ライフサイエンスコーパス: plasminogen

1 n vitro, irrespective of its ability to bind plasminogen.

2 responsible for capturing the bulk of bound plasminogen.

3 atriptase, through plasminogen activator, to plasminogen.

4 triptase zymogen activation, was shown to be plasminogen.

5 ted by t-PA, and uPA activates the remaining plasminogens.

6 gen in aqueous media even in the presence of plasminogen, a potentially interfering molecule in the c

7 own PPARgamma target genes with PGC1beta and plasminogen-activated inhibitor-1 being increased, no ch

8 nolytic failure, and compared the effects of plasminogen activation and alpha2-antiplasmin inactivati

9 The plasminogen activation and plasmin inhibition system ass

10 Plasminogen activation by betaFXIIa was minimal and not

11 This effect depended on plasminogen activation by Sak.

12 Catalytically inactive tPA-S(481)A inhibited plasminogen activation by tPA and uPA, attenuated ICH, l

13 elet-derived polyP significantly augment the plasminogen activation capacity of alphaFXIIa.

14 roduction, but whether CLEC3A contributes to plasminogen activation is unknown.

15 The plasminogen activation system is best known as an extrac

16 vivo extracellular proteostasis system, the plasminogen activation system may work synergistically w

17 results reveal a novel role for Sak-induced plasminogen activation that prevents S. aureus biofilm f

18 ed the autoactivation of FXII and subsequent plasminogen activation, indicating that once activated,

19 of a widely used, pharmacologic inhibitor of plasminogen activation, tranexamic acid, also delays the

20 and the balance between fibrin formation and plasminogen activation, with tissue plasminogen activato

21 nergistically to enhance alphaFXIIa-mediated plasminogen activation.

22 plasminogen and participates in tPA-mediated plasminogen activation.

23 nds to plasminogen and enhances tPA-mediated plasminogen activation.

24 Intravenous recombinant tissue plasminogen activator (alteplase) was approved by the US

25 Although intravenous tissue plasminogen activator (IV-rtPA) was approved nearly 2 de

26 as an inhibitor of urokinase and tissue-type plasminogen activator (PA), PA inhibitor-1 (PAI-1) has a

27 ent with intravenous (IV) recombinant tissue plasminogen activator (rtPA) after mild stroke.

28 andidates for intravenous recombinant tissue plasminogen activator (rtPA) because their symptoms are

29 trievers with intravenous recombinant tissue plasminogen activator (rtPA) compared with rtPA alone.

30 As thrombolysis with recombinant tissue plasminogen activator (rtPA) is a standard of care withi

31 Currently, tissue plasminogen activator (t-PA) is the only approved thromb

32 dominated by the experience with tissue-type plasminogen activator (t-PA), which proved little better

33 ove current thrombolytic therapy with tissue plasminogen activator (t-PA).

34 f fibrinolysis after recombinant tissue-type plasminogen activator (tPA) administration revealed that

35 endovascular therapy plus intravenous tissue plasminogen activator (tPA) administration versus tPA ad

36 reduction in treatment times for tissue-type plasminogen activator (tPA) administration.

37 mized treatment with intravenous (IV) tissue plasminogen activator (tPA) alone versus IV tPA + endova

38 ulation of 2 fibrinolytic parameters, tissue plasminogen activator (tPA) and its physiological inhibi

39 ofibrinolytic enzymes, urokinase, and tissue plasminogen activator (TPA) as a source for plasmin form

40 nce-dependent proteolytic activity of tissue plasminogen activator (tPA) becomes restricted in the ad

41 nce-dependent proteolytic activity of tissue plasminogen activator (tPA) becomes restricted in the ad

42 d recipient WIT along with the use of tissue plasminogen activator (tPA) flush during DCD procurement

43 edema is a recognised complication of tissue plasminogen activator (tPA) for ischaemic stroke.

44 Thrombolytic therapy using tissue plasminogen activator (tPA) in acute stroke is associate

45 Intravenous tissue plasminogen activator (tPA) is known to improve outcomes

46 Tissue-type plasminogen activator (tPA) is the major intravascular a

47 rombolytic treatment with recombinant tissue plasminogen activator (tPA) may exacerbate blood-brain b

48 gen and enhances its association with tissue plasminogen activator (tPA) thereby enhancing plasmin pr

49 ients with acute ischemic stroke with tissue plasminogen activator (tPA) within 4.5 hours of symptom

50 ue factor, fibrinogen-like protein 2, tissue plasminogen activator (tPA), and plasminogen activator i

51 nd peritoneal fluid concentrations of tissue plasminogen activator (tPA), d-dimer, thrombin-antithrom

52 ection of a plasmid encoding for tissue-type plasminogen activator (tPA).

53 which includes the use of intravenous tissue plasminogen activator (tPA).

54 lytic treatment with recombinant tissue-type plasminogen activator (tPA).

55 use of a fibrinolytic enzyme such as tissue plasminogen activator (tPA).

56 we show that neurons release urokinase-type plasminogen activator (uPA) and astrocytes recruit the u

57 ing the enzymatic activity of urokinase-type plasminogen activator (uPA) and matrix metalloproteinase

58 apoptosis with suppression of urokinase-type plasminogen activator (uPA) and the uPA receptor in AECs

59 of the plasminogen activators urokinase-type plasminogen activator (uPA) and tissue plasminogen activ

60 diac fibrosis by inactivating urokinase-type plasminogen activator (uPA) and ultimately plasmin (Pm)

61 Mice lacking urokinase-type plasminogen activator (uPA) are highly susceptible, wher

62 Urokinase plasminogen activator (uPA) converts plasminogen to plas

63 EGFR TKIs, elevated expression of urokinase plasminogen activator (uPA) drives signaling through the

64 Urokinase plasminogen activator (uPA) is a biomarker and therapeut

65 Urokinase-type plasminogen activator (uPA) is a serine proteinase that

66 Urokinase-type plasminogen activator (uPA) is a serine proteinase that,

67 elet (PLT) alpha granule-delivered urokinase plasminogen activator (uPA) is highly effective in preve

68 Genetic absence of the urokinase-type plasminogen activator (uPA) reduces arthritis progressio

69 Urokinase-type plasminogen activator (uPA) regulates angiogenesis and v

70 trypsin-like serine protease, urokinase-type plasminogen activator (uPA), is central in tissue remode

71 tment increased endocytosis of the urokinase plasminogen activator (uPA), its receptor (uPAR), and pl

72 chitosan, targeting acidic pH, and urokinase plasminogen activator (UPA), targeting UPAR.

73 is due to the effects of t-PA and urokinase plasminogen activator (uPA).

74 n consensus cleavage motif of urokinase-type plasminogen activator (uPA).

75 ary biochemical target of SerpinB2-urokinase plasminogen activator (uPA).

76 d angiomyolipomas overexpress urokinase-type plasminogen activator (uPA).

77 olytic cascade of cathepsin B/urokinase-type plasminogen activator (uPA)/matrix metalloproteinase-2 (

78 or, fatty acid-binding protein 4, and tissue plasminogen activator [t-PA]) as IR biomarkers.

79 derately reduced single-chain urokinase-type plasminogen activator activation.

80 The plasminogen activator activity of the alphaFXIIa-polyP70

81 e: intravenous thrombolysis with tissue-type plasminogen activator and endovascular treatment for pro

82 nents of the fibrinolytic pathway (urokinase plasminogen activator and plasmin) are elaborated in ple

83 t, PAM50, Breast Cancer Index, and urokinase plasminogen activator and plasminogen activator inhibito

84 the fibrinolytic system (plasma tissue-type plasminogen activator and plasminogen activator inhibito

85 D-dimer, plasmin-antiplasmin complex, tissue plasminogen activator and plasminogen activator inhibito

86 protein aggregates interact with tissue-type plasminogen activator and plasminogen, via an exposed ly

87 PPXbd enhanced fibrin sensitivity to tissue plasminogen activator and promoted clot retraction durin

88 intrathrombus delivery of recombinant tissue plasminogen activator and thrombus aspiration or macerat

89 lations of PAs such as streptokinase, tissue-plasminogen activator and urokinase have been developed

90 erwent MT with or without intravenous tissue plasminogen activator and were admitted to endovascular-

91 Activated factor XII (FXIIa) has plasminogen activator capacity but its relative contribu

92 ic protein-1), and formation of PAI-1/tissue plasminogen activator complexes.

93 protein-1 and the formation of PAI-1/tissue plasminogen activator complexes.

94 Intravenous tissue plasminogen activator did not impact outcomes.

95 onsisting of 1mg of recombinant human tissue plasminogen activator every 8 hours until clot clearance

96 Patients were treated with IVT with tissue plasminogen activator followed by MT (IVT and MT group)

97 obal Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Arteries [GUSTO] clas

98 obal Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Arteries moderate or

99 obal Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Arteries moderate/sev

100 obal Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GU

101 obal Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries-def

102 investigate the contribution of polyP to the plasminogen activator function of alphaFXIIa.

103 March 31, 2015 and who received tissue-type plasminogen activator in the emergency department at 15

104 atalytic and thrombolytic activity of tissue plasminogen activator in vitro and ex vivo.

105 hesion molecules, fibrinogen-like protein 2, plasminogen activator inhibitor (PAI)-1), secretion of p

106 n 2, tissue plasminogen activator (tPA), and plasminogen activator inhibitor (PAI)-1.

107 ghly susceptible, whereas those deficient in plasminogen activator inhibitor (PAI-1) are resistant to

108 ) (by confocal microscopy), plasma levels of plasminogen activator inhibitor (PAI-1), and factor XIII

109 chemotactic protein-1 (CCL2) (MCP-1), tissue plasminogen activator inhibitor (PAI-1), and regulated o

110 connective tissue growth factor (CTGF), and plasminogen activator inhibitor (PAI-1).

111 Plasminogen activator inhibitor 1 (PAI-1) is a serpin in

112 (MS, n = 20; control, n = 10), expression of plasminogen activator inhibitor 1 (PAI-1), a key enzyme

113 vator (tPA) and its physiological inhibitor, plasminogen activator inhibitor 1 (PAI-1), in Puumala ha

114 with diabetes experience elevated levels of plasminogen activator inhibitor 1 (PAI-1), regardless of

115 isolated a high-quality DNA aptamer pair for plasminogen activator inhibitor 1 (PAI-1).

116 Plasminogen activator inhibitor 1 (PAI-1/serpinE1) can b

117 Increased activated plasminogen activator inhibitor 1 had a strong associati

118 king BDNF maturation in the hippocampus with plasminogen activator inhibitor 1 hinders the persistenc

119 s and levels of the coagulation intermediary plasminogen activator inhibitor 1 in three mouse models

120 as observed, but a trend toward lower plasma plasminogen activator inhibitor 1 with higher excretion

121 Tests for FXI and FXII activity, plasminogen activator inhibitor 1, and activated partial

122 Plasminogen activator inhibitor 1, vascular cell adhesio

123 r slows down matrix degradation by increased plasminogen activator inhibitor 1.

124 Recently it has been demonstrated that plasminogen activator inhibitor serpins promote brain me

125 complex, plasmin-alpha2-antiplasmin complex, plasminogen activator inhibitor type 1 [PAI-1], D-dimer,

126 dex, and urokinase plasminogen activator and plasminogen activator inhibitor type 1 in specific subgr

127 SerpinB2 (plasminogen activator inhibitor type 2) is constitutivel

128 Increased levels of plasminogen activator inhibitor type I (PAI-1) have been

129 plasma tissue-type plasminogen activator and plasminogen activator inhibitor type I) was not influenc

130 in complex, tissue plasminogen activator and plasminogen activator inhibitor-1 (markers for fibrinoly

131 Higher plasminogen activator inhibitor-1 (p = 0.002), E-selecti

132 Similarly, higher plasminogen activator inhibitor-1 (p = 0.007) and S100B

133 l transition (EMT), TNBC cells could produce plasminogen activator inhibitor-1 (PAI-1) and stimulate

134 ctivatable fibrinolysis inhibitor (TAFI) and plasminogen activator inhibitor-1 (PAI-1) are causal fac

135 Basal expression of plasminogen activator inhibitor-1 (PAI-1) in human and m

136 en activator (uPA), its receptor (uPAR), and plasminogen activator inhibitor-1 (PAI-1) into the early

137 Plasminogen activator inhibitor-1 (PAI-1) is known to pr

138 Plasminogen activator inhibitor-1 (PAI-1) is the main in

139 iation of a gain-of-function polymorphism in plasminogen activator inhibitor-1 (PAI-1) with airway ob

140 t gene SERPINE1 that is encoding the protein plasminogen activator inhibitor-1 (PAI-1), an establishe

141 NADPH oxidases (NOXs), and fibrotic markers, plasminogen activator inhibitor-1 (PAI-1), and fibronect

142 VEGF, plasminogen activator inhibitor-1 (PAI-1), and pigment e

143 nase-9 (MMP-9), tumor necrosis factor-alpha, plasminogen activator inhibitor-1 (PAI-1), and urinary o

144 In infected mice that overexpress plasminogen activator inhibitor-1 (PAI-1), S. aureusclfA

145 leomycin failed to induce miR-34a in p53- or plasminogen activator inhibitor-1 (PAI-1)-deficient mice

146 tions and is characterized by high levels of plasminogen activator inhibitor-1 (PAI-1).

147 xia-inducible factor-1alpha (HIF-1alpha) and plasminogen activator inhibitor-1 (PAI-1).

148 Adjusting for S100B did not alter plasminogen activator inhibitor-1 and E-selectin associa

149 with increased alpha-smooth muscle actin and plasminogen activator inhibitor-1 expression.

150 S-1 peptide had increased efficacy in plasminogen activator inhibitor-1 serpin-deficient trans

151 mediated connective tissue growth factor and plasminogen activator inhibitor-1 up-regulation.

152 There was a 51.8% net decrease in PAI-1 (plasminogen activator inhibitor-1), a 12.1% net decrease

153 d2 phosphorylation, normalized expression of plasminogen activator inhibitor-1, and mitigated PH and

154 pression of interleukin-6, thrombospondin-1, plasminogen activator inhibitor-1, and tissue factor, wh

155 We measured plasma concentrations of plasminogen activator inhibitor-1, E-selectin, and angio

156 on of genes downstream of Smad2/3, including plasminogen activator inhibitor-1, fibronectin, and conn

157 ependent connective tissue growth factor and plasminogen activator inhibitor-1-induced proliferative

158 or pathway inhibitor, fibrinogen-like 1, and plasminogen activator inhibitor-1.

159 Plasminogen activator inhibitors (PAIs) 1 and 2 were als

160 tor and histidine-rich glycoprotein, but not plasminogen activator inhibitors 1 and 2.

161 ute ischemic stroke treated with tissue-type plasminogen activator is associated with improved outcom

162 protease thrombin and release the urokinase plasminogen activator loaded into the polymer capsules,

163 ential association between soluble urokinase plasminogen activator receptor (suPAR) and incident non-

164 cent studies describe soluble urokinase-type plasminogen activator receptor (suPAR) as a circulating

165 Soluble urokinase plasminogen activator receptor (suPAR) independently pre

166 Systemic soluble urokinase plasminogen activator receptor (suPAR) is a circulating

167 We investigated whether soluble urokinase plasminogen activator receptor (suPAR), a marker of immu

168 nase that upon binding to the urokinase-type plasminogen activator receptor (uPAR) catalyzes the conv

169 The urokinase-type plasminogen activator receptor (uPAR) has a well-establi

170 tential of PET imaging of the urokinase-type plasminogen activator receptor (uPAR) in glioblastoma.

171 is capable of recognizing the urokinase-type plasminogen activator receptor (uPAR), a uniquely overex

172 gy: 1) an elevated tumor receptor, urokinase plasminogen activator receptor (UPAR), and 2) the acidic

173 eted factors, including CD73, urokinase-type plasminogen activator receptor (uPAR), and serum amyloid

174 Transcripts of the urokinase plasminogen activator receptor (uPAR), which facilitates

175 sion levels of alpha5 integrin and urokinase plasminogen activator receptor (uPAR).

176 in the asthma susceptibility gene, urokinase plasminogen activator receptor (uPAR/PLAUR) have been as

177 eraction with a region of the urokinase-type plasminogen activator receptor (uPAR88-92), able to inte

178 Sirt6 also reduces urokinase plasminogen activator receptor expression, which is a ke

179 imicrobial peptides antigen-6/urokinase-type plasminogen activator receptor related protein-1 and bet

180 phropathy biomarkers, soluble urokinase-type plasminogen activator receptor, suPAR and neutrophil gel

181 The overexpression of urokinase-type plasminogen activator receptors (uPARs) represents an es

182 ion, partly caused by hypoxia induced tissue plasminogen activator release.

183 Intravenous thrombolysis with tissue-type plasminogen activator remains the mainstay of acute stro

184 administered before or together with tissue plasminogen activator therapy due to the risk of inhibit

185 ) and had higher rates of intravenous tissue plasminogen activator treatment (174 [74.4%] vs 172 [59.

186 ographic Score (ASPECTS), intravenous tissue plasminogen activator treatment, and time from LKN to ar

187 ix patients (4%) received intravenous tissue plasminogen activator without complications.

188 d patients suggested that intravenous tissue plasminogen activator would be delayed by 12 minutes, bu

189 e radius from onset, then intravenous tissue plasminogen activator would be delayed by 7 minutes and

190 Urokinase (uPA, urinary plasminogen activator) is a serine protease belonging to

191 Intravenous rt-PA (recombinant tissue-type plasminogen activator) is effective in improving outcome

192 i acutely and r-tPA (recombinant tissue-type plasminogen activator) therapy may be required, despite

193 in >50% of patients treated with tissue-type plasminogen activator), and (5) face-to-face meetings wi

194 hemorepulsive: alpha-2-macroglobulin, tissue plasminogen activator, and metallothionein III.

195 to activate the single-chain urokinase-type plasminogen activator, and the G221A and G221S variants

196 onists, alpha2-macroglobulin and tissue-type plasminogen activator, attenuated expression of inflamma

197 l approaches such as recombinant tissue-type plasminogen activator, direct thrombin inhibitors, and a

198 cluding alpha2-macroglobulin and tissue-type plasminogen activator, failed to cause LRP1 shedding.

199 efficacy of desmoteplase, a fibrin-dependent plasminogen activator, given between 3 h and 9 h after s

200 efficacy of alteplase, a recombinant tissue plasminogen activator, in combination with minimally inv

201 interacts with the thrombolytic drug tissue plasminogen activator, the only approved therapy of acut

202 be one-directional: from matriptase, through plasminogen activator, to plasminogen.

203 ty and efficacy of leukocyte antigen, PLAUR (plasminogen activator, urokinase receptor) domain-contai

204 ory increase in expression of urokinase-type plasminogen activator, which activates uPAR-dependent ce

205 -type plasminogen activator (uPA) and tissue plasminogen activator, which binds tightly to the cleara

206 ain neuroprotection and inhibition of tissue plasminogen activator-induced brain hemorrhages.

207 neuroprotective agent if given after tissue plasminogen activator-induced reperfusion.

208 raischemic helium at 75 vol% inhibits tissue plasminogen activator-induced thrombolysis and subsequen

209 after ischemia, in order not to block tissue plasminogen activator-induced thrombolysis and to obtain

210 the risk of inhibiting the benefit of tissue plasminogen activator-induced thrombolysis; and 2) could

211 tion and plasminogen activation, with tissue plasminogen activator-mediated lysis being more efficien

212 ed lysis being more efficient than urokinase plasminogen activator-mediated lysis.

213 rotease plasmin by staphylokinase and tissue plasminogen activator.

214 ke was strictly dependent on plasminogen and plasminogen activator.

215 bolytic and proteolytic properties of tissue plasminogen activator.

216 phaFXIIa is a highly efficient and favorable plasminogen activator.

217 marginal compared with urokinase and tissue plasminogen activator.

218 ukemia inhibitory factor, and urokinase-type plasminogen activator.

219 ptase and subsequent activation of urokinase plasminogen activator.

220 ular endothelial growth factor and urokinase plasminogen activator.

221 ation with phorbol esters and urokinase-type plasminogen activator.

222 ma treated with therapeutic levels of tissue plasminogen activator.

223 lular adhesion molecule-1 and urokinase-type plasminogen activator.

224 rrelated significantly with levels of tissue plasminogen activator.

225 ecreting enzymatic factors, including tissue plasminogen activator.

226 te CgA C-terminal cleavage by activating the plasminogen activator/plasmin system.

227 ntal vascular-endothelial function [ratio of plasminogen-activator inhibitor (PAI) 1 to PAI-2 and mea

228 Several plasminogen activators (PAs) have been found effective i

229 where it can be converted to plasmin by host plasminogen activators or by endogenously expressed stap

230 bitor 1 (PAI-1) is a serpin inhibitor of the plasminogen activators urokinase-type plasminogen activa

231 rt plasminogen to plasmin in the presence of plasminogen activators.

232 ibitor of the tissue type and urokinase type plasminogen activators.

233 tetranectin binds to the kringle 4 domain of plasminogen and enhances its association with tissue pla

234 , we found that CLEC3A specifically binds to plasminogen and enhances tPA-mediated plasminogen activa

235 Binding of plasminogen and fibrinogen co-localized with PAC-1 in th

236 t mice or mice with combined deficiencies of plasminogen and fibrinogen had decreased EAE severity, t

237 ing platelets were PAC-1 negative, and bound plasminogen and fibrinogen in a protruding "cap." These

238 nfocal microscopy revealed direct binding of plasminogen and fibrinogen to different platelet subpopu

239 htE), pneumococcal surface protein A (PspA), plasminogen and fibronectin binding protein B (PfbB), an

240 lectin CLEC3A and show that CLEC3A binds to plasminogen and participates in tPA-mediated plasminogen

241 Together, these data suggest that plasminogen and plasmin-mediated fibrinolysis is a key m

242 ular fibrin uptake was strictly dependent on plasminogen and plasminogen activator.

243 ivator inhibitor-1), a 12.1% net decrease in plasminogen, and a 17.8% net increase in D-dimer.

244 binding proteins A and B, were found to bind plasminogen, and one of them, FnBPB, was studied in deta

245 CL5, IL8, CCL2), cytokines (IL1B, IFNG), and plasminogen- and coagulation-related molecules (SERPINB2

246 Plasminogen binding did not to occur by the same mechani

247 , confirming a role for fibrin in amplifying plasminogen binding to PS-exposing platelets.

248 Hirudin attenuates, but does not abolish plasminogen binding, denoting the importance of fibrin.

249 Here, we identified a novel plasminogen-binding protein, termed CipA.

250 The N3 subdomain of FnBPB contains the full plasminogen-binding site, and this includes, at least in

251 Plasminogen bound to recombinant FnBPB with a KD of 0.53

252 A sub-pM concentration of plasminogen (but not plasmin) acting at the cell surface

253 0 was found to bind to FXII, alphaFXIIa, and plasminogen, but not betaFXIIa.

254 timulated activation of Glu and Lys forms of plasminogen by alphaFXIIa.

255 different subpopulations of platelets harbor plasminogen by diverse mechanisms and provide an essenti

256 Plasminogen captured on the surface of S. aureus- or Lac

257 MMP-2 and the uPA/uPAR/plasminogen cascade provide therapeutic targets to decre

258 y in EAE disease onset, as seen in mice with plasminogen deficiency alone.

259 psilon) activity, cobalamin C deficiency, or plasminogen deficiency.

260 rary to initial expectations, EAE-challenged plasminogen-deficient (Plg(-)) mice developed significan

261 Pharmacological fibrinogen depletion in plasminogen-deficient animals restored a normal pattern

262 re to clear fibrin from the fracture site in plasminogen-deficient mice severely impaired fracture va

263 ssessed by a model of bacteremia using human plasminogen-expressing mice.

264 er invasive pathogens, S. aureus can capture plasminogen from the human host where it can be converte

265 for subsequent surface binding of human-host plasminogen (hPg) to the E-domain of hFg.

266 The binding of human plasminogen (hPg) to the surface of the human pathogen g

267 attern D M-protein strains that also express plasminogen (human Pg (hPg)) binding Group A streptococc

268 rthermore, C4BP readily forms complexes with plasminogen in fluid phase and such complexes are presen

269 sminogen kringle domains facilitate the C4BP-plasminogen interaction.

270 receptor (uPAR) catalyzes the conversion of plasminogen into plasmin on the cell surface.

271 receptor (uPAR), catalyzes the conversion of plasminogen into plasmin on the cell surface.

272 Specifically, uPA cleaves the zymogen plasminogen into the active form (plasmin), which then d

273 Moreover, the lysine-binding sites in plasminogen kringle domains facilitate the C4BP-plasmino

274 ent inhibitor C4b-binding protein (C4BP) and plasminogen of the fibrinolytic pathway.

275 y regulate urokinase -mediated activation of plasminogen (Pg).

276 strain AP53, which strongly binds host human plasminogen/plasmin (hPg/hPm) directly via an hPg/hPm su

277 In previous studies, plasminogen (Plg) cross-reactive Abs, which can recogniz

278 We detected a mutation in the plasminogen (PLG) gene in patients with HAEnCI.

279 ular attention has focused on the binding of plasminogen (Plg) to bacterial surfaces, as it has been

280 The participation of the plasminogen (Plg)/plasmin (Pla) system in the productive

281 Fluorescently labeled plasminogen radiates from platelet aggregates at the bas

282 33-fold in human hepatoma cells in which the plasminogen receptor (KT) was knocked out.

283 nd 1.6-fold in human hepatoma cells in which plasminogen receptor (KT) was overexpressed, showing for

284 is internalized by the plasminogen receptor, plasminogen receptor (KT), and the apo(a) component is r

285 ng for the first time the role of a specific plasminogen receptor in Lp(a) uptake.

286 l findings that Lp(a) is internalized by the plasminogen receptor, plasminogen receptor (KT), and the

287 rombin/convulxin significantly increased the plasminogen signal associated with phosphatidylserine (P

288 scribe for the first time that deficiency of plasminogen, the key fibrinolytic enzyme, delays disease

289 Plasminogen, the primary fibrinolytic enzyme, also modif

290 The ability of plasminogen to induce matriptase zymogen activation and

291 late release of urokinase, which can convert plasminogen to plasmin and represents a possible source

292 en bound to plasminogen, was able to convert plasminogen to plasmin in the presence of plasminogen ac

293 okinase plasminogen activator (uPA) converts plasminogen to plasmin, resulting in a proteolytic casca

294 Bound plasminogen, upon conversion to active plasmin, degraded

295 t with tissue-type plasminogen activator and plasminogen, via an exposed lysine-dependent mechanism,

296 notypes, suggesting that the contribution of plasminogen was downstream of the T-cell response.

297 The link between matriptase and plasminogen was initially thought to be one-directional:

298 the main substrate cleaved by Sak-activated plasminogen, was a major component of biofilm matrix, an

299 e range of host molecules, and when bound to plasminogen, was able to convert plasminogen to plasmin

300 The interaction of plasminogen with platelets and their localization during

301 to evaluate the hypothesis that the loss of plasminogen would exacerbate neuroinflammatory disease.