ライフサイエンスコーパス: thrombin

1 mice have impaired activation in response to thrombin.

2 ly correlated with the inhibition of PAF and thrombin.

3 lot blood, unlike PLGA particles loaded with thrombin.

4 nd is affected minimally by interaction with thrombin.

5 hrombin than PLGA particles loaded only with thrombin.

6 face protease-activated receptor 1 (PAR1) by thrombin.

7 lly-observed residency times of fibrin-bound thrombin.

8 rleukin (IL)-1alpha is directly activated by thrombin.

9 led to the discovery of a 1 nM inhibitor of thrombin.

10 were similar with adenosine diphosphate and thrombin.

11 nd 21m with 27 nM inhibitory activity toward thrombin.

12 Affinity selection of the library with thrombin, a common protease, revealed a number of enrich

13 Thrombin, a procoagulant protease, cleaves and activates

14 uce the complications of VTE, attenuation of thrombin activatable fibrinolysis inhibitor activity is

15 atelet aggregates and competitively inhibits thrombin-activatable fibrinolysis inhibitor (carboxypept

16 mbomodulin, and inhibiting thrombomodulin or thrombin-activatable fibrinolysis inhibitor (TAFI) norma

17 phil percentage of white cells with LAS, and thrombin-activatable fibrinolysis inhibitor activation p

18 tivator inhibitor 1, and decreased levels of thrombin-activatable fibrinolysis inhibitor and alpha2-a

19 d murine bone-marrow-derived macrophages and thrombin activated human platelets yields results in agr

20 more efficiently killed by human platelets, thrombin-activated platelet releasate, and synthetic pla

21 Interestingly, enhanced thrombin activation in C3(-/-) TM mice and reduction of

22 Direct thrombin activation of platelets through protease-activa

23 d by thrombin, while tissue factor, a potent thrombin activator, colocalized with pro-IL-1alpha in th

24 The device was optimised to detect thrombin activities in serum, achieving a thrombin detec

25 , ASA-treated mice had reduced intravascular thrombin activity and microvascular occlusion as compare

26 techniques, this is the only one to measure thrombin activity in serum dilutions, rather than simply

27 lly and survive into early adulthood without thrombin activity will provide important insight into it

28 trical distribution of fibrin deposition and thrombin activity.

29 ugh animal studies have demonstrated that WE thrombin acts as an anticoagulant through activated prot

30 ied on representative slice before and after thrombin administration (22.20 +/- 6.31 cm(2) vs. 13.28

31 Thrombin also binds to the formed fibrin matrix, but thi

32 Comparative analysis of thrombin and a single-point mutant reveals that the simu

33 It blocks the contact system, but also thrombin and activated protein C (APC), making it an una

34 tly shown, that the FVL mutation accelerates thrombin and APC (activated protein C) formation in carr

35 These studies define distinct thrombin and APC dynamic signaling profiles and a rich a

36 ion (S->V) eliminates residual inhibition of thrombin and APC for both variants, while retaining thei

37 report the global phosphoproteome induced by thrombin and APC signaling in endothelial cells with the

38 l unique dynamic phosphoproteome profiles of thrombin and APC signaling, an enrichment of associated

39 cale simulation, this reduced model predicts thrombin and fibrin co-regulation during thrombosis unde

40 In predicting intrathrombus thrombin and fibrin during 15-min microfluidic experimen

41 induced clot strengthening, but they require thrombin and fibrin generation and are unable to measure

42 and -2 expressions and their main activators thrombin and FXa in the plaque were determined in the pl

43 re, expression of PARs and their activators, thrombin and FXa was diminished after rivaroxaban treatm

44 Inflammatory mediators, such as thrombin and histamine, increase intracellular calcium l

45 omparison of the SC(1-325) fragment bound to thrombin and its inactive precursor prethrombin 2 has in

46 -glycolic acid) (PLGA) particles loaded with thrombin and MnO(2) nanosheets that decompose H(2)O(2) t

47 , NOX1 does not affect platelet responses to thrombin and normal hemostasis, as assayed in tail bleed

48 The thrombin and plasmin concentration peak heights (PH) and

49 its deposition and clearance, including (pro)thrombin and plasmin(ogen), have powerful roles in drivi

50 th factor C (VEGFC) and VEGFD are cleaved by thrombin and plasmin, serine proteases generated during

51 structural architecture of the free forms of thrombin and prethrombin-2, consistent with an E*-E equi

52 ffect is plasma dependent but independent of thrombin and rivaroxaban's anticoagulatory capacity.

53 rm anticoagulation with dabigatran inhibited thrombin and the formation of occlusive thrombi in AD; p

54 pounds were inactive against the off-targets thrombin and trypsin.

55 ntrations of clinically relevant human alpha-thrombin and vascular endothelial growth factor using ch

56 ers with single dithiophosphate moieties and thrombin and VEGF, respectively, display equilibrium dis

57 tion and more substantial production of FXa, thrombin, and fibrin as compared with controls.

58 agulant properties and the ability to affect thrombin- and cancer-cell-induced platelet aggregation.

59 Indeed, in EA.hy926 cells, thrombin- and histamine-stimulated p38 activation depend

60 g mediators and the deficiency of endogenous thrombin antagonists.

61 predicted the measured clot elution rate of thrombin-antithrombin (TAT) and fragment F1.2 in the pre

62 easing baseline prothrombin fragment 1.2 and thrombin-antithrombin complex levels in the placebo grou

63 hrombin activation fragment 1+2 (F1+2), TAT (thrombin-antithrombin complex), APC, and D-dimer were mo

64 higher baseline prothrombin fragment 1.2 or thrombin-antithrombin complex.

65 easing baseline prothrombin fragment 1.2 and thrombin-antithrombin complex.

66 cted increased circulating tissue factor and thrombin-antithrombin complexes in patients with NEC.

67 F1+2 (prothrombin fragment 1+2) and TAT (thrombin-antithrombin III) were assessed immediately bef

68 posed sensor was tested for the detection of thrombin-aptamer interactions based on silane-coupling s

69 the capacitive biosensor is validated using thrombin as a model analyte.

70 Using the clotting protease thrombin as a model system, we investigate the molecular

71 Using the trypsin-like, clotting protease thrombin as a relevant model system, we show that its co

72 serum-transfer nephrotoxic model identified thrombin as a surrogate pathway for complement activatio

73 c acid, collagen, adenosine diphosphate, and thrombin as secondary endpoints.

74 Specific binding to human thrombin as well as high stability in the presence of RN

75 atelet/neutrophil extracellular traps (NETs)/thrombin axis, using COVID-19 specimens, cell-based inhi

76 d; we hypothesized that this could be due to thrombin becoming physically trapped within fibrin fiber

77 Nucleic acid aptamers selected for thrombin binding have been previously shown to possess a

78 lecular dynamics (MD) simulations of the TBA-thrombin binding indicated enhanced Guanine 4 (G4) struc

79 alue changes of capacitance originating from thrombin binding with the aptamers modified on the biose

80 eters affecting the molecular anchoring of a thrombin-binding aptamer (TBA) onto polymethacrylate mon

81 ional RNA origami molecules bearing multiple thrombin-binding RNA aptamers and showing significantly

82 Thrombin binds a specific Na(+) ion next to Asp189, whic

83 ing antibody could significantly shorten the thrombin burst in response to tissue factor in platelet-

84 ontrast, alpha1AT-SLLR/S residually inhibits thrombin, but no longer APC.

85 alpha1AT-SMTR/S no longer inhibits thrombin, but residually inhibits APC.

86 Targeted inhibition of thrombin by a nanomedicine-based approach was protective

87 abel-free sensitive detection of human alpha-thrombin by an aptamer-functionalized nanoporous alumina

88 Ca(2+)] response to stimulation with 5-HT or thrombin, by an estimated 25%, with an effect size of 0.

89 esized that a particle designed to discharge thrombin cargos in response to an external stimulus, suc

90 plex that upon activation by calcium binding/thrombin cleavage covalently cross-links preformed fibri

91 Mice bearing a mutation in the IL-1alpha thrombin cleavage site (R114Q) exhibited defects in effi

92 Thrombin cleaved pro-IL-1alpha at a site perfectly conse

93 Thrombin-cleaved IL-1alpha was detected in humans during

94 e proteases, recognize different substrates; thrombin cleaves after Arg, whereas trypsin cleaves afte

95 eneration of activated protein C (APC) by TM-thrombin complex and in upregulation of intercellular ad

96 structures of the native and PS2-RNA aptamer:thrombin complexes reveals an RNA-induced fit in the lat

97 d on silane-coupling surface chemistry, with thrombin concentrations ranging from 2.5 to 40 nM.

98 ms, with aggregation occurring at suboptimal thrombin concentrations.

99 um dilutions, rather than simply quantifying thrombin concentrations.

100 al stem cells is modified to display a novel thrombin construct, giving rise to spontaneous fibrin hy

101 yte proliferation after PHx, indicating that thrombin contributes to liver regeneration primarily by

102 Thrombin-derived C-terminal peptides (TCPs), including a

103 The linear range for thrombin detection in human serum solution is from 10 pM

104 ct thrombin activities in serum, achieving a thrombin detection limit of 38 muU/mul in 10% (v/v) huma

105 tal platelets showed enhanced sensitivity to thrombin due to higher expression of several downstream

106 Thrombin enhanced CSF-2 secretion in TDC cultures fourfo

107 s of human blood coagulation factor XIIa and thrombin exhibiting a 1,2,4-triazol-5-amine scaffold.

108 Thrombin-feedback activation of FXIa became prominent an

109 /VIIa or FIXa), FIXa (via TF/FVIIa or FXIa), thrombin, fibrin, and FXIa.

110 Thrombin-fibrin binding is often described as two indepe

111 These studies establish that the thrombin/fibrinogen axis is fundamental to host antimicr

112 telet aggregation in response to full-length thrombin, followed by clinical association analyses, Men

113 phenotype that is characterized by increased thrombin formation after coagulation activation.

114 ets (PS(plt)) by showing that PS(plt) limits thrombin formation in large veins.

115 ced FVIII-SQ accelerated early factor Xa and thrombin formation, which may explain the higher OS acti

116 toprotective properties that is generated by thrombin from the zymogen precursor protein C in a react

117 ynamic T2*w MRI facilitated visualization of thrombin + Gd solution transiting through cerebral vascu

118 dependent increase in the rate and amount of thrombin generated and overall clot strength.

119 During thrombosis, thrombin generates fibrin, however fibrin reversibly bin

120 tor vWbp was identified as the source of the thrombin-generating potential underlying fibrin(ogen)-de

121 Simultaneously, the thrombin generation (TG) assay was used to assess their

122 Concurrent to impaired PG, HFD also enhanced thrombin generation (TG).

123 Both mAbs increase thrombin generation and promote plasma clotting.

124 monocytes, thereby liberating factor Xa for thrombin generation and protease activated receptor 1/2

125 By using the calibrated automated thrombin generation assay, we showed that a PN-1-neutral

126 oration into prothrombinase was supported by thrombin generation assays in plasma.

127 oluble thrombomodulin having higher baseline thrombin generation biomarker levels had lower mortality

128 Moreover, the PZ antibody enhanced thrombin generation both in the absence and presence of

129 on of kidney injury following attenuation of thrombin generation by argatroban in a serum-transfer ne

130 m premature rupture of membranes (PPROM) and thrombin generation by decidual cell-expressed tissue fa

131 activation of protein C, which downregulates thrombin generation by enzymatically inactivating factor

132 ce given human FXII-Lys/Arg309, induction of thrombin generation by infusion of tissue factor results

133 vity that is based on its ability to enhance thrombin generation due to binding coagulation factors X

134 PI-PZ complex produced a major inhibition of thrombin generation during prothrombinase-catalyzed acti

135 actions are compared with published data for thrombin generation in vitro in 1) quiescent plasma expo

136 ses, and some models qualitatively replicate thrombin generation thresholds across a series of tissue

137 in our understanding of the contribution of thrombin generation to arterial thrombosis and the role

138 he capacity of published numerical models of thrombin generation to reproduce experimentally observed

139 Because beta2-GPI-mediated MBL-dependent thrombin generation was increased after priming the endo

140 ed with a PZ-specific antibody and decreased thrombin generation when exogenous ZPI-PZ complex was ad

141 These showed enhanced thrombin generation when the inhibitor was neutralized w

142 ed activated partial thromboplastin time and thrombin generation), similar to human samples containin

143 tions of the usual target, minimal effect on thrombin generation, and adverse effects on portal press

144 on exhibits a severe reduction in secretion, thrombin generation, and fibrinogen cleavage.

145 s recombinant TFshort inhibited factor Xa or thrombin generation, excluding a dominant-negative mecha

146 re all lower, which, together with increased thrombin generation, indicate hypercoagulability.

147 try, thromboelastography, sonorheometry, and thrombin generation, may eventually have a role in the e

148 thelial inflammation, complement activation, thrombin generation, platelet, and leukocyte recruitment

149 complement and promotes complement-dependent thrombin generation.

150 ophilia, PN-1 neutralization did not improve thrombin generation.

151 C, protein S, and antithrombin) factors and thrombin generation.

152 y activates FIX, which ultimately results in thrombin generation.

153 ent with measured albumin elution, with most thrombin (>99%) being fibrin-bound.

154 The thrombin mutant W215A/E217A (WE thrombin) has been one of the best characterized constru

155 tion by selective inhibition of factor Xa or thrombin, has renewed the interest in dual-pathway inhib

156 Moreover, multiple GPCRs agonists, including thrombin, histamine, prostaglandin E(2), and ADP, stimul

157 in C is a natural anticoagulant activated by thrombin in a reaction accelerated by the cofactor throm

158 tural stability of TBA upon interaction with thrombin in an ionic environment.

159 or has detection limits of 1 pM and 10 pM of thrombin in phosphate buffered saline and mimic serum so

160 cal tools for studying the role of FXIIa and thrombin in physiological and pathological processes.

161 1 and PAR4 are drug targets, but the role of thrombin in platelet aggregation remains largely unexplo

162 iable signal/noise ratio, was 10 pM of alpha-thrombin in presence of 500 muM HSA.

163 gel formed by directly mixing fibrinogen and thrombin in solution.

164 h tumor necrosis factor alpha (TNFalpha) and thrombin in the activation and permeability of primary h

165 The model required free thrombin in the clot (~100 nM) to have an elution half-l

166 We further estimated that ~30% of thrombin in the experiments to which we compare our mode

167 binds to trypsin in protonated state and to thrombin in unprotonated state at P1 along with differen

168 e data demonstrate the conserved function of thrombin in zebrafish and provide insight into the role

169 hozoite-stage P. falciparum-IE and prolonged thrombin-induced barrier disruption in both resting and

170 ereas adducin-1 depletion completely ablated thrombin-induced barrier disruption without compromising

171 CXCR4-associated effects on thrombin-induced beta-arrestin-2 recruitment to and sign

172 recruitment to recombinant PAR1 and enhanced thrombin-induced Ca(2+) mobilization.

173 Importantly, thrombin-induced Ca(2+) signaling and EC permeability we

174 h stemness (Nestin, Sox2) was regulated, and thrombin-induced cell death was prevented.

175 We hypothesized that thrombin-induced colony-stimulating factor-2 (CSF-2) in

176 Surprisingly, the thrombin-induced degradation of IkappaBalpha in the cyto

177 adin and adducin-1 actin binding proteins in thrombin-induced endothelial barrier disruption is unvei

178 In hPPECs, TM2 inhibited thrombin-induced ERK1/2 phosphorylation and activation o

179 CXCR4 siRNA knockdown inhibited thrombin-induced ERK1/2 phosphorylation.

180 f ATG7 using si-RNA significantly attenuated thrombin-induced expression of proinflammatory molecules

181 Whereas thrombin-induced extracellular signal-regulated protein

182 trophoblast-expressed CSFR2, contributes to thrombin-induced fetal membrane weakening, eliciting abr

183 The thermodynamic profile of calcium/thrombin-induced FXIII-A activation explains the role of

184 st that CXCR4:PAR1 heteromerization enhances thrombin-induced G protein signaling of PAR1 and PAR1-me

185 Finally, TM2 dose-dependently inhibited thrombin-induced impairment of hPPEC monolayer permeabil

186 an be minimized, and that MAP sensitivity to thrombin-induced increase in monolayer permeability is s

187 act on human platelets, suppressing classic thrombin-induced inside-out signaling events (eg, Akt ac

188 rombin signaling proteins blocks effectively thrombin-induced junction disassembly, and that MAPs car

189 This is likely due to suppression of thrombin-induced phosphorylation and thereby inactivatio

190 p = 3.0 x 10(-42)) associated with increased thrombin-induced platelet aggregation (beta = 0.70, SE =

191 against platelet-activating factor (PAF) and thrombin-induced platelet aggregation.

192 venous thromboembolism through its effect on thrombin-induced platelet reactivity.

193 We show that thapsigargin and thrombin-induced SOCE was markedly reduced in Mylk-L(-/-

194 Actin stress fiber dynamics are required for thrombin-induced translocation of RelA/p65 to the nucleu

195 also revealed subtleties in the mechanism of thrombin inhibition, between and within the families, th

196 VT is fatal but is fully rescued by thrombin inhibition.

197 zed to a highly potent, neutral, non-prodrug thrombin inhibitor by designing, synthesizing, and testi

198 abigatran, a clinically approved oral direct thrombin inhibitor with a low risk of intracerebral hemo

199 consisting of targeting a natural and potent thrombin inhibitor, expressed by platelets, called prote

200 tamin K antagonists, heparins, fondaparinux, thrombin inhibitors and factor Xa inhibitors.

201 Despite extensive research on small molecule thrombin inhibitors for oral application in the past dec

202 ng anticoagulants, such as the factor Xa and thrombin inhibitors, are relatively safe and effective i

203 o identify seven tick proteins with putative thrombin inhibitory activity that we predict to be postt

204 nto considerations its anti-inflammatory and thrombin-inhibitory actions, a bioavailable form of quer

205 Although thrombin is a key enzyme in the coagulation cascade and

206 Thrombin is an enzyme that plays many important roles in

207 used in the experiments or, less likely, 2) thrombin is irreversibly inhibited at a faster-than-expe

208 exists predominantly in the E* form, whereas thrombin is more rigid and exists predominantly in the E

209 While thrombin is the key protease in thrombus formation, othe

210 s cast doubts on recent hypotheses that free thrombin is zymogen-like and transitions to protease-lik

211 ilibrium and providing no evidence that free thrombin is zymogen-like.

212 st gamma-thrombin, which is a modified alpha-thrombin lacking the aptamer binding epitope.

213 pite the faster onset of coagulation, global thrombin levels were unaffected.

214 in-specific and not likely due to effects on thrombin levels.

215 We present a congeneric series of thrombin ligands with a variety of functional groups tri

216 of detection (LOD) of 0.1 nM), a biomarker (thrombin, LOD of 50 pM), and a drug (cocaine, LOD of 5 n

217 provide evidence that parasite products and thrombin may interact to increase brain endothelial perm

218 The notion of physically trapped thrombin may provide new insights into conflicting obser

219 , a variant refractory to prothrombinase- or thrombin-mediated cleavage, we observed variant affiniti

220 ATG7 silencing also reduced thrombin-mediated EC permeability by inhibiting the disa

221 al, we used intra-arterial administration of thrombin mixed with gadolinium and visualized the occlus

222 ed biosensor was tested for the detection of thrombin molecule concentrations ranging from 0.625 mug/

223 The thrombin mutant W215A/E217A (WE thrombin) has been one o

224 the antithrombotic potency of this or other thrombin mutants.

225 genes that mediate the disruptive effect of thrombin on endothelial cell junctions.

226 vation marker expression, while responses to thrombin or adhesion to fibrinogen were not affected.

227 phorylated proteins not previously linked to thrombin or APC signaling, a function for afadin and add

228 Thrombin or NETosis inhibition or C5aR1 blockade attenua

229 ylcoumarin (AMC) from substrates specific to thrombin or plasmin was monitored.

230 The tissue factor-thrombin-PAR-1 signaling axis in tumor cells promotes PD

231 f KPC and KPC-Par-1(KO) cells indicated that thrombin-PAR-1 signaling significantly altered immune re

232 d further indicate that one key mechanism of thrombin/PAR-1-mediated tumor growth is suppression of a

233 ulmonary fibrosis (PF); TGF-beta, Factor Xa, thrombin, plasmin and uPA all induced fibroblast/myofibr

234 alpha-Thrombin plays a critical role in coordinating thromboti

235 ynthesis of a membrane-binding supercationic thrombin-polymer surfactant complex.

236 Thrombin-pretreated TDC-derived conditioned media supern

237 edroxyprogesterone acetate (MPA) +/- 1 IU/mL thrombin pretreatment for 4 hours, washed, and then incu

238 ed bacterial clearance was dependent on (pro)thrombin procoagulant function, supporting a suspected r

239 vere disease led to a significantly improved thrombin production in PRP, underlining the regulatory r

240 IX (FIX) respectively, lead to insufficient thrombin production, and therefore to bleeding.

241 Afadin depletion resulted in enhanced thrombin-promoted barrier permeability, whereas adducin-

242 We previously showed that thrombin promotes endothelial barrier disruption through

243 examining cytokine proproteins for potential thrombin protease consensus sites.

244 dence suggests that CXCR4 activation reduces thrombin/protease-activated receptor 1 (PAR1)-induced im

245 Changes in plasma levels of thrombin, prothrombin activation fragment 1+2 (F1+2), TA

246 et Inhibition and Patient Outcomes], TRACER [Thrombin Receptor Antagonist for Clinical Event Reductio

247 the protease-activated receptor-1 (PAR-1), a thrombin receptor expressed by vECs, neuronal cells, and

248 We find that the thrombin receptor PAR4 triggers cell membrane blebbing i

249 ntly discovered that global knock-out of the thrombin receptor, also known as Protease Activated Rece

250 Pharmacologic inhibition of the principal thrombin receptor, protease activated receptor-1 (PAR-1)

251 ited increased platelet aggregation to TRAP (thrombin receptor-activating peptide) (children with SDB

252 a leftward shift in the dose/response for a thrombin receptor-activating peptide, an increased maxim

253 Thrombin receptors PAR1 and PAR4 are drug targets, but t

254 Protease-activated receptor 1 (PAR1), a thrombin-responsive G protein-coupled receptor (GPCR), i

255 group and others have previously shown that thrombin's procoagulant and anticoagulant activities can

256 Addition of the trigger protein, thrombin, selectively opens the gate and enables a 330-f

257 er-soluble fibrinogen, following cleavage by thrombin, self-polymerize to form water-insoluble fibrin

258 Of the recently reported ultra-sensitive thrombin sensing techniques, this is the only one to mea

259 tivated receptor 4 (PAR4) mediates sustained thrombin signaling in platelets and is required for a st

260 As (sgRNAs) that target genes encoding known thrombin signaling proteins blocks effectively thrombin-

261 wnstream coagulation proteases factor Xa and thrombin significantly attenuates heme-induced microvasc

262 mutagenesis results in a mutant activated by thrombin significantly faster than wild type.

263 lso more rigid than the blood clot formed by thrombin solution.

264 t the allelic effect is highly platelet- and thrombin-specific and not likely due to effects on throm

265 We then repeated Candida killing assays with thrombin-stimulated or unstimulated washed platelets and

266 Moreover, dilution of releasates from thrombin-stimulated platelets showed that the toxicity o

267 Whereas thrombin stimulation reduced surface expression of PAR1,

268 Trypsin and thrombin, structurally similar serine proteases, recogni

269 significantly active toward the fluorescent thrombin substrate used in the experiments or, less like

270 all shear rate, high muM-levels of intraclot thrombin suggest robust prothrombin penetration into clo

271 Ligand binding to thrombin takes place exclusively in the E form without s

272 Simultaneous thrombin (TG) and plasmin (PG) generation is useful to a

273 e particles released a 3-fold larger mass of thrombin than PLGA particles loaded only with thrombin.

274 the central blood-clotting serine proteinase thrombin that is also the target of several clinically a

275 or II, is a multidomain zymogen precursor of thrombin that undergoes an allosteric equilibrium betwee

276 zymogen protein C likely interacts with the thrombin-thrombomodulin complex through a rigid body ass

277 dabigatran plasma concentration and diluted thrombin time and ecarin clotting time, and a non-linear

278 ed by the dabigatran-specific assays diluted thrombin time and ecarin clotting time.

279 21 patients (97.5%) with an elevated diluted thrombin time at presentation and 95 of 131 patients (72

280 function, median reversal measured by dilute thrombin time was 100% within 4 h of idarucizumab admini

281 domain, which is able to effectively prolong thrombin time.

282 sic tenase to 15 nM prothrombinase to 15 muM thrombin to 90 muM fibrin.

283 he presence of CXCR4 reduced the efficacy of thrombin to induce beta-arrestin-2 recruitment to recomb

284 ect percutaneous delivery of fibre coils and thrombin to the venous aneurysm of the AVM.

285 sn-1 esterification is markedly activated by thrombin treatment of murine platelets to generate oxidi

286 their receptor N terminus by enzymes such as thrombin, trypsin, and cathepsin-G.

287 and activated by serine proteinases such as thrombin, trypsin, and cathepsin-G.

288 d ligands formed through cleavage of PAR1 by thrombin versus APC result in unique active receptor con

289 aling, the proteins and pathways utilized by thrombin versus APC signaling to induce opposing cellula

290 e microbes in WT mice was restored if active thrombin was administered to the peritoneal cavity.

291 The sensor response to alpha-thrombin was determined in the presence of a high concen

292 data, we made an additional assumption that thrombin was irreversibly sequestered; we hypothesized t

293 is mediated by an ordered water molecule, in thrombin, water is scattered over three hydration sites.

294 ating either human or mouse whole blood with thrombin, we saw a significant decrease in C. albicans s

295 itivity was also characterized against gamma-thrombin, which is a modified alpha-thrombin lacking the

296 nuated by charged Glu192 at the rim of S1 in thrombin, which is replaced by uncharged Gln192 in tryps

297 Platelet activation was triggered by thrombin, which, in turn, was activated by tissue factor

298 vated platelets was cleaved and activated by thrombin, while tissue factor, a potent thrombin activat

299 ates fibrin, however fibrin reversibly binds thrombin with low affinity E-domain sites (KD = 2.8 muM)

300 at three sites in the middle of factor V by thrombin, yielding an N terminus-derived heavy chain and