ライフサイエンスコーパス: factor V

1 -3, platelet activating factor receptor, and factor V.

2 )) was 79.7 kb downstream of F5, coagulation factor V.

3 domains of blood coagulation factor VIII and factor V.

4 lactadherin as compared with factor VIII and factor V.

5 as EAD was not significant when adjusted for factor V.

6 pplemented with increasing concentrations of factor V.

7 res with the anticoagulant pathway involving factor V.

8 e proteolytic activity of CpaA against human Factor V.

9 deposition (for >/=2 late-life vascular risk factors vs 0: OR, 1.66; 95% CI, 0.75-3.69).

10 ncordance index significantly (0.61 for risk factors vs. 0.81 for the CAC score, p < 0.0001).

11 ctors vs none: HR 0.04, CI 0.01 to 0.20; 4-5 factors vs 1-3 factors: HR 0.38, CI 0.22 to 0.66; trend

12 ctors vs none: HR 0.15, CI 0.02 to 1.15; 4-5 factors vs 1-3 factors: HR 0.53, CI 0.28 to 0.98; trend

13 llele-specific polymerase chain reaction for factor V 1691A (Leiden), factor II 20 210A, methylenetet

14 relative risks (RR) for coronary disease of factor V 1691A and of prothrombin 20210A were 1.17 (95%

15 Phe, Asp(697) --> Lys, and Tyr(698) --> Phe (factor V(2K2F)) was partially resistant to activation by

16 .0% in smokers with 3 or more metabolic risk factors vs 3.87% in smokers with none; P < .0001) in smo

17 acid regions 334-335 and 695-698 as follows: factor V(3K) ((334)DY(335) --> KF and (695)DYDY(698) -->

18 the (695)DYDY (698) --> AAAA substitutions (factor V(4A)).

19 51% of these 49 patients had 3 or more risk factors (vs 5.7% in the rest of the cohort, P < 0.001).

20 to either lysine (factor V(5K)) or alanine (factor V(5A)).

21 all residues were mutated to either lysine (factor V(5K)) or alanine (factor V(5A)).

22 tly named at least 1 established stroke risk factor vs 68% in 1995.

23 35) --> KF and (695)DYDY(698) --> AAAA), and factor V(6A) ((334)DY(335) --> AA and (695)DYDY(698) -->

24 iewed as factor X(a) (FX(a)) in complex with factor V(a) (FV(a)) on a phosphatidylserine (PS)-contain

25 Tightly associated factor V(a) (FVa) and factor X(a) (FXa) serve as the ess

26 We expressed human factor V(a) (rFVa) with mutations in either the C1 domai

27 C(6)PS also mediates the interaction between factor V(a) heavy (V(a)-HC) and light (V(a)-LC) chains.

28 Factors V(a) and X(a) (FV(a) and FX(a), respectively) as

29 V (KF)) and D (334) --> A and Y (335) --> A (factor V (AA)).

30 by platelets) were sufficient to accelerate factor V activation and abrogate the anticoagulant funct

31 functions as an amplifier of the process of factor V activation and thus has an important procoagula

32 Reaction pathways for factor V activation are similar for all thrombin forms.

33 formed incorporating the various pathways of factor V activation including the presence or absence of

34 In a mechanism distinct from factor VIII, factor V activation involves proteolytic removal of inhi

35 triggers the contact pathway, it accelerates factor V activation, and it enhances fibrin polymerizati

36 from activated human platelets) accelerates factor V activation, completely abrogates the anticoagul

37 much to be learned about parahemophilia and factor V activation, two seemingly well studied areas of

38 act pathway of blood clotting and accelerate factor V activation.

39 ts provide new insight into the mechanism of factor V activation.

40 ed by exosite 2 in the rate-limiting step of factor V activation.

41 The active component was identified as factor V activator (RVV-V).

42 mediate abundance were selected, coagulation factor V, adiponectin, C-reactive protein (CRP), and thy

43 17.0, 25.4, 24.2, and 14.0% for coagulation factor V, adiponectin, CRP, and thyroxine binding globul

44 2, 110, 120, and 246 pmol/mL for coagulation factor V, adiponectin, CRP, and thyroxine binding globul

45 Factor V also enhances both cleavage rates when protein

46 esis that proteolysis within the B-domain of factor V, although necessary, is incidental to the mecha

47 Factor V Amsterdam binds to TFPI, prolonging its half-li

48 no acids from the B domain), which we called factor V Amsterdam.

49 ch has been shown previously to cleave human Factor V and deregulate blood coagulation, as the most a

50 omologous to a putative Ca2+ binding site in factor V and expression of B-domainless factor VIII mole

51 Combined deficiency of factor V and factor VIII (F5F8D) is a bleeding disorder

52 Combined deficiency of factor V and factor VIII (F5F8D) is caused by mutations

53 d ERGIC-53) result in combined deficiency of factor V and factor VIII (F5F8D), an autosomal recessive

54 IC-53) or MCFD2 cause combined deficiency of factor V and factor VIII (F5F8D).

55 Alpha-thrombin catalyzes the activation of factor V and factor VIII following discrete proteolytic

56 substrate specificity of MzT, in activating factor V and factor VIII on membranes, and the anticoagu

57 n-like effect; falls in thrombin generation, Factor V and Factor VIII to 52%, 19% and 17% normal resp

58 MCFD2 may function to specifically recruit factor V and factor VIII to sites of transport vesicle b

59 A) were able to induce clotting and activate factor V and factor VIII with rates similar to the plasm

60 the C domains of blood coagulation proteins factor V and factor VIII.

61 disorder, combined deficiency of coagulation factor V and factor VIII.

62 D could result from a defect in secretion of factor V and factor VIII.

63 LMAN1 causing a selective block to export of factor V and factor VIII.

64 are conserved in murine, bovine, and porcine factor V and in human factor VIII.

65 of an association between a shorter form of factor V and increased TFPI levels, resulting in severel

66 oes not require factor VII, but does require factor V and lipid.

67 s are given of new findings on the source of factor V and the synthesis of factor VIII, the mechanism

68 he membrane-binding sites of factor VIII and factor V and to function as an anticoagulant.

69 These include platelet factor V and, surprisingly, plasma tissue factor pathway

70 DAII) and combined deficiency of coagulation factors V and VIII (F5F8D) are the 2 known hematologic d

71 C2 structure is similar to the C2 domains of factors V and VIII (rmsd of C(alpha) atoms of 0.9 A and

72 acterized by inactivation of the coagulation factors V and VIII and a derepression of the fibrinolysi

73 The discoidin C2 domains of coagulation factors V and VIII are known to interact with extracellu

74 s than is found in other vertebrates in that factors V and VIII seem to be represented by a single ge

75 In analogy with the C2 domains of factors V and VIII, some or all of these solvent-exposed

76 o membrane-binding domains of blood-clotting factors V and VIII.

77 , and IRAK3; and a disruption of coagulation factors V and VIII.

78 The activation of coagulation factors V and X by Russell's viper venom (RVV) has been

79 vated protein C (APC) resistance, and plasma factor V antigen in 335 participants who developed VTE d

80 of proconvertin (factor VII), proaccelerin (factor V), antihemophilic globulin (factor VIII), or Chr

81 We aimed to assess factor V as a biomarker of EAD and a predictor of graft

82 anistic insights responsible for maintaining factor V as an inactive procofactor will be discussed.

83 contrast, beta-thrombin was unable to cleave factor V at Arg(1545) and factor VIII at both Arg(372) a

84 Beta-thrombin was found to cleave factor V at Arg(709) and factor VIII at Arg(740), albeit

85 om Russell's viper venom (RVV) cleaves human factor V at Arg1018 and Arg1545 to produce a Mr 150,000

86 Naja nigricollis nigricollis, cleaves human factor V at Asp697, Asp1509, and Asp1514 to produce a mo

87 an factor V, single-chain B-domain-truncated factor V bound to FXa membranes with an affinity that wa

88 FX by FVIIa/TF and inactivation of activated factor V by APC.

89 Direct activation of factor V by factor Xa at physiologically relevant concen

90 r the activation of phospholipid-bound human factor V by native and recombinant thrombin and meizothr

91 by cleavage at three sites in the middle of factor V by thrombin, yielding an N terminus-derived hea

92 or prothrombin of 850 nm), and activation of factor V by thrombin.

93 ogous with the factor VIII C2 (fVIII-C2) and factor V C2 (fV-C2) domains.

94 Blood coagulation factor V circulates as a procofactor with little or no p

95 n the variable bleeding tendencies in severe factor V deficiency.

96 The bleeding manifestation of severe factor V-deficient patients varies dramatically.

97 esistance when added to normal plasma and to factor V-deficient plasma supplemented with increasing c

98 a mutant molecule with this region deleted (factor V(Delta659-663)).

99 he last 30 amino acids from the heavy chain (factor V(Delta680-709)) and a mutant molecule with the (

100 were employed to assess the ability of these factor V derivatives to assemble and function in prothro

101 Factor V enhances Arg(562) cleavage more than Arg(336) c

102 reviously reported for both prothrombin- and factor V (F5)-deficient mice.

103 e recombinant molecules along with wild-type factor V (factor V(WT)) were transiently expressed in ma

104 idual components of the network (factor IIa, factor V, factor VIII, and thrombomodulin), did not affe

105 lation factors (fibrinogen, prothrombin, and factor V); fibrinolytic factors (plasminogen activator i

106 Alpha-thrombin readily activated factor V following cleavages at Arg(709), Arg(1018), and

107 in competes efficiently with factor VIII and factor V for binding sites on synthetic phosphatidylseri

108 tudies continue to move our understanding of factor V forward.

109 nt partial B-domain-truncated derivatives of factor V (FV(des811-1491) and FV(des811-1491) with Arg(7

110 ndividuals have normal levels of coagulation factor V (FV) activity, but demonstrate inhibition of gl

111 N1 or MCFD2 cause the combined deficiency of factor V (FV) and factor VIII (FVIII; F5F8D), suggesting

112 s responsible for the efficient secretion of factor V (FV) and FVIII to the plasma.

113 ELISA data reveal that TFPI-2 binds factor V (FV) and partially B-domain-deleted FV (FV-1033

114 PAR4-AP-mediated factor V (FV) association with the platelet surface was

115 equence nearly identical to a portion of the factor V (FV) B domain necessary for maintaining FV in a

116 how that selective expression of coagulation factor V (FV) by resident peritoneal macrophages in mice

117 Coagulation factor V (FV) circulates as an inactive procofactor and

118 Single chain factor V (fV) circulates as an Mr 330,000 quiescent pro-

119 ce site in a patient with severe coagulation factor V (FV) deficiency and life-threatening bleeding e

120 ndocytoses fluorescently labeled coagulation factor V (FV) from the media into alpha-granules and rel

121 sue of Blood, Nogami et al report on a novel factor V (FV) gene mutation (FV Trp1920-->Arg, FVNara) a

122 etely devoid of plasma- and platelet-derived factor V (FV) identified 167 variants in his F5 gene inc

123 fense, we challenged mice with deficiency of factor V (FV) in either the plasma or platelet compartme

124 Coagulation factor V (FV) is a central regulator of the coagulation

125 Activation of blood coagulation factor V (FV) is a key reaction of hemostasis.

126 ipt, which encodes a previously unrecognized factor V (FV) isoform they call FV-short.

127 (APC) resistance, often associated with the factor V (FV) Leiden mutation, is the most common risk f

128 Measurement of platelet factor V (FV) levels in 7 F5F8D patients (4 with LMAN1 a

129 fically to the FXa binding site expressed on factor V (FV) upon activation to factor Va (FVa) by thro

130 Factor V (FV), a central regulatory protein in hemostasi

131 The deficiency of fibrinogen, prothrombin, factor V (FV), FVII, FVIII, FIX, FX, FXI, and FXIII, cal

132 bly by directly interacting with coagulation factor V (FV), which has been activated by FXa.

133 re replaced by the corresponding residues of factor V (FV).

134 may also interact with platelet coagulation factor V (FV).

135 The C domains of coagulation factors V (FV) and VIII (FVIII) are structurally conserv

136 argo receptor complex transports coagulation factors V (FV) and VIII (FVIII) from the endoplasmic ret

137 receptor MCFD2, LMAN1 transports coagulation factors V (FV) and VIII (FVIII).

138 thrombin activator homologous to coagulation factors V (FV) and Xa (FXa).

139 yses were done of 191 studies in relation to factor V G1691A (ie, factor V Leiden), factor VII G10976

140 factor II G202010A, 0.25% (0.12%-0.53%) for factor V G1691A, and 0.10% (0.06%-0.17%) in relatives wi

141 for IT (antithrombin, protein C, protein S, factor V G1691A, factor II G20210A) and determined the i

142 risk of severe preeclampsia with coagulation factor V gene (proaccelerin, labile factor) (F5) polymor

143 The 1691A variant of the factor V gene and the 20210A variant of the prothrombin

144 G20210A prothrombin and factor V gene mutations were assessed in sera stored at

145 Molecular analysis of the factor V gene revealed a novel homozygous mutation in th

146 agulation Factor II gene and the Coagulation Factor V gene.

147 pathway, catalyzes the initial activation of factor V; generation of factor Va in a milieu already co

148 or less and in 20/153 (13.1%) patients with factor V >36.1 U/mL (P < 0.001).

149 5%, and 95%, respectively, for patients with factor V >36.1 U/mL (P = 0.001).

150 h factor V of 36.1 U/mL or less and 153 with factor V >36.1 U/mL.

151 Factor V has never been compared to a validated early al

152 The relative risk of thrombosis in factor V heterozygotes is at least 3 times higher than i

153 677T, factor XIII Val34Leu, PAI-1 4G/5G, and factor V HR2) did not modify the association of hormone

154 tain Australian snakes have a unique form of factor V in their venom with these inhibitory sequences

155 is full-length EPCR (49 kDa) and APC retains factor V-inactivating activity.

156 ng the presence or absence of the pathway of factor V-independent prothrombin activation by factor Xa

157 Factor V is an early marker for EAD and is a continuous

158 They also bear on how factor V is converted into a cofactor capable of assembl

159 Targets of the oncogenic transcription factor v-Jun in the murine cell line C3H 10T1/2 cells ha

160 e mutations D (334) --> K and Y (335) --> F (factor V (KF)) and D (334) --> A and Y (335) --> A (fact

161 DY(335) --> KF and (695)DYDY(698) --> KFKF), factor V(KF/4A) ((334)DY(335) --> KF and (695)DYDY(698)

162 lower and upper), with corresponding filling factors, v(l) and v(u).

163 The effect of prothrombotic polymorphism, factor V Leiden (Arg506Gln; FV Leiden), was examined in

164 Factor V Leiden (F5(L) ) is a common genetic risk factor

165 Activated protein C resistance due to factor V Leiden (FVL) is a common genetic risk factor fo

166 We describe a mouse model of fetal loss in factor V Leiden (FvL) mothers in which fetal loss is tri

167 nous thromboembolism (VTE) in relatives with factor V Leiden (FVL) or G20210A prothrombin (PT20210A)

168 A well-known example is the factor V Leiden (FVL) paradox: the FVL mutation poses a

169 rdiac surgery, we tested the hypothesis that factor V Leiden (FVL), a common coagulation factor polym

170 anticardiolipin antibodies and genotyping of factor V Leiden (FVL), factor II G20210A (FII), and meth

171 gle gene mutation in factor V, the so called factor V Leiden (FVL), is the most common cause of throm

172 onwhite ethnicity, heterozygous carriers for factor V Leiden (P=0.001) and obesity (P=0.002) are sign

173 Studies examining the role of factor V Leiden among patients at higher risk of atherot

174 of synthetic nucleic acid targets including Factor V Leiden and methylenetetrahydrofolate reductase.

175 genetic factors involved in thrombotic risk, factor V Leiden and prothrombin G20210A.

176 (1) report that thrombotic disorders such as factor V Leiden are often treated with drugs like low mo

177 As has already been shown, heterozygous factor V Leiden carrier status improves the survival of

178 The effect of the factor V Leiden carrier status in severe sepsis in the P

179 nvestigated the hypothesis that heterozygous factor V Leiden carrier status might protect against the

180 e survival benefit derived from heterozygous factor V Leiden carrier status was only evident at doses

181 vival advantage associated with heterozygous factor V Leiden carrier status.

182 The proportion of factor V Leiden carriers in patients with severe sepsis

183 Therefore, factor V Leiden carriers should not be excluded from thi

184 No homozygous factor V Leiden carriers were identified.

185 those without), and inherited thrombophilia (factor V Leiden carriers with a 10-year cumulative incid

186 tein C (drotrecogin alfa [activated]) as non-factor V Leiden carriers.

187 in patients with severe sepsis suggest that factor V Leiden constitutes a rare example of a balanced

188 edication was rivaroxaban for her homozygous Factor V Leiden deficiency.

189 Previous findings in the mouse factor V Leiden endotoxemia model and in patients with s

190 Factor V Leiden enhanced the hormone-associated risk of

191 Participants were screened for factor V Leiden G1691A and prothrombin G20210A mutation

192 show for the first time that a heterozygous factor V Leiden genotype is associated with improved 30-

193 Compared with non-Leiden carriers, factor V Leiden heterozygous carriers may have a slightl

194 lerotic plaque rupture, we hypothesized that factor V Leiden may be a stronger risk factor for athero

195 The survival of homozygous factor V Leiden mice did not differ from that of normal

196 polysaccharide, the survival of heterozygous factor V Leiden mice did not differ from that of wild-ty

197 els (thrombomodulin-deficient TMPro mice and factor V Leiden mice), in which the endogenous protein C

198 factor V proteolysis by activated protein C (factor V Leiden mice), were employed.

199 relative survival advantage of heterozygous factor V Leiden mice.

200 of this study was to investigate whether the factor V Leiden mutation (Arg506Gln) is associated with

201 with severe thrombophilia such as homozygous factor V Leiden mutation (FVL) depend on a positive fami

202 rvival was significantly associated with the factor V Leiden mutation (p = .049).

203 The factor V Leiden mutation (R506Q), a prothrombotic gene p

204 proved survival of mice heterozygous for the factor V Leiden mutation complements results from the an

205 confirm that carriers of this prothrombotic factor V Leiden mutation do not have an increased risk o

206 The high prevalence of the factor V Leiden mutation in certain populations has prom

207 ly relevant than genetic testing to detect a factor V Leiden mutation in identifying persons who are

208 different species strongly suggest that the factor V Leiden mutation is indeed a potent modifier of

209 A factor V Leiden mutation was present in 6 patients, prot

210 Genotyping for the factor V Leiden mutation.

211 that the system successfully identified the factor V Leiden mutations from human blood specimens.

212 first-degree relatives of an index case with factor V Leiden or the prothrombin 20210A gene variant,

213 g and old patients of both sexes, those with factor V Leiden or the prothrombin gene mutation, and th

214 3 (CI, 0.50 to 1.39) among women with either factor V Leiden or the prothrombin mutation and 1.36 (CI

215 Women with either factor V Leiden or the prothrombin mutation had a 49% ha

216 embolism risk to carriers of the established factor V Leiden p.R506Q and prothrombin G20210A mutation

217 hisms that increase coagulability, including factor V Leiden R506G, factor II (prothrombin) G20210A,

218 Participating studies genotyped factor V Leiden status and shared risk estimates for the

219 The combined data on factor V Leiden status from 3894 adult patients with sev

220 Routine assessment of factor V Leiden status is unlikely to improve atherothro

221 complements results from the analysis of the factor V Leiden subgroup of patients enrolled in the PRO

222 The striking magnitude of the factor V Leiden survival benefit in the initial PROWESS

223 roves pregnancy outcome in a murine model of factor V Leiden that is unrelated to its anticoagulation

224 Factor V Leiden was not associated with increased risk o

225 Factor V Leiden was not associated with the combined out

226 Defects in this mechanism (eg, factor V Leiden) are associated with thrombosis but resu

227 ain haemostatic genes (such as that encoding factor V Leiden) are involved in the development of veno

228 studies in relation to factor V G1691A (ie, factor V Leiden), factor VII G10976A, prothrombin G20210

229 m (hepatic lipase, APOE, PON1) and clotting (factor V Leiden, fibrinogen).

230 blood samples, which were used to determine factor V Leiden, G20210A prothrombin, and 677C>T MTHFR p

231 ation-based prospective studies, we measured factor V Leiden, HR2 haplotype, activated protein C (APC

232 nce of such genetic thrombophilia markers as factor V Leiden, prothrombin 20210A mutation, and antiph

233 hereditary thrombophilic defects, including factor V Leiden, prothrombin G20210A defect, and deficie

234 philic risk factors prevalent in Caucasians (factor V Leiden, Prothrombin G20210A) are distinctly rar

235 rrent use of a panel of three genetic tests (factor V Leiden, prothrombin variant G20210A, and protei

236 Using a murine model of factor V Leiden-associated placental failure, we show th

237 VIIIa, and APC resistance is often caused by factor V Leiden.

238 eterozygous or homozygous (n=47) carriers of factor V Leiden.

239 resistance independently of the presence of factor V Leiden.

240 ociated with age, overweight or obesity, and factor V Leiden.

241 For idiopathic VTE, in addition to the factor V (Leiden) mutation (odds ratio [OR], 5.13; 95% c

242 Factor V(Leiden) (fV(Leiden)) predisposes to thrombosis

243 d normal factor Va as well as membrane-bound factor V(LEIDEN) by APC at Arg(306) is required for the

244 On a factor V(Leiden) genetic background, ZPI deficiency prod

245 trast, thrombogenic effects in patients with factor V-Leiden.

246 In the multivariate analysis, factor V level less than 40% at day 0 and factor V level

247 Patients were divided according to their factor V levels into the <=36.1 U/mL and > 36.1 U/mL gro

248 s, factor V level less than 40% at day 0 and factor V levels of 40% or greater at admission but decre

249 We retrospectively assessed the serum factor V levels on postoperative day 1 after LT.

250 omain (rFV(a2)-C2) and of a B domain-deleted factor V light isoform (rFV(a2)) in Hi-5 and COS cells,

251 In contrast, the factor V-like, homologous subunit (Pt-FV) of a prothromb

252 xpression of the RXR-dependent transcription factor v-maf musculoaponeurotic fibrosarcoma oncogene fa

253 egions, we have created a mutant recombinant factor V molecule that is missing the last 30 amino acid

254 A recombinant factor V molecule with the mutations Asp(695) --> Lys, T

255 We have generated factor V molecules in which all residues were mutated to

256 The recombinant factor V molecules were expressed and purified to homoge

257 We constructed recombinant factor V molecules with the mutations D (334) --> K and

258 intermediate in thrombin formation, cleaves factor V more slowly than does thrombin, resulting in a

259 mologous residues of the other protein and a factor V mutant with 5 amino acids changed to those from

260 Some factor V mutants, including FV(MTTS/Y), had increased me

261 ctors vs none: HR 0.12, CI 0.03 to 0.47; 4-5 factors vs none: HR 0.04, CI 0.01 to 0.20; 4-5 factors v

262 e observed for cardiovascular mortality (4-5 factors vs none: HR 0.08, CI 0.01 to 0.66; 1-3 factors v

263 th higher numbers of healthy behaviours (1-3 factors vs none: HR 0.12, CI 0.03 to 0.47; 4-5 factors v

264 ctors vs none: HR 0.08, CI 0.01 to 0.66; 1-3 factors vs none: HR 0.15, CI 0.02 to 1.15; 4-5 factors v

265 patients were included in the study: 74 with factor V of 36.1 U/mL or less and 153 with factor V >36.

266 4%, and 74%, respectively, for patients with factor V of 36.1 U/mL or less and 98%, 95%, and 95%, res

267 diagnosed in 41 (55.4%) of 74 patients with factor V of 36.1 U/mL or less and in 20/153 (13.1%) pati

268 should also be tested for genetic defects in factor V or concomitant thrombophilia.

269 rombotic phenotype, such as selective plasma factor V or factor Xa inhibition.

270 Factor V plays an essential role in hemostasis and has a

271 ant splicing of F5 and ultimately to a short factor V protein (missing 623 amino acids from the B dom

272 C activation (TMPro mice) or at the level of factor V proteolysis by activated protein C (factor V Le

273 venous thromboembolism (VTE) in relation to factor V-related risk factors.

274 od to a tryptic digest of bovine coagulation factor V resulted in identification of sulfation on tyro

275 Factor VIII and factor V share structural homology and bind to phospholi

276 nterpretation that proteolytic activation of factor V simply eliminates steric and/or conformational

277 In contrast to human factor V, single-chain B-domain-truncated factor V bound

278 ntangle the relative importance of extrinsic factors vs. species characteristics for the establishmen

279 l of DR and the association of systemic risk factors vs the CDI and FD.

280 Factor V, the precursor of factor Va, circulates in plas

281 nce as a result of a single gene mutation in factor V, the so called factor V Leiden (FVL), is the mo

282 nd was sufficient for the ability of cleaved factor V to bind Xa and assemble into the prothrombinase

283 The proteolytic conversion of factor V to factor Va is central for amplified flux thro

284 roteolysis indicating that the conversion of factor V to factor Va results in appropriate structural

285 ust thrombin generation is the activation of factor V to factor Va.

286 The activation of the procofactor, factor V, to factor Va is an essential reaction that occ

287 unanticipated insights into ways to modulate factor V/Va function for therapeutic benefit.

288 Dynamic variables regarding factor V values are predictive of a poor outcome.

289 t VTE was found for all IT traits except the factor V variant and elevated lipoprotein(a).

290 h reduced plasma levels of blood coagulation factors V, VII, VIII, IX, X, and XII.

291 Better repletion of factors V, VIII, and IX was seen longitudinally, and bot

292 ich contains an RGD motif) and two discoidin/Factor V/VIII C domains.

293 tibody (YW107.4.87) binds to the coagulation factor V/VIII domains (b1b2) of NRP1 and blocks VEGF bin

294 rding to the multivariable regression model, factor V was a continuous marker of EAD (odds ratio [OR]

295 Factor V was a continuous predictor for 3- and 6-month g

296 ances in our understanding of the biology of factor V which shed light on the variable bleeding tende

297 tact pathway and promoting the activation of factor V, which in turn results in abrogation of the fun

298 ant molecules along with wild-type factor V (factor V(WT)) were transiently expressed in mammalian ce

299 c defects in thrombus formation, in cases of factor V, XI or XII deficiency; and in contrast, thrombo

300 identified across 3 of the candidate genes (factors V, XI, and protein C) in SNP analyses.