists.

198 ion of a two-segment fluorogenic analogue of vitamin K, B-VKQ, prepared by coupling vitamin K3, also

199 served functional associations occur between vitamin K biosynthesis and NDC1 homologs throughout the

200 Higher vitamin K concentrations can restore up to 60% of coagul

201 n fecal menaquinone concentrations and serum vitamin K concentrations, gut microbiota composition, an

202 assigned patients in a 1:1 ratio to receive vitamin K concomitant with a single dose of either 4F-PC

203 1 (VKORC1) reduces vitamin K epoxide in the vitamin K cycle for post-translational modification of p

204 Thus, our understanding of the vitamin K cycle is only partial at the molecular level.

205 by the complex multicomponent nature of the vitamin K cycle.

206 RC1 and oral anticoagulant inhibition of the vitamin K cycle.

207 Vitamin K deficiency associated with lower relative cMGP

208 ceiving dialysis and examined the effects of vitamin K deficiency on MGP carboxylation.

209 In conclusion, vitamin K deficiency-mediated reduction in relative cMGP

210 ycles vitamin K to support the activation of vitamin K-dependent (VKD) proteins, which have diverse f

211 a-carboxylase for gamma-carboxylation of all vitamin K-dependent (VKD) proteins.

212 Protein C, a secretory vitamin K-dependent anticoagulant serine protease, inact

213 the bloodstream, Ad vectors can bind several vitamin K-dependent blood coagulation factors, which con

214 KORC1L1 reduces vitamin K epoxide to support vitamin K-dependent carboxylation as efficiently as does

215 reductase (VKOR) is an essential enzyme for vitamin K-dependent carboxylation, while the physiologic

216 quired for posttranslational modification of vitamin K-dependent clotting factors.

217 Vitamin K-dependent coagulation factors deficiency is a

218 bit calcification requires the activity of a vitamin K-dependent enzyme, which mediates MGP carboxyla

219 Analyses of vitamin K-dependent factors in 6 cancer patients with av

220 Vitamin K-dependent factors protect against vascular and

221 Protein S is a vitamin K-dependent glycoprotein, which, besides its ant

222 CDP is also related to disruption of vitamin K-dependent metabolism, causing secondary effect

223 in K antagonists on the functionality of the vitamin K-dependent protein produced by extrahepatic tis

224 anin-A[rs9658644], Cystatin-C[rs2424577] and Vitamin K-Dependent Protein S[rs6123] in the schizophren

225 Activation of Axl by its ligand Gas6, a vitamin K-dependent protein, is inhibited at doses of wa

226 TAM receptors can be activated by the vitamin K-dependent proteins Gas6 and protein S.

227 Severe deficiency of vitamin K-dependent proteins in patients not maintained

228 No binding of PTX2 to other vitamin K-dependent proteins was observed.

229 s involved in the gamma-carboxylation of the vitamin K-dependent proteins, and vitamin K epoxide is a

230 tamin K that is required for modification of vitamin K-dependent proteins.

231 n/phospholipid binding) for a Gla residue in vitamin K-dependent proteins.

232 eated zebrafish, which have decreased active vitamin K, display similar vascular degeneration as reh

233 bjects who increased their dietary intake of vitamin K during the follow-up had a 51% reduced risk of

234 The vitamin K epoxide (KO) product is recycled by two reacti

235 carboxylated reporter when fed vitamin K or vitamin K epoxide (KO).

236 reductase complex subunit 1 (VKORC1) reduces vitamin K epoxide in the vitamin K cycle for post-transl

237 ion of the vitamin K-dependent proteins, and vitamin K epoxide is a by-product of this reaction.

238 arfarin and other 4-hydroxycoumarins inhibit vitamin K epoxide reductase (VKOR) by depleting reduced

239 oralis, and revealed the essential role of a vitamin K epoxide reductase (VKOR) gene in pilus assembl

240 Vitamin K epoxide reductase (VKOR) is an essential enzym

241 Vitamin K epoxide reductase (VKOR) is essential for the

242 The intramembrane vitamin K epoxide reductase (VKOR) supports blood coagul

243 ts quiescin-sulfhydryl oxidase 1 (QSOX1) and vitamin K epoxide reductase (VKOR).

244 Using the mammalian membrane protein vitamin K epoxide reductase (VKORc1) as a reporter, we d

245 Vitamin K epoxide reductase complex subunit 1 (VKORC1) r

246 on its interaction with a splice variant of vitamin K epoxide reductase complex subunit 1 (VKORC1),

247 mented but uncharacterized splice variant of vitamin K epoxide reductase complex subunit 1 (VKORC1),

248 eviously uncharacterized ER membrane protein vitamin K epoxide reductase complex subunit 1 variant 2

249 ociates with a novel membrane protein termed vitamin K epoxide reductase complex subunit 1 variant 2

250 largely uncharacterized ER-resident protein vitamin K epoxide reductase complex subunit 1 variant 2

251 ctions of vIL-6 with the ER membrane protein vitamin K epoxide reductase complex subunit 1 variant 2

252 macromolecular interactions by inhibition of vitamin K epoxide reductase, cellular responses includin

253 We show that in vivo VKORC1L1 reduces vitamin K epoxide to support vitamin K-dependent carboxy

254 suggests novel roles for bacterially derived vitamin K forms known as menaquinones in health and dise

255 human and animal studies has suggested that vitamin K has a potentially beneficial role in glucose m

256 ex, and diet are determinants of circulating vitamin K; however, there is still large unexplained int

257 ation, which depends upon the oxygenation of vitamin K hydroquinone (KH2).

258 of vitamin K 2,3-epoxide to vitamin K and to vitamin K hydroquinone, the latter required by the enzym

259 agonists, clinicians are accustomed to using vitamin K if there is a need to reverse the anticoagulan

260 apid progression to end-stage liver disease, vitamin K-independent coagulopathy, low-to-normal serum

261 homeostasis; however, an alternative UBIAD1/vitamin K-independent pathway may regulate cardiac funct

262 to patient because of differences in dietary vitamin K intake, common genetic polymorphisms, and mult

263 Vitamin K is involved in the gamma-carboxylation of the

264 K 2,3-epoxide, suggesting that supplemented vitamin K is reduced in vivo.

265 methylation of the demethylated precursor of vitamin K is strictly dependent on the reduced form of i

266 Due to the limited intake of vitamin K, its regeneration is necessary and involves vi

267 scribed as being responsible for driving the vitamin K-mediated antioxidation pathways.

268 e candidate genes related to lipoprotein and vitamin K metabolism were identified as potential determ

269 lines secrete carboxylated reporter when fed vitamin K or vitamin K epoxide (KO).

270 Non-vitamin K oral anticoagulants (NOACs) are commonly presc

271 Non-vitamin K oral anticoagulants (NOACs) are now widely use

272 Non-vitamin K oral anticoagulants (NOACs) do not require rou

273 ials will assess the risk and benefit of non-vitamin K oral anticoagulants among patients at high ris

274 lighting the greater absolute benefit of non-vitamin K oral anticoagulants in patients with type 2 di

275 ents who have both and the potential for non-vitamin K oral anticoagulants to have greater benefits t

276 al anticoagulants (NOACs), also known as non-vitamin K oral anticoagulants, were at least noninferior

277 The vitamin K oxidoreductase (VKORC1) recycles vitamin K to

278 able a better understanding of the role that vitamin K plays in biological redox reactions ubiquitous

279 eversible redox behavior on par with that of vitamin K, provides a high-sensitivity fluorescence sign

280 ycled by two reactions, i.e. KO reduction to vitamin K quinone (K) and then to KH2, and recent studie

281 Direct detection of the vitamin K reaction products is confounded by KH2 oxidati

282 ic variants in VKORC1, which are involved in vitamin K reduction and associated with DVT, correlate w

283 of menaquinones produced by gut bacteria to vitamin K requirements and inflammation is undetermined.

284 In the presence of warfarin, vitamin K rescued carboxylation in HEK293 cells but not

285 We determined the association between vitamin K status and coronary artery calcium (CAC) progr

286 Poor vitamin K status is linked to greater risk of several ch

287 e unexplained interindividual variability in vitamin K status.

288 sults obtained from the patient treated with vitamin K, suggesting that the D153G alteration in GGCX

289 Whether vitamin K supplementation can prevent and/or treat calci

290 Vitamin K supplementation increased in ALGS after PEBD (

291 Daily supraphysiological vitamin K supplementation restores clotting for VKCFD2 p

292 amma-glutamyl carboxylation of F9CH required vitamin K supplementation, and was dose-dependently inhi

293 ) is essential for the production of reduced vitamin K that is required for modification of vitamin K

294 poxide reductase (VKOR) by depleting reduced vitamin K that is required for posttranslational modific

295 uthentic step in the biosynthetic pathway of vitamin K, that this reaction is enzymatically driven, a

296 e vitamin K oxidoreductase (VKORC1) recycles vitamin K to support the activation of vitamin K-depende

297 Animal studies have shown that vitamin K treatment reduced vascular calcification, but

298 genital/acquired FX deficiency or after anti-vitamin K treatment) were characterized by concomitantly

299 s, a cellular process requiring reduction of vitamin K (VK) by a second enzyme, a reductase called VK

300 ole in blood coagulation and bone formation, vitamin K (VK) has begun to emerge as an important nutri