ライフサイエンスコーパス: prothrombin

1 domain determine the functional behavior of prothrombin.

2 m a staphylothrombin complex upon binding to prothrombin.

3 ciate with, and non-proteolytically activate prothrombin.

4 n of prothrombinase on two cleavage sites in prothrombin.

5 ses binding sites for factor Xa and possibly prothrombin.

6 gle-1 to kringle-2 in the coagulation factor prothrombin.

7 activation and conformational plasticity of prothrombin.

8 ic or pharmacologic reduction of circulating prothrombin.

9 of an index case with factor V Leiden or the prothrombin 20210A gene variant, the presence of these a

10 and factor X(a) (FXa) serve as the essential prothrombin-activating complex that assembles on phospha

11 apedesis/adhesion, Fc macrophage activation, prothrombin activation and hepatic stellate cell activat

12 propiece plays essential roles in regulating prothrombin activation and proteinase function.

13 ignificant implications for the mechanism of prothrombin activation and the zymogen --> protease conv

14 In FXa-catalyzed prothrombin activation assays, both FV and FV(DeltaIIa)

15 Gel electrophoresis analyzing prothrombin activation by prothrombinase assembled with

16 ntapeptide from this region (DYDYQ) inhibits prothrombin activation by prothrombinase by inhibiting m

17 The rate of prothrombin activation by vWbp(1-263) is controlled by a

18 Prothrombin activation can proceed through the intermedi

19 ses of plasma-derived and recombinant mutant prothrombin activation demonstrated delayed cleavage of

20 A molecular mechanism of prothrombin activation emerges from the structure.

21 ributions that these 2 intermediates make to prothrombin activation in tissue factor (Tf)-activated b

22 critical length of 15 residues, the rate of prothrombin activation increases (10-fold) in the absenc

23 ssembled on synthetic phospholipid vesicles, prothrombin activation proceeds with an initial cleavage

24 ariants of meizothrombin, an intermediate of prothrombin activation that contains the propiece covale

25 ed blood, producing a membrane that supports prothrombin activation through the meizothrombin pathway

26 When prothrombin activation was monitored at a typical venous

27 e role of this flexibility in the context of prothrombin activation was tested with several deletions

28 These findings support a molecular model of prothrombin activation where Lnk2 presents the sites of

29 ith the mutant molecules revealed a delay in prothrombin activation with persistence of meizothrombin

30 ermediates from the two possible pathways of prothrombin activation.

31 pathophysiologic conditions characterized by prothrombin activation.

32 echanistic basis for its accumulation during prothrombin activation.

33 es were contributing to approximately 35% of prothrombin activation.

34 ctor V-like, homologous subunit (Pt-FV) of a prothrombin activator from Pseudonaja textilis venom is

35 nake Pseudonaja textilis has a venom-derived prothrombin activator homologous to coagulation factors

36 platelet and fibrinogen levels and increased prothrombin and activated partial thromboplastin times a

37 G20210A prothrombin and factor V gene mutations were assessed in

38 Finally, we present steady-state models of prothrombin and factor X activation under flow showing t

39 When prothrombin and factor X are activated coincident with e

40 dary progressive MS had significantly higher prothrombin and factor X levels than healthy donors, whe

41 ), which, following an association with host prothrombin and fibrinogen, form fibrin clots and enable

42 nd factor XIII, whereas Coa co-purified with prothrombin and fibrinogen.

43 Based on residual serum prothrombin and flow cytometric assays, CSS segregates a

44 ctor-binding protein (vWbp) to activate host prothrombin and form fibrin cables, thereby promoting th

45 cretes coagulase (Coa), which activates host prothrombin and generates fibrin fibrils that protect th

46 In the blood, the zymogens prothrombin and prethrombin-2 require the prothrombinase

47 e substrate binding channel on fVa, to which prothrombin and the intermediate meizothrombin bind in 2

48 The three-dimensional architecture of prothrombin and the molecular basis of its activation re

49 d factor XIII, but not fibronectin, required prothrombin and triggered the non-proteolytic activation

50 family with a bleeding diathesis, prolonged prothrombin, and activated partial thromboplastin times,

51 tures composed only of factor Xa, factor Va, prothrombin, and calcium ions, myosin greatly enhanced p

52 It is synthesized in the zymogen form, prothrombin, and its activation at the end of the blood

53 activated platelet surface, the cleavage of prothrombin, and prothrombin mutants lacking either one

54 ding factors IXa (FIXa), FXa/FX, FVa, FVIII, prothrombin, and PS-sensitive marker Annexin V were dist

55 with and activate the host hemostatic factor prothrombin, and the bacterial surface display of agglut

56 report the first x-ray crystal structure of prothrombin as a Gla-domainless construct carrying an Al

57 our self-similar recycling model applied to prothrombin assays reproduces the empirical equations fo

58 o thrombin exosite II and has no affinity to prothrombin at all.

59 he activated platelet surface, which cleaves prothrombin at Arg271 and Arg320.

60 activation demonstrated delayed cleavage of prothrombin at both Arg(320) and Arg(271) by prothrombin

61 Burial of Arg-320 prevents prothrombin autoactivation and directs prothrombinase to

62 Prothrombin autoactivation induced by histone H4 emerges

63 Whether prothrombin autoactivation occurs in the wild-type under

64 of prothrombinase, factors (f) Xa and Va and prothrombin, bind to negatively charged membrane phospho

65 overned by a differential ability to support prothrombin binding and the variable accumulation of int

66 hat antibodies directed against the variable prothrombin binding portion of coagulases confer type-sp

67 ative selection, the coding sequence for the prothrombin-binding D1-D2 domain is highly variable and

68 in the rate of thrombin formation for desGla prothrombin but with a major effect on the pathway for s

69 ) restored most of the catalytic defect with prothrombin, but not with the synthetic substrate.

70 ade where cofactor Va enhances activation of prothrombin by factor Xa by compressing Lnk2 and morphin

71 binase regulating cleavage and activation of prothrombin by factor Xa.

72 The present study evaluates activation of prothrombin by full-length vWbp(1-474) through activity

73 to the regulation of the rate of cleavage of prothrombin by prothrombinase.

74 framework for the mechanism of activation of prothrombin by prothrombinase.

75 Although the activation of prothrombin by surface-localized prothrombinase is clear

76 alpha-thrombin in vivo is the activation of prothrombin by the prothrombinase complex assembled on e

77 ains in the pathophysiological activation of prothrombin by vWbp, and may reveal a function for autoc

78 ogenous fII gene, resulting in expression of prothrombin carrying 3 amino acid substitutions (R157A,

79 the NH(2)-terminal residues of vWbp into the prothrombin catalytic domain.

80 nt is evident as a switch in the pathway for prothrombin cleavage and the intermediate produced but w

81 cofactor with factor Xa and optimum rates of prothrombin cleavage.

82 Among the two conformations of prothrombin, collapsed and fully extended, histone H4 bi

83 nical trial to compare nonactivated 4-factor prothrombin complex concentrate (4F-PCC) with plasma for

84 pared the efficacy and safety of four-factor prothrombin complex concentrate (4F-PCC) with that of pl

85 measures and biomarkers by using a 4-factor prothrombin complex concentrate (4F-PCC).

86 efficacy of fresh frozen plasma (FFP) versus prothrombin complex concentrate (PCC) in patients with V

87 actice include fresh frozen plasma (FFP) and prothrombin complex concentrate (PCC).

88 therapies that promote formation of fibrin (prothrombin complex concentrate [PCC], activated PCC [aP

89 ecombinant activated factor VII or activated prothrombin complex concentrate did not alter the delaye

90 rventional treatment was needed in 37.8% and prothrombin complex concentrate in 9.1%.

91 circumstances, avoiding the use of plasma or prothrombin complex concentrate in the nonemergent rever

92 rgent reversal with frozen plasma versus the prothrombin complex concentrate Octaplex.

93 ntial hematoma expansion (43% [12 of 28] for prothrombin complex concentrate vs 29% [5 of 17] for no

94 ng administration of hemostatic factors (eg, prothrombin complex concentrate), were left to the discr

95 ntial ability of a low dose of the activated prothrombin complex concentrate, FEIBA, to reestablish h

96 complex concentrate vs 29% [5 of 17] for no prothrombin complex concentrate, P = .53), or on the occ

97 agents with a fast onset of action, such as prothrombin complex concentrate, recombinant factor VIIa

98 pplied to guide the dosing of fibrinogen and prothrombin complex concentrate, which are selectively u

99 all, 57% (35 of 61) of the patients received prothrombin complex concentrate, with no statistically s

100 rfarin anticoagulation with frozen plasma or prothrombin complex concentrate.

101 romboembolic events in patients treated with prothrombin complex concentrates (PCCs) for the manageme

102 Nonspecific hemostatic agents such as prothrombin complex concentrates and recombinant factor

103 Recombinant factor VIIa and activated prothrombin complex concentrates are similarly effective

104 of coagulation factors (fresh frozen plasma, prothrombin complex concentrates or recombinant activate

105 he coagulation factor levels and contents of prothrombin complex concentrates; ambiguity about the op

106 therapy; the variability in availability of prothrombin complex concentrates; the variability in the

107 eal a function for autocatalysis of the vWbp.prothrombin complexes during initiation of blood coagula

108 rol, n = 1), bolus administration of a human prothrombin concentrate complex (hPCC; 2.5 mL/kg, n = 2)

109 Prothrombin concentrate may be considered in life-threat

110 Mice with a genetic deficit in prothrombin confirmed the specificity of the thrombin pr

111 normal clotting times, but markedly reduced prothrombin consumption.

112 re used to directly test the hypothesis that prothrombin contributes to tumor development in colitis-

113 Furthermore, the K(m) for prothrombin conversion with the factor Xa variants assem

114 Here we report that an engineered analog of prothrombin could be used to detect S. aureus in endocar

115 Des-gamma carboxy-prothrombin (DCP) and lectin-bound AFP (AFP-L3%) are pot

116 lpha-fetoprotein (AFP) and des-gamma-carboxy prothrombin (DCP) in the early diagnosis of HCC.

117 as strongly inferred by the observation that prothrombin deficiency dramatically reduced the formatio

118 These prothrombin derivatives bound staphylocoagulase and inte

119 were compared by equilibrium binding to the prothrombin derivatives prethrombin 1, prethrombin 2, th

120 Active site labeling of all prothrombin derivatives with D-Phe-Pro-Arg-chloromethyl

121 The results suggest a role for prothrombin domains in the pathophysiological activation

122 findings confirm the molecular plasticity of prothrombin emerged from recent structural studies and s

123 Prothrombin exists in equilibrium between two alternativ

124 re obtained with pharmacologic inhibition of prothrombin expression or inhibition of thrombin proteol

125 Reduced prothrombin expression was associated with lower mitotic

126 No significant increase in prothrombin F1 + 2 was noted during NMP.

127 To explore the hypothesis that reduced prothrombin (factor II [FII]) levels in SCD will limit v

128 irect comparison of the binding constants of prothrombin, factor X, activated factor VII, and activat

129 Prothrombin features a conformation 80 A long, with frag

130 vWbp bound to prothrombin, fibrinogen, fibronectin, and factor XIII, w

131 Prothrombin (FII) is activated to alpha-thrombin (IIa) b

132 o Gln reveals that prothrombinase can cleave prothrombin following Arg side chains shifted by as many

133 mbin is produced from the C-terminal half of prothrombin following its proteolytic activation.

134 Prethrombin-1 differs from prothrombin for the absence of 155 residues in the N-ter

135 investigate the binding of the Gla domain of prothrombin fragment 1 (PT1) to anionic lipids in the pr

136 thrombin generation in vivo), tissue factor, prothrombin fragment 1 + 2 (F1+2), and normalized APC se

137 and future VTE have been found for d-dimer, prothrombin fragment 1+2, and soluble P-selectin and als

138 extracorporeal membrane oxygenation therapy, prothrombin fragment 1.2 (F1.2) (1.36-2.4 microM), throm

139 ligand), coagulation activation/inhibition (prothrombin fragment 1.2, thrombin/antithrombin complex,

140 7.6 ng/ml to 33.2 +/- 17.4 ng/ml, p = 0.003; prothrombin fragment 1.2: 95.6 +/- 45.6 micromol/l to 24

141 Concentration of prothrombin fragment F1 + 2 (marker of coagulation activ

142 Levels of prothrombin fragment F1 + 2 (P = 0.031) and D-dimers (P

143 The PAI-1/tPA complexes, D-dimers, and prothrombin fragment F1 + 2 were measured in plasma samp

144 , as reflected by lower plasma levels of the prothrombin fragment F1+2 (mean peak levels 57.9% [p<0.0

145 or necrosis factor receptor-1), coagulation (prothrombin fragment F1+2 and d-dimer), and endothelial

146 d-dimer, prothrombin fragment F1.2 and TATc concentrations were l

147 and amyloid-P) and coagulation (D-dimer and prothrombin-fragment 1+2) markers were determined.

148 transient increases in levels of d-dimer and prothrombin fragments 1 and 2 were observed, which resol

149 lasma was associated with the recruitment of prothrombin, FXIII, and fibronectin as well as the forma

150 n probands compared with individuals without prothrombin G20210A (OR, 1.45; 95% CI, 0.96-2.2).

151 bophilic defects, including factor V Leiden, prothrombin G20210A defect, and deficiencies of the natu

152 sufficient regarding the predictive value of prothrombin G20210A homozygosity for recurrent VTE and t

153 er, it is unknown whether testing for FVL or prothrombin G20210A improves outcomes in adults with VTE

154 Carrier frequencies for prothrombin G20210A in fatal PE were 2- to 10-fold highe

155 Heterozygosity for prothrombin G20210A is not predictive of recurrent VTE i

156 a history of VTE who were tested for FVL or prothrombin G20210A or in family members of individuals

157 of VTE in family members of individuals with prothrombin G20210A.

158 homozygous FVL; 0.6% (0.4%) for heterozygous prothrombin G20210A; 8.2% (5.5%) for compound heterozygo

159 5.5%) for compound heterozygotes for FVL and prothrombin G20210A; 9.0% (6.1%) for antithrombin defici

160 the fII(WE) mutations within the endogenous prothrombin gene.

161 The coagulation factor prothrombin has a complex spatial organization of its mo

162 Prothrombin has three linkers connecting the N-terminal

163 profound contribution of membrane binding by prothrombin in determining the rate at which it is conve

164 posing a modest 50% reduction in circulating prothrombin in fII+/- mice, a level that carries no sign

165 details on the conformational plasticity of prothrombin in solution and the drastic structural diffe

166 er to access the conformational landscape of prothrombin in solution and uncover structural features

167 rements detect two distinct conformations of prothrombin in solution, in a 3:2 ratio, with the distan

168 we prepared deletion derivatives of fXa and prothrombin in which both the Gla and first EGF-like dom

169 tivated partial thromboplastin time (but not prothrombin index) differed significantly between cirrho

170 Platelets, fibrinogen, prothrombin index, activated partial thromboplastin time

171 based on platelets, fibrinogen, d-dimer, and prothrombin index.

172 ransferase and alanine aminotransferase, and prothrombin international normalized ratio; LR, 0.09; 95

173 y factor Xa by compressing Lnk2 and morphing prothrombin into a conformation similar to the structure

174 Taken together, these data establish that prothrombin is a powerful modifier of SCD-induced end-or

175 of cofactor Va and offers insights into how prothrombin is activated at the molecular level.

176 n important physiological role for Lnk2 when prothrombin is anchored to the membrane.

177 The zymogen prothrombin is composed of fragment 1 containing a Gla d

178 Prothrombin is conformationally activated by von Willebr

179 uring activation of the coagulation cascade, prothrombin is converted to thrombin by prothrombinase,

180 The structure of prothrombin is currently unknown.

181 That prothrombin is linked to early events in CAC was strongl

182 which of these intermediates is formed when prothrombin is processed on the activated platelet surfa

183 The zymogen prothrombin is proteolytically converted by factor Xa to

184 Prothrombin is the zymogen precursor of the clotting enz

185 Two new crystal structures of prothrombin lacking 22 (ProTDelta146-167) or 14 (ProTDel

186 rethrombin-2 into the conventional assay for prothrombin level in human plasma, employing ecarin and

187 olitis showed that mice carrying half-normal prothrombin levels were comparable to control mice in mu

188 , hepatic encephalopathy, variceal bleeding, prothrombin <45%, serum bilirubin >45 mumol/L, albumin <

189 ts for kringle-1 relative to the rest of the prothrombin molecule.

190 et surface, the cleavage of prothrombin, and prothrombin mutants lacking either one of the cleavage s

191 otease thrombin, which is unable to activate prothrombin or prethrombin-2.

192 w the complex assembles and its mechanism of prothrombin processing are of central importance to huma

193 Notecarin D (NotD) is a prothrombin (ProT) activator in the venom of the tiger s

194 Mouse and human prothrombin (ProT) active site specifically labeled with

195 e factor Xa (FXa)-mediated conversion of the prothrombin (ProT) zymogen to active alpha-thrombin (alp

196 activator of the blood coagulation zymogen, prothrombin (ProT).

197 gam et al report that long-term reduction of prothrombin (PT) expression results in diminished vascul

198 atives with factor V Leiden (FVL) or G20210A prothrombin (PT20210A) gene polymorphisms may differ acc

199 strengthened the initial binding of vWbp to prothrombin, resulting in higher activity and an approxi

200 and endothelial cells on fully carboxylated prothrombin reveals new mechanistic insights into functi

201 nonreactive species arising from the loss of prothrombin's phospholipid binding domain (des F1 specie

202 The generation of proteolyzed prothrombin species by preassembled prothrombinase in ph

203 eukocyte and platelet counts, tissue factor, prothrombin split products, D-dimer, P-selectin, factor

204 are 10(6)- to 10(7)-fold less active toward prothrombin than the monomer, with the decrease being at

205 cular species such as the thrombin precursor prothrombin, thrombin in complex with some of its natura

206 fined according to the "50-50 criteria" (ie, prothrombin time <50% and serum bilirubin >50 micromol/L

207 /= 127 g/L; odds ratio, 0.99; p < 0.01), and prothrombin time (</= 58%; odds ratio, 0.98; p < 0.05) w

208 irect bilirubin (0.13 versus 0.1, P = 0.01), prothrombin time (14.4 versus 12.4, P = 0.002), and AST-

209 nd 2.3 [0.8-8.7] microg/mL, p = .05), longer prothrombin time (19.3 [15.4-25.9] vs. 15.3 [14.8-17.1],

210 ody mass index (HR 1.40; 95% CI: 1.01-1.95), prothrombin time (HR 0.79; 95% CI: 0.70-0.90), serum alb

211 We analyzed altered prothrombin time (measured as international normalized r

212 0.0001), alkaline phosphatase (P = 0.0009), prothrombin time (P = 0.0005), and maximal vital capacit

213 h baseline esophageal varices (P = 0.01) and prothrombin time (P = 0.002), but not with disease progr

214 Coagulation studies revealed prothrombin time (PT) 13.5 seconds, internationalized no

215 The low hemolysis of 2.39% with short prothrombin time (PT) and activated partial thromboplast

216 Increases in prothrombin time (PT) and international normalised ratio

217 Prothrombin time (PT) and the associated international n

218 vated partial thromboplastin time (aPTT) and prothrombin time (PT) are clinical tests commonly used t

219 vated partial thromboplastin time (APTT) and prothrombin time (PT) are less sensitive and may be norm

220 neral overview of the plasmatic coagulation, prothrombin time (PT) tests are frequently combined with

221 e (MA), LY30] with their corresponding CCTs [prothrombin time (PT)/activated partial thromboplastin t

222 thod affected only by factors II and X (Fiix-prothrombin time [Fiix-PT]) compared with standard PT-IN

223 s prothrombinase activity and increases both prothrombin time and activated partial thromboplastin ti

224 Knockout FVII mice demonstrated a delayed prothrombin time and decreased plasma FVII expression.

225 varices demonstrated a significantly longer prothrombin time and lower platelet count, there was no

226 d patients had more severe injury, prolonged prothrombin time and partial thromboplastin time (PTT),

227 er 90%, whereas fVII knockdown prolonged the prothrombin time and reduced fVII activity to a similar

228 inverse correlation with platelet count and prothrombin time but not with serum albumin level.

229 r months to years, to maintain a near-normal prothrombin time can reverse the coagulopathy associated

230 ed activated partial thromboplastin time and prothrombin time clotting times to baseline at 60 mins.

231 f seven serine proteases, and FVII-deficient prothrombin time EC2x = 1.2 muM.

232 markers for liver function are bilirubin and prothrombin time expressed as International Normalized R

233 s thrombin potential and partial reversal of prothrombin time following 50 IU/kg.

234 el greater than or equal to 250 mumol/L, and prothrombin time greater than or equal to 30 seconds was

235 actors, and treatment of prolongation of the prothrombin time in critically ill patients using the in

236 ma activated partial thromboplastin time and prothrombin time increased over 10-fold during the bleed

237 owed that patient age older than 65 years, a prothrombin time international normalized ratio greater

238 e influence of several anticoagulants on the prothrombin time limits its diagnostic value.

239 factors that influence dosing, conscientious prothrombin time monitoring, and sage dosage adjustment

240 rtate aminotransferase, cholinesterases, and prothrombin time not differed in 2 groups.

241 hromboplastin time of 49.2 seconds, a normal prothrombin time of 12.4 seconds, and a platelet count o

242 lation panel was unremarkable and included a prothrombin time of 15.4 seconds, an international norma

243 national normalized ratio of more than 11, a prothrombin time of more than 120 seconds, and an activa

244 times are best suited for dabigatran and the prothrombin time or the anti-FXa for rivaroxaban.

245 emia, renal insufficiency, hyponatremia, and prothrombin time prolongation (all P < 0.001).

246 Prothrombin time prolongation is prevalent in critically

247 nsfusion (detection rate of 71%, vs. 43% for prothrombin time ratio >1.2, p < .001).

248 traumatic coagulopathy defined as laboratory prothrombin time ratio >1.2.

249 Point-of-care prothrombin time ratio had reduced agreement with labora

250 ratio had reduced agreement with laboratory prothrombin time ratio in patients with acute traumatic

251 In trauma hemorrhage, prothrombin time ratio is not rapidly available from the

252 Prothrombin time ratio was calculated and acute traumati

253 Laboratory prothrombin time results were available at a median of 7

254 Baseline prothrombin time was 28+/-0.8 secs (n=8) and followed a

255 Mean prothrombin time was shorter in arterial strokes (P < .0

256 Effects on prothrombin time were partially reversed at 50 IU/kg.

257 clotting test with the quick clotting time (prothrombin time), it was possible to diagnose factor VI

258 thological grades, total bilirubin, albumin, prothrombin time, alpha-fetoprotein, and tumor number, w

259 Mean activated partial thromboplastin time, prothrombin time, and international normalized ratio wer

260 , D-dimer, alpha-2-antiplasmin, antitrombin, prothrombin time, and platelet count) and the DIC score

261 A combination of prothrombin time, endothelium-derived CD105-microparticl

262 survival was independently predicted by PS, prothrombin time, extrahepatic tumor spread, macrovascul

263 had hepatic encephalopathy; median levels of prothrombin time, INR, and total bilirubin were, respect

264 iabetes mellitus, relative lymphocyte count, prothrombin time, peripheral artery disease, and contral

265 nogen at the time of surgery, with unchanged prothrombin time.

266 m: age, Glasgow Coma Scale, base excess, and prothrombin time.

267 brain "thromboplastic" activity used in the prothrombin time.

268 or Xa inhibitor which has a strong impact on prothrombin time.

269 , specifically baseline levels of bilirubin, prothrombin time/international normalized ratio, and Mod

270 irubin, albumin, creatinine, and hemoglobin; prothrombin time; and numbers of platelets and white cel

271 ith CO maintained liver function with normal prothrombin times versus a 2-fold prolongation in contro

272 th a relatively modest 1.25-fold increase in prothrombin times, and in the absence of hemorrhagic com

273 g activated partial thromboplastin times and prothrombin times.

274 The prothrombinase complex converts prothrombin to alpha-thrombin through the intermediate m

275 S), binds to discrete sites on FXa, FVa, and prothrombin to alter their conformations, to promote FXa

276 ar-mediated binding to VWF and activation of prothrombin to form S aureus-fibrin-platelet aggregates.

277 secreted coagulase that activates the host's prothrombin to generate fibrin.

278 Exosite-dependent binding of prothrombin to prothrombinase facilitates active site do

279 gnificant flexibility in solution and enable prothrombin to sample alternative conformations.

280 ecent studies have documented the ability of prothrombin to spontaneously convert to the mature prote

281 sembled on the surface of platelets converts prothrombin to thrombin by cleaving at Arg-271 and Arg-3

282 (f)Xa and cofactor fVa, efficiently converts prothrombin to thrombin by specific sequential cleavage

283 Prothrombinase converts prothrombin to thrombin via cleavage at Arg(320) followe

284 es the rate of the proteolytic conversion of prothrombin to thrombin.

285 is catalyzing the proteolytic activation of prothrombin to thrombin.

286 ere, we report that binding of histone H4 to prothrombin under physiological conditions generates thr

287 Prothrombin uses the intramolecular collapse of kringle-

288 To explore the hypothesis that a prothrombin variant favoring antithrombotic pathways wou

289 y normal cleavage at Arg(320) in recombinant prothrombin variants bearing additional Arg side chains

290 Using desGla prothrombin variants in which the individual cleavage si

291 the action of prothrombinase on full-length prothrombin variants lacking gamma-carboxyglutamate modi

292 platelet-associated prothrombinase activates prothrombin via an efficient concerted mechanism in whic

293 d show little specificity of interaction for prothrombin vs. thrombin.

294 In addition to alpha-thrombin enrichment, prothrombin was also efficiently captured from plasma sa

295 Regardless of the agonist used, prothrombin was initially cleaved at Arg271 generating p

296 unchallenged adults genetically depleted of prothrombin was very short ( approximately 5-7 days).

297 More interestingly, prothrombin(WE) expression significantly ameliorated the

298 y, gene-targeted mice carrying low levels of prothrombin were used to directly test the hypothesis th

299 Small angle x-ray scattering measurements of prothrombin wild type stabilized 70% in the closed confo

300 ons document direct binding of histone H4 to prothrombin with an affinity in the low nm range.