ライフサイエンスコーパス: thrombin

1 compared to the substrate-bound form (PPACK-thrombin).

2 Antithrombin mainly inhibits factor Xa and thrombin.

3 lly, tightly, and quickly binds and inhibits thrombin.

4 to single strand of DNA sequence and release thrombin.

5 nalized nucleic acid aptamer for human alpha-thrombin.

6 er tumor necrosis factor-alpha (TNFalpha) or thrombin.

7 have not been established in the context of thrombin.

8 ly regulate blood coagulation in response to thrombin.

9 g to its primary endogenous activator, alpha-thrombin.

10 s killed to equal extent but did not require thrombin.

11 he proteinase-activated receptor 1 (PAR1) by thrombin.

12 e zymogen from autoproteolytic conversion to thrombin.

13 d is enzymatically activated specifically by thrombin.

14 n 1 (HC1) was confirmed to be a substrate of thrombin.

15 to the generation of tissue factor (TF) and thrombin.

16 stin-2 biased PAR1 signaling by both APC and thrombin.

17 nt first-in-class, sub-maximal inhibitors of thrombin.

18 and also the interaction between aptamer and thrombin.

19 ecificity of interaction for prothrombin vs. thrombin.

20 tion independently of cofactor activation by thrombin.

21 injury induced by the inflammatory stimulus thrombin.

22 50 x 0.25 mm) for studying the stability of thrombin (0-1400 nM) adhered to a fibrin matrix (0.1-0.4

23 The day after, under CT guidance, human thrombin (1,000 IU) was injected inside the aneurysmatic

24 Ultralow concentrations of thrombin (10(-18) m) as well as a low molecular weight a

25 Thrombin, a critical regulator of the Rho-mediated barri

26 a significant increase in the activation of thrombin, a recognized target of SE2, and excess stimula

27 eral hemostasis-related genes, including the thrombin-activatable receptor PAR-1 (protease-activated

28 gion of an anti-alphaIIbbeta3 mAb fused to a thrombin-activatable, low-molecular-weight pro-uPA (PLT/

29 The i.v. injection of thrombin-activated platelets into CD40(-/-)apoE(-/-) mic

30 brinogen and PAR1, the trypsin-like protease thrombin activates the anticoagulant protein C in a reac

31 We show that platelet-like thrombin activation is apparently responsible for the di

32 partially inhibited by hirudin, which blocks thrombin activation of FXI.

33 , we observed profound platelet aggregation, thrombin activation, and fibrin clot formation within (a

34 creased adhesion in the basal state and upon thrombin activation.

35 protein C in hepatocytes is critical for its thrombin activation.

36 vealing that convertase cleavage can precede thrombin activation.

37 A revealed that avathrin interacts with the thrombin active site and exosite-I.

38 Elevated thrombin activity underlies obesity-linked thromboemboli

39 nificantly lower quantities of intravascular thrombin activity, reduced platelet aggregation, and imp

40 ases and proteins granted the measurement of thrombin added to healthy human plasma with same high se

41 re also supported by a mathematical model of thrombin adhesion to fibrin, which demonstrates that thr

42 phaIIbbeta3 activation upon stimulation with thrombin, ADP-mediated alphaIIbbeta3 activation is reduc

43 cells, and exenatide significantly inhibited thrombin-, ADP-, and collagen-induced platelet aggregati

44 U/mL) inhibits 72% of the active clot-bound thrombin after approximately 10 min at 92 s(-1), while n

45 e prothrombin (ProT) zymogen to active alpha-thrombin (alphaT).

46 ch was exemplified on QiShenYiQi Pills using thrombin and angiotensin converting enzyme as "quality b

47 Thrombin and collagen increased exosome content of alpha

48 lified by specific fluorescence detection of thrombin and factor Xa at only 500 fM concentration.

49 d receptors (PARs) can activate HSCs through thrombin and factor Xa, which are known PAR agonists, an

50 Our aim was to investigate the role of thrombin and fibrinogen gamma' in modulating fibrin stru

51 of fibers is an important mechanism by which thrombin and fibrinogen gamma' modulate fibrin clot stru

52 d extrinsic coagulation cascades upstream of thrombin and fX.

53 nts (DOAC), and currently such inhibitors of thrombin and fXa are in clinical use.

54 We used three endogenous GPCR agonists: thrombin and histamine, which disrupt endothelial barrie

55 vident in microvessels directly treated with thrombin and in those located in adjoining thrombin-free

56 ive inhibitor with an affinity of 545 pM for thrombin and is 4 orders of magnitude more selective tow

57 ) is a G protein-coupled receptor (GPCR) for thrombin and is proteolytically activated, similar to th

58 ence the free energy of binding, between the thrombin and its aptamer reduce as the applied electric

59 t from identifying a function of proteolyzed thrombin and its fragments, our findings provide an inte

60 The serpin antithrombin III (ATIII) targets thrombin and other proteases involved in blood coagulati

61 Our results suggest that in vivo-generated thrombin and plasmin do not directly activate the comple

62 h FXa/PCPS and E coli infusion led to robust thrombin and plasmin generation.

63 Despite inducing a strong burst of thrombin and plasmin, FXa/PCPS infusion did not produce

64 ier dysfunction caused by vasoactive peptide thrombin and proinflammatory bacterial wall lipopolysacc

65 The aptamer was found to be selective for thrombin and required the modifications for binding affi

66 ed that although recombinant wild type alpha-thrombin and rIIa(S478A) were able to induce clotting an

67 microneedle-based patch can sense activated thrombin and subsequently releases heparin to prevent co

68 Here, we present a fusion protein where thrombin and the EGF456 domain of thrombomodulin are con

69 amer TBA15 to its protein target human-alpha-thrombin and to probe the hybridization of DNA.

70 Instillation of thrombin and XeC into adjacent restricted regions increa

71 te injury during nephrosis, and suggest that thrombin and/or podocyte-expressed thrombin receptors ma

72 al distributions of the key enzymatic (i.e., thrombin) and structural (i.e., platelets and fibrin) co

73 vation at low but not high concentrations of thrombin, and maximal platelet activation at high concen

74 xposure to inflammatory factors such as LPS, thrombin, and TNFalpha, as has been observed in vivo.

75 ges in activation biomarkers of coagulation (thrombin-antithrombin [TAT]), fibrinolysis (plasmin-anti

76 ombin fragment 1.2 (F1.2) (1.36-2.4 microM), thrombin-antithrombin complex (14.5-50 microg/L), and D-

77 ng tissue factor production, reducing plasma thrombin-antithrombin complex levels and fibrinogen depo

78 leukin-6, and -10); "coagulation" (D-dimers, thrombin-antithrombin complex); "oxidative stress" (urin

79 stasis (endogenous thrombin potential [ETP], thrombin-antithrombin complex, plasmin-alpha2-antiplasmi

80 Microvesicle tissue factor activity, thrombin-antithrombin complexes, and D-dimers were measu

81 e was no difference in levels of circulating thrombin-antithrombin complexes.

82 in increased platelet activation, increased thrombin/antithrombin complex, and decreased bleeding ti

83 v/TM injected after endotoxin did not reduce thrombin/antithrombin complexes; nor did antibodies that

84 sTM did not, and augmented APC production by thrombin approximately 50-fold more than sTM.

85 iosensor requires the clear understanding of thrombin-aptamer interaction properties in real-like env

86 influence of electrostatic potential on the thrombin/aptamer complex, our computations show that the

87 streptavidin can combine with biotin labeled thrombin aptamers.

88 Using thrombin as a model, a relationship was established betw

89 Using thrombin as the protease, Cdc50p remains intact and in c

90 2.8 muM) and approximately 0.3 molecules of thrombin at high-affinity binding sites (Kd = 0.15 muM).

91 The crystal structure of thrombin-avathrin complex at 2.09 A revealed that avathr

92 o model of infection, a dynamic NET-platelet-thrombin axis that promotes intravascular coagulation an

93 ts shed additional light on the mechanism of thrombin binding and inhibition by this family of saliva

94 , is the region mainly responsible for alpha-thrombin binding and inhibition.

95 Indeed, we observed decreased thrombin binding and inhibitory properties even when usi

96 Thrombin binding aptamers represent promising candidates

97 thrombin initially binds to the low-affinity thrombin binding sites before preferentially equilibrati

98 models of fibrin formation, exosite-mediated thrombin binding to fibrin contributes to clot stability

99 We present thrombin-binding aptamer amphiphiles that self-assemble

100 n situ-generated adherent, resorbable plasma-thrombin biologic scaffold, was evaluated in diabetic ra

101 e biological element in the realization of a thrombin biosensor.

102 ng elements for the development of real-time thrombin biosensors; however implementation of such bios

103 ctions has a powerful influence on whether a thrombin burst occurs and the thrombin response when it

104 ased significantly 45 min after injection of thrombin but not with injection of PBS as a vehicle cont

105 vates the clotting proteinases factor Xa and thrombin by forming covalent complexes with them.

106 (APC) breaks down the complex that produces thrombin by proteolytically inactivating factor Va.

107 ngside PAR1 and PAR4 to the targets, whereby thrombin can affect tissue function.

108 st that the protein response, which involves thrombin-catalyzed conversion of a soluble plasma protei

109 Thrombin-catalyzed fibrin formation and fibrin susceptib

110 ese data establish a novel mechanism whereby thrombin cleavage of HC1 regulates the adhesive properti

111 In humans, thrombin cleavage of the propeptide at PR(221) downward

112 onical extracellular site different from the thrombin-cleavage site and thus initiates biased recepto

113 troma-derived OPN for HSC aging and identify thrombin-cleaved OPN as a novel niche informed therapeut

114 Exposure of aged HSCs to thrombin-cleaved OPN attenuates aging of old HSCs, resul

115 proteinuria in two rat nephrosis models, and thrombin colocalized with a podocyte-specific marker in

116 bility to GO, leads to the desorption of TBA-thrombin complex from electrode surface and significant

117 rombin solution and formation of the aptamer-thrombin complexes which had weak binding ability to GO,

118 e biosensor's signal was proportional to the thrombin concentration from 0.1 to 10nM with a detection

119 inear relationship between RLS increment and thrombin concentration in the range of 60pM-6.0nM with a

120 ril packing was confirmed in plasma for high thrombin concentrations and fibrinogen-deficient plasma

121 , a relationship was established between the thrombin concentrations and the PA ratio, with a dynamic

122 ation thrombin may be cytoprotective, higher thrombin concentrations may contribute to podocyte injur

123 R4 signaling, leaving a narrow window of low thrombin concentrations that exclusively engage PAR1.

124 We thus hypothesized that thrombin contributes to podocyte injury in a protease-ac

125 ted platelet activation and monocyte-derived thrombin contributes to thrombosis in HIT and identifies

126 initiated the contact pathway and amplified thrombin-dependent factor XI activation.

127 before further coagulation amplification by thrombin-dependent feedback loops enhances the risk of t

128 n and coimmunoprecipitation assays confirmed thrombin-dependent interactions between human protease-a

129 lled by platelets (>40% killing in 2 h) in a thrombin-dependent manner whereas a methicillin-sensitiv

130 s thrombomodulin, unlike other anticoagulant thrombin derivatives engineered to date.

131 elastase cleaves thrombin, generating 11-kDa thrombin-derived C-terminal peptides (TCPs), which bind

132 interconversion for the application of human thrombin detection.

133 ulation receptors in vivo High-concentration thrombin directly injured conditionally immortalized hum

134 or 1 (PAR1) by activated protein C (APC) and thrombin elicits paradoxical cytoprotective and cytotoxi

135 When treated with TNFalpha or thrombin, endothelial monolayers on stiffer substrates s

136 Results indicate that similar to APC, thrombin exerts cytoprotective effects via beta-arrestin

137 bimanus orthologue anophelin, cE5 binds both thrombin exosite I with segment Glu-35-Asp-47 and the ca

138 22, on the other hand, binds specifically to thrombin exosite II and has no affinity to prothrombin a

139 trinsic coagulation pathway independently of thrombin feedback loops.

140 vents, but the mechanistic links between the thrombin/fibrin(ogen) axis and obesity-associated pathol

141 ut not tissue factor- or nucleic acid-driven thrombin formation.

142 d interendothelially to the spatially remote thrombin-free microvessels.

143 h thrombin and in those located in adjoining thrombin-free regions.

144 tive electric field successfully unbinds the thrombin from the aptamer.

145 show that human neutrophil elastase cleaves thrombin, generating 11-kDa thrombin-derived C-terminal

146 FP, purified DNA triggered contact-dependent thrombin generation (TG) and amplified TG initiated by l

147 ng synchronised membrane ballooning requires thrombin generation acting effectively in a positive fee

148 ascade, representing the relevant biology of thrombin generation and the subsequent fibrin deposition

149 We posit that myosin enhancement of thrombin generation could contribute either to promote h

150 g time of FXII-deficient plasma and enhanced thrombin generation in a surface-dependent manner.

151 ring of the antithrombin level and increased thrombin generation in participants with hemophilia A or

152 n vitro, increasing the hematocrit increased thrombin generation in the absence of platelets; however

153 The lead candidate was shown to promote thrombin generation in vitro and to restore fibrin and p

154 us, TF synergistically primes FIXa-dependent thrombin generation independently of cofactor activation

155 others have demonstrated that ex vivo plasma thrombin generation is enhanced during nephrosis, sugges

156 Partial restoration of thrombin generation with recombinant activated factor VI

157 IIa mutants deficient in direct TF-dependent thrombin generation, but preserving FVIIIa generation by

158 G profile with heparin-like effect; falls in thrombin generation, Factor V and Factor VIII to 52%, 19

159 After superficial injury without thrombin generation, no multigranular compartments were

160 We also assessed thrombin generation, platelet-thrombus interactions, and

161 uble TM showed reduced tissue factor-induced thrombin generation.

162 severe laser injury of the vessel wall with thrombin generation.

163 yme that is involved in the amplification of thrombin generation.

164 thrombosis by exhibiting a strong endogenous thrombin-generation capacity that relied on the enzymati

165 a cell-membrane-bound (myristoyl tail) anti-thrombin (hirudin-like peptide [HLL]), which can be perf

166 Thrombin however failed to induce the spatially extensiv

167 Prothrombin (FII) is activated to alpha-thrombin (IIa) by prothrombinase.

168 The results confirm a pivotal role for thrombin in AMR in vivo.

169 The abnormal level of thrombin in body fluids may lead to different diseases,

170 s, we monitored the signaling specificity of thrombin in endothelial cells in response to lipopolysac

171 biosensor was successfully applied to detect thrombin in human plasma.

172 e a promising tool for clinical diagnosis of thrombin in human urine.

173 Detection of thrombin in plasma raises timely challenges to enable th

174 ed a role for the blood-coagulation protease thrombin in regulating the adhesion of monocytic cells t

175 baraensis, and bovine and porcine fibrinogen/thrombin in restructured meat was developed using trypti

176 h2-GFP based assay allowed quantification of thrombin in solution with a detection limit of 2.27aM.

177 Thrombin increased endothelial permeability (evident by

178 Thrombin-induced aggregation was decreased in PP1calpha(

179 -181b and Card10 are important regulators of thrombin-induced EC activation and arterial thrombosis.

180 However, SK1-I pretreatment rescued thrombin-induced EC permeability in Trpc1(-/-) ECs.

181 e siRNA-induced cingulin knockdown augmented thrombin-induced EC permeability monitored by measuremen

182 nhancement or the protective effects against thrombin-induced EC permeability, but abolished the adva

183 g the PP1c binding site moderately decreased thrombin-induced human platelet aggregation.

184 Subsequently, the thrombin-induced increase in endothelial F-actin was det

185 XeC also inhibited the thrombin-induced increase in the amplitude of endothelia

186 Increased thrombin-induced permeability in ECs with depleted cingu

187 oteins that could be processed into multiple thrombin inhibiting peptides appear to be widespread amo

188 Moreover, nonspecific thrombin inhibition has been shown to decrease proteinur

189 enotype is fatal but can be fully rescued by thrombin inhibition.

190 e preparation of a nonpeptidic, polar direct thrombin inhibitor as a single, macrocyclic esterase-cle

191 ated bleeding in vivo that is induced by the thrombin inhibitor dabigatran.

192 Avathrin: a novel thrombin inhibitor derived from a multicopy precursor in

193 e, which we previously identified as a novel thrombin inhibitor from the same tick species.

194 ontrast, treatment with dabigatran, a direct thrombin inhibitor, limited HFD-induced obesity developm

195 ing thrombalexin (TLN), a novel cell binding thrombin inhibitor, using porcine and unused human kidne

196 ing Thrombalexin (TLN), a novel cell binding thrombin-inhibitor, using porcine and unused human kidne

197 Therefore, direct thrombin inhibitors may represent an alternative to vita

198 here how this technology has been applied to thrombin inhibitors to generate a novel class of drugs t

199 nt tissue-type plasminogen activator, direct thrombin inhibitors, and antiplatelet treatments.

200 adhesion to fibrin, which demonstrates that thrombin initially binds to the low-affinity thrombin bi

201 Thrombin initiates human platelet aggregation by coordin

202 otic stroke induced by either intra-arterial thrombin injection or ferric chloride application follow

203 During injury, the key enzyme thrombin is formed, leading to generation of fibrin.

204 relaxation dispersion data revealed that apo-thrombin is highly dynamic, with mus-ms motions througho

205 As the concentration of thrombin is increased, PAR1 signaling is quickly overcom

206 Thrombin is known to signal to cells by cleaving/activat

207 Thrombin is produced from the C-terminal half of prothro

208 Overall, thrombin is robustly generated within clots by the extri

209 Ang-2 and thrombin levels were measured by ELISA and Western blott

210 ne, higher C-reactive protein, D-dimer, peak thrombin, lower Ks, shorter lag phase, decreased D-Drate

211 RIIA and transactivation by monocyte-derived thrombin markedly increases Annexin V and factor Xa bind

212 First, evidence that thrombin may be as important as platelets to thrombosis

213 s have shown that, whereas low-concentration thrombin may be cytoprotective, higher thrombin concentr

214 s enhanced during nephrosis, suggesting that thrombin may contribute to nephrotic progression.

215 form and the possible modes of deactivation (thrombin mediated secondary cleavage) of the activated f

216 ontrast the contribution of PAR1 and PAR4 to thrombin-mediated activation of the platelet fibrin rece

217 MicroRNA-181b inhibits thrombin-mediated endothelial activation and arterial th

218 such as platelet spreading on fibrinogen and thrombin-mediated fibrin clot retraction.

219 and activation peptides, we determined that thrombin-mediated injury depended upon interactions betw

220 controls but was completely restored when TM/thrombin-mediated TAFI activation was inhibited.

221 By pairing localized vascular injury with thrombin microinjection in the mesenteric circulation of

222 olecule of fibrin can bind approximately 1.6 thrombin molecules at low-affinity binding sites (Kd = 2

223 is the result of a constant rearrangement of thrombin molecules within a dense matrix of binding site

224 demonstrate that the proteolytic activity of thrombin negatively regulates the adhesion of monocytes

225 markedly reduced generation of factor Xa and thrombin on platelets.

226 othelial monolayers treated with TNFalpha or thrombin on stiffer substrates, indicating elevated cell

227 Blocking phosphatidylserine, inhibiting thrombin or blocking PAR1 receptor, largely prevented sy

228 S365L did not form stable complexes with thrombin or factor Xa, and the I207T/I207A variants inhi

229 data provide proof of concept that targeting thrombin or fibrin(ogen) may limit pathologies in obese

230 ltaIIa)) that cannot be cleaved/activated by thrombin or FXa also enhanced TFPI-mediated inhibition o

231 d peptide, adenosine 5'-diphosphate, A23187, thrombin, or U46619).

232 Thrombin- or collagen-induced platelet aggregation and s

233 ct platelets with PAD4 suppressed ADAMDEC1-, thrombin-, or collagen-induced release of HMW-EGF.

234 As models, several proteins, including human thrombin, PDGF-BB, Avidin, and His-tagged recombinant pr

235 rly, ex vivo incubation of baboon serum with thrombin, plasmin, or FXa did not show noticeable comple

236 okinase was released by IL-1, TNF-alpha, and thrombin (positive control), but not estrogen.

237 outcome was percentage change in endogenous thrombin potential (ETP) from randomisation to day 42, w

238 phils) and markers of hemostasis (endogenous thrombin potential [ETP], thrombin-antithrombin complex,

239 When the thrombin present in the target solution specifically hyd

240 lin-mutant ThbdPro mice, which have elevated thrombin procoagulant function, gained more weight and d

241 telet deposition) was largely sufficient for thrombin production.

242 tivation of the collagen glycoprotein VI and thrombin protease-activated receptor (PAR) 1.

243 Endothelial stimulation with thrombin rapidly increased the endothelial release of ET

244 let Inhibition and Patient Outcomes (PLATO), Thrombin Receptor Antagonist for Clinical Event Reductio

245 TRA2P-TIMI 50 (Thrombin Receptor Antagonist in Secondary Prevention of

246 ease in vascular permeability induced by the thrombin receptor, protease activated receptor 1 (PAR1).

247 imal mechanical ventilation and injection of thrombin receptor-activating peptide.

248 of cg03636183 in the coagulation factor II (thrombin) receptor-like 3 gene (F2RL3) (M = -0.64, 95% c

249 ors on platelets F2R (coagulation factor II (thrombin) receptor; PAR1) and GP5 (glycoprotein 5), as w

250 gest that thrombin and/or podocyte-expressed thrombin receptors may be novel therapeutic targets for

251 activation of protease-activated receptor 4 thrombin receptors noted in black subjects compared with

252 especially thrombin signaling, including the thrombin receptors on platelets F2R (coagulation factor

253 Stimulation of MEG-01 with thrombin reduced levels of WDR1 transcripts and protein.

254 A subpopulation of active thrombin remains stably adhered to a fibrin matrix over

255 latelet activation at high concentrations of thrombin requires PAR4.

256 Notably, the thrombin-resistant R221A mutant is still cleaved by thes

257 PAR4 antagonism reduces the maximum thrombin response by over 50%.

258 e on whether a thrombin burst occurs and the thrombin response when it does.

259 A thrombin-responsive closed-loop patch is developed for p

260 ibril content of the fibers produced by high thrombin resulted in weakened clot architecture as analy

261 and 200 nM) inhibits (50 and 93%) clot-bound thrombin reversibly (87 and 66% recovery).

262 mics of the coagulation serine protease, apo-thrombin (S195M-thrombin), were compared to the substrat

263 sac vascular defects, suggesting a role for thrombin signaling in vessel development.

264 enesis of cardiovascular disease, especially thrombin signaling, including the thrombin receptors on

265 regarded as a target for trypsin but not for thrombin signaling.

266 nsformation of TBA after incubating with the thrombin solution and formation of the aptamer-thrombin

267 nous flow conditions was developed using the thrombin-specific, fluorogenic substrate SN-59 (100 muM)

268 This model illustrates that clot-bound thrombin stability is the result of a constant rearrange

269 In thrombin-stimulated HUVECs, Kindlin-2 and cortical actin

270 Interestingly, thrombin-stimulated platelets also significantly enhance

271 Thrombin stimulation of platelets induced the dissociati

272 omplexes were predicted to contain conserved thrombin-susceptible cleavage sites based on sequence an

273 4 orders of magnitude more selective towards thrombin than to the other serine proteases of the coagu

274 In the presence of thrombin, the aptamer on the adsorbent layer captures th

275 In the absence of thrombin, the aptamers adsorbed onto the surface of GO l

276 Although avathrin is cleaved by thrombin, the C-terminal cleavage product continues to e

277 Conversely, in the presence of thrombin, the conformational transformation of TBA after

278 e linked by the specific cutting site of the thrombin, the fusion protein was used as the active biol

279 n molecule 1, and (3) a stimulatory role for thrombin, the thrombospondin-1/CD36 axis and cyclooxygen

280 nse still active at higher concentrations of thrombin, this response is superseded by PAR4.

281 functional and structural properties of the thrombin-thrombomodulin complex, prolongs the clotting t

282 of idarucizumab, on the basis of the diluted thrombin time or ecarin clotting time.

283 to 100), on the basis of either the diluted thrombin time or the ecarin clotting time.

284 ons increased F-actin in microvessels in the thrombin-treated and adjacent regions but not in those i

285 monolayer were increased by proinflammatory thrombin treatment.

286 rating peptide, we were able to inhibit both thrombin-triggered platelet aggregation in vitro and clo

287 y is to assess the stability of fibrin-bound thrombin under venous flow conditions and to determine b

288 brin matrix (0.1-0.4 mg/mL fibrinogen, 10 nM thrombin) under a variety of venous flow conditions was

289 an 75% from baseline resulted in median peak thrombin values at the lower end of the range observed i

290 e FXIa contributions, with fibrin localizing thrombin via its antithrombin-I activity as a potentiall

291 When thrombin was added a sandwich structure can form on the

292 In particular, thrombin was identified as a key mediator of the effects

293 Antithrombin inactivation of thrombin was impaired in the presence of the sulfated co

294 groups, a highly functionalized aptamer for thrombin was raised with a dissociation constant of 1.6

295 Toward this, the receptor-mediated agonist, thrombin, was instilled into microvessels in a restricte

296 rst 500 s, approximately 92,000 molecules of thrombin were generated per surface TF molecule for the

297 ulation serine protease, apo-thrombin (S195M-thrombin), were compared to the substrate-bound form (PP

298 Blood clotting in vivo is catalyzed by thrombin, which simultaneously induces fibrinogen bindin

299 Here, we show that specific inhibition of thrombin with hirudin reduced proteinuria in two rat nep

300 , which both interact with multiple sites of thrombin with low nanomolar affinities and show little s