ライフサイエンスコーパス: plasminogen activator

1 phaFXIIa is a highly efficient and favorable plasminogen activator.

2 marginal compared with urokinase and tissue plasminogen activator.

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

4 ptase and subsequent activation of urokinase plasminogen activator.

5 ular endothelial growth factor and urokinase plasminogen activator.

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

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

8 ma treated with therapeutic levels of tissue plasminogen activator.

9 investigate whether hypoxia releases tissue plasminogen activator.

10 n of recanalization after intravenous tissue plasminogen activator.

11 h sensitivity C-reactive protein, and tissue plasminogen activator.

12 rrelated significantly with levels of tissue plasminogen activator.

13 ecreting enzymatic factors, including tissue plasminogen activator.

14 rotease plasmin by staphylokinase and tissue plasminogen activator.

15 ke was strictly dependent on plasminogen and plasminogen activator.

16 bolytic and proteolytic properties of tissue plasminogen activator.

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

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

19 minutes of forearm-ischemia increased tissue plasminogen activator 31-fold (p<0.001).

20 ved treatment for ischaemic stroke is tissue plasminogen activator, a clot-buster.

21 sed expression of its target, urokinase-type plasminogen activator, a known tumor-associated protease

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

23 The plasminogen activator activity of the alphaFXIIa-polyP70

24 complications after intravenous tissue-type plasminogen activator administration to patients with IS

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

26 nB2, an inhibitor of extracellular urokinase plasminogen activator and deletion of DUSP5 acts synergi

27 at the combination of an intrapleural tissue plasminogen activator and deoxyribonuclease therapy can

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

29 cific plasmids pFra (murine toxin) and pPla (plasminogen activator and pesticin).

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

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

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

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

34 proteolytic center by recruiting the tissue plasminogen activator and plasminogen and mediating the

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

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

37 of action of intravenous recombinant tissue plasminogen activator and the rationale of various poten

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

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

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

41 Newly discovered roles for plasminogen activators and plasminogen activator inhibit

42 Moreover, plasminogen activators and the respective inhibitors wer

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

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

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

46 Patients treated with intravenous tissue plasminogen activator at Suburban Hospital, Bethesda, Ma

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

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

49 of action of intravenous recombinant tissue plasminogen activator, clinical studies could include ag

50 ad lower HbA1c, insulin, HOMA-IR, and tissue plasminogen activator compared with those taking placebo

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

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

53 Intravenous tissue plasminogen activator did not impact outcomes.

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

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

56 in which hepatocyte ER stress is induced by plasminogen activator expression, with high-fat diet.

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

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

59 cardiac arrest and birth asphyxia and tissue plasminogen activator for ischemic stroke) have proved t

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

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

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

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

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

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

66 obal Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries), a

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

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

69 transgenic mice carrying the urokinase-type plasminogen activator gene driven by the major urinary p

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

89 ral function for the gene SERPINE1, encoding plasminogen activator inhibitor 1 (PAI-1).

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

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

92 Increased activated plasminogen activator inhibitor 1 had a strong associati

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

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

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

96 ion of inflammatory mediators such as PAI-1 (plasminogen activator inhibitor 1), suggesting that gluc

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

98 lammatory cytokines such as TNF-alpha, IL-6, plasminogen activator inhibitor 1, and IL-1beta.

99 Plasminogen activator inhibitor 1, vascular cell adhesio

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

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

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

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

104 SerpinB2 (plasminogen activator inhibitor type 2) is constitutivel

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

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

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

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

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

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

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

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

113 Levels of plasminogen activator inhibitor-1 (PAI-1) increased sign

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

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

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

117 he morning surge of the prothrombotic factor plasminogen activator inhibitor-1 (PAI-1) observed in hu

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

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

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

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

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

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

124 Plasminogen activator inhibitor-1 (PAI-1), which inhibit

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

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

127 ata for the latency transition of the serpin plasminogen activator inhibitor-1 (PAI-1).

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

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

130 both murine models while decreasing alveolar plasminogen activator inhibitor-1 and promoting myofibro

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

132 matrix metalloproteinase (MMP)-8, MMP-9, and plasminogen activator inhibitor-1 levels were determined

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

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

135 In contrast, both LOX-1 and CD32 mediate plasminogen activator inhibitor-1 upregulation in arteri

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

137 evented CRP-induced arteriolar expression of plasminogen activator inhibitor-1, a thrombogenic protei

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

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

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

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

142 tronectin was enhanced by uPA and blocked by plasminogen activator inhibitor-1, the latter approach a

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

144 nectin, X-linked inhibitor of apoptosis, and plasminogen activator inhibitor-1.

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

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

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

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

149 covered roles for plasminogen activators and plasminogen activator inhibitors in these diseases provi

150 n the time intervals from intravenous tissue plasminogen activator initiation to groin puncture (medi

151 with IS treated with intravenous tissue-type plasminogen activator is associated with higher unadjust

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

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

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

155 om onset with intravenous recombinant tissue plasminogen activator (IV rtPA) therapy.

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

157 Tissue plasminogen activator levels were significantly increase

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

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

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

161 ADAMTS13, after activation by urokinase-type plasminogen activator or the thrombolytic agent streptok

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

163 "thrombolysis" OR "fibrinolysis" OR "tissue plasminogen activator" OR "streptokinase" OR "urokinase.

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

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

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

167 the causative agent of plague, expresses the plasminogen activator protease Pla, which has been shown

168 l guidelines endorse recombinant tissue-type plasminogen activator (r-tPA) in eligible patients with

169 The soluble cleaved urokinase plasminogen activator receptor (scuPAR) is a circulating

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

171 ng levels of soluble forms of urokinase-type plasminogen activator receptor (suPAR) are generally ele

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

173 high plasma levels of soluble urokinase-type plasminogen activator receptor (suPAR) have been associa

174 Soluble urokinase plasminogen activator receptor (suPAR) independently pre

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

176 eased plasma level of soluble urokinase-type plasminogen activator receptor (suPAR) was associated re

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

178 , procalcitonin (PCT), and soluble urokinase plasminogen activator receptor (suPAR).

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

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

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

182 The urokinase-type plasminogen activator receptor (uPAR) is a glycosylphosp

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

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

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

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

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

188 inase plasminogen activator (uPA); urokinase plasminogen activator receptor (uPAR); plasminogen; and

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

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

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

192 ell surface-associated HS and urokinase-type plasminogen activator receptor in the accumulation of FX

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

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

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

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

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

198 randomized trial, weekly recombinant tissue plasminogen activator (rt-PA), 1 mg per lumen, once per

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

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

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

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

203 benefit of intravascular recombinant tissue plasminogen activator (rtPA) on functional outcome in is

204 treated with intravenous recombinant tissue plasminogen activator (rtPA) within 4(1/2) hours after s

205 We fused single-chain urokinase plasminogen activator (scuPA) to a small recombinant ant

206 Humanized urokinase plasminogen activator/severe combined immunodeficiency m

207 sminogen activator start; intravenous tissue plasminogen activator start to randomization; randomizat

208 ed tomography (CT); CT to intravenous tissue plasminogen activator start; intravenous tissue plasmino

209 dosomes containing proteins of the urokinase plasminogen activator system (uPAS) to relocate to perin

210 evidence suggests an association between the plasminogen activator system and its inhibitors in a var

211 y, the newly characterized regulation of the plasminogen activator system by endogenous microRNAs pro

212 The plasminogen activator system is also involved in the pat

213 endence when treated with intravenous tissue plasminogen activator (t-PA) alone.

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

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

216 strate that GRP78 also binds the tissue-type plasminogen activator (t-PA), which results in a decreas

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

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

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

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

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

222 activation of plasminogen by urokinase-type plasminogen activator to active plasmin was significantl

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

224 ultaneously binds plasminogen and its tissue plasminogen activator tPA.

225 ropeptide-Y (NPY) (within 200 ms) and tissue plasminogen activator (tPA) (over many seconds) in adren

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

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

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

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

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

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

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

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

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

235 , namely, that marked release of tissue-type plasminogen activator (tPA) followed by delayed synthesi

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

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

238 The benefits of intravenous tissue plasminogen activator (tPA) in patients with acute ische

239 e window available for treatment with tissue plasminogen activator (tPA) in patients with acute ische

240 Here, we show that the expression of tissue plasminogen activator (tPA) is increased in glial cells

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

242 Tissue-type plasminogen activator (tPA) is known to promote macropha

243 200 ms after fusion, whereas labeled tissue plasminogen activator (tPA) is often discharged over man

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

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

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

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

248 Tissue-type plasminogen activator (tPA), a protease up-regulated in

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

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

251 gen (Pg) binding and/or activation by tissue plasminogen activator (tPA), reduced plasmin-mediated pr

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

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

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

255 system for site-specific delivery of tissue plasminogen activator (tPA).

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

257 ar vs 38% [27 of 70] intravenous [IV] tissue-plasminogen activator [tPA]; relative risk, 1.07 [99% co

258 clot dissolution in recombinant tissue-type plasminogen activator-treated animals, but enduring high

259 191 of 44 410 (34%) intravenous tissue-type plasminogen activator-treated IS patients with CKD.

260 mbus was detected in recombinant tissue-type plasminogen activator-treated rats but not in vehicle-in

261 s model) followed by recombinant tissue-type plasminogen activator treatment (10 mg/kg, IV).

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

263 Outcomes after intravenous tissue plasminogen activator treatment via telemedicine (telest

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

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

266 Urokinase plasminogen activator (uPA) and its receptor (uPAR) coor

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

268 d that the expression of both urokinase-type plasminogen activator (uPA) and the uPA receptor are ele

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

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

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

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

273 Urokinase plasminogen activator (uPA) converts plasminogen to plas

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

275 y delayed synthesis and release of urokinase plasminogen activator (uPA) from injured brain leads to

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

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

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

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

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

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

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

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

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

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

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

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

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

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

290 matrix metalloproteinase (MMP)-2; urokinase plasminogen activator (uPA); urokinase plasminogen activ

291 ed the active form of the protease urokinase plasminogen activator (uPA, PLAU).

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

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

294 d by exposure to specific ligands (urokinase plasminogen activator, vitronectin), but not via adjustm

295 ug-entrapped vascular grafts: urokinase-type plasminogen activator was entrapped within a porous alum

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

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

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

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

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