ライフサイエンスコーパス: factor V

1 domains of blood coagulation factor VIII and factor V.

2 lactadherin as compared with factor VIII and factor V.

3 pplemented with increasing concentrations of factor V.

4 res with the anticoagulant pathway involving factor V.

5 e proteolytic activity of CpaA against human Factor V.

6 -3, platelet activating factor receptor, and factor V.

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

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

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

10 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

11 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

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

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

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

15 .0% in smokers with 3 or more metabolic risk factors vs 3.87% in smokers with none; P < .0001) in smo

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

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

18 51% of these 49 patients had 3 or more risk factors (vs 5.7% in the rest of the cohort, P < 0.001).

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

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

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

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

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

24 Factor X(a) (FX(a)) binding to factor V(a) (FV(a)) on platelet-derived membranes contai

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 n prothrombin was examined in the absence of factor V(a) and in the absence and presence of bovine ph

28 results presented here we conclude that both factor V(a) and PS-containing membranes induce similar r

29 ing at 50 microm membrane concentration, but factor V(a) extends the range of efficient channeling to

30 asurements to demonstrate the following: (1) Factor V(a) has four sites for dicaproyl-sn-glycero-3-ph

31 Moreover, we have determined: 1) factor V(a) has the greatest effect in enhancing rates o

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

33 Factor V(a) is a cofactor for the serine protease factor

34 ous results, which were obtained either with factor V(a) or with membranes individually, with results

35 lates the structure and cofactor activity of factor V(a), which is a heterodimer composed of one heav

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

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

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

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

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

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

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

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

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

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

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

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

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

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

50 17.0, 25.4, 24.2, and 14.0% for coagulation factor V, adiponectin, CRP, and thyroxine binding globul

51 2, 110, 120, and 246 pmol/mL for coagulation factor V, adiponectin, CRP, and thyroxine binding globul

52 Factor V also enhances both cleavage rates when protein

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

86 tes, namely mucin, pepsin, human coagulation factor V, and erythroid spectrin.

87 Factor V antigen also was not associated with VTE overal

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

89 or participants with the combination of high factor V antigen plus factor V Leiden the OR of idiopath

90 e proband has a severe bleeding disorder and factor V antigenic and functional levels of 8% and less

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

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

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

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

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

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

97 Specific cleavage of factor V at several P1Arg sites is critical for maintena

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

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

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

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

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

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

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

105 Few factor V deficiency mutations have been identified as ye

106 ygous splice site mutation in a patient with factor V deficiency.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

137 Factor V (FV) is a single-chain plasma protein containin

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

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

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

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

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

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

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

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

146 The coagulation factors V (FV) and VIII (FVIII) are important at sites o

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

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

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

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

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

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

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

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

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

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

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

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

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

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

161 677T, factor XIII Val34Leu, PAI-1 4G/5G, and factor V HR2) did not modify the association of hormone

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

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

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

165 ma demonstrated that the antibody recognizes factor V, is polyclonal, and has conformational epitopes

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

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

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

169 in the heterozygous form in combination with factor V Leiden (Arg506Gln).

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

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

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

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

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

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

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

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

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

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

180 of 186 white control subjects possessed the factor V Leiden allele (P <.001; odds ratio, 17.1; 95% c

181 No factor V Leiden alleles were detected in 19 white TM pat

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

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

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

185 -1.72), but double heterozygotes for HR2 and factor V Leiden carried an OR of idiopathic VTE of 16.3

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

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

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

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

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

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

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

193 No homozygous factor V Leiden carriers were identified.

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

195 (95% CI, 2.20-6.12) in participants carrying factor V Leiden compared with noncarriers.

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

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

198 Factor V Leiden enhanced the hormone-associated risk of

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

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

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

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

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

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

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

206 relative survival advantage of heterozygous factor V Leiden mice.

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

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

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

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

211 d risk of thrombosis for women who carry the factor V Leiden mutation and use oral contraceptive pill

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

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

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

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

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

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

218 Genotyping for the factor V Leiden mutation.

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

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

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

222 3 (CI, 0.50 to 1.39) among women with either factor V Leiden or the prothrombin mutation and 1.36 (CI

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

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

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

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

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

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

229 he combination of high factor V antigen plus factor V Leiden the OR of idiopathic VTE was 11.5 (95% C

230 The prevalence of factor V Leiden was significantly increased among the wh

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

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

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

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

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

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

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

238 Available evidence indicates that factor V Leiden, prothrombin 20210A, and lipoprotein (a)

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

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

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

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

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

244 resistance independently of the presence of factor V Leiden.

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

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

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

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

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

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

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

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

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

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

255 nd has conformational epitopes on the entire factor V molecule (heavy and light chains, and B region)

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

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

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

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

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

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

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

263 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

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

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

266 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

267 nd thrombin express functional alpha-granule factor V only on a subpopulation of cells.

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 ty chromatography on protein G-Sepharose and factor V-Sepharose.

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

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

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

279 ponding residues of the APC cleavage site in factor V spanning residues 504-509 (Asp(504)-Arg-Arg-Gly

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

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

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

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

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 lation factor activities measured, including factors V, VII, VIII, and IX.

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

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

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

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

295 teins, including fibrinogen, thrombospondin, factor V, von Willebrand factor, and fibronectin.

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 eg, fibrinogen with glycoprotein IIb/IIIa or factor V with phosphatidylserine) as well as serotonin b

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

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