ライフサイエンスコーパス: plasminogen

1 ibrin matrix did not occur in the absence of plasminogen.

2 of uPA and the P3 residue of both PAI-1 and plasminogen.

3 was significantly impaired in the absence of plasminogen.

4 t were significantly associated with PEs and plasminogen.

5 ndocardium, resulting in increased levels of plasminogen.

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

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

8 The mammalian plasminogen activation (PA) system catalyzes the generat

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

10 The plasminogen activation and plasmin inhibition system ass

11 Plasminogen activation by betaFXIIa was minimal and not

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

13 Soluble urokinase plasminogen activation receptor (suPAR) is risk factor f

14 further pharmacological interventions of the plasminogen activation system and other proteolytic syst

15 Protein sequences of members of the plasminogen activation system are present throughout the

16 The plasminogen activation system is best known as an extrac

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

18 odel treated with amiloride, an inhibitor of plasminogen activation, and measured changes in plasmin

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

20 smin generation assays determined effects on plasminogen activation.

21 plasminogen and participates in tPA-mediated plasminogen activation.

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

23 iNPC with enzymatically-inactive tissue-type plasminogen activator (EI-tPA), prior to grafting into a

24 system, and eliminated harmful factors like plasminogen activator (Pla) and murine toxin from the OM

25 old increase in platelet stores of urokinase plasminogen activator (PLAU/uPA); subsequent plasmin-med

26 zed octafluoropropane and recombinant tissue plasminogen activator (rt-PA)-loaded echogenic liposomes

27 male C57bl/6 mice, thrombolysis using tissue-plasminogen activator (t-PA) reduced injury and improved

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

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

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

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

32 ed delivery and controlled release of tissue plasminogen activator (tPA) at the thrombus site.

33 ral activation through a reduction in tissue plasminogen activator (tPA) caused by upregulation of it

34 Earlier administration of intravenous tissue plasminogen activator (tPA) in acute ischemic stroke is

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

36 on-advection model of thrombolysis by tissue plasminogen activator (TPA) in an occluded vessel with a

37 Tissue-type plasminogen activator (tPA) is a major mediator of fibri

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

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

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

41 Emerging evidence suggests that tissue plasminogen activator (tPA), currently the only FDA-appr

42 rin more resistant to fibrinolysis by tissue plasminogen activator (tPA), exacerbating the prothrombo

43 ed partial prothrombin time, D-dimer, tissue plasminogen activator (tPA), plasminogen activator inhib

44 ernational normalized ratio, D-dimer, tissue plasminogen activator (tPA), plasminogen activator inhib

45 Tissue plasminogen activator (tPA), which is reduced in Alzheim

46 into the source of intravascular tissue-type plasminogen activator (tPA).

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

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

49 o bind fibrinogen D fragment close to tissue plasminogen activator (tPA; residues gamma312-324) and p

50 njury following activation by urokinase-type plasminogen activator (u-PA; encoded by the PLAU gene).

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

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

53 to analyze the interaction between urokinase plasminogen activator (uPA) and monoclonal uPAR antibody

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

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

56 upregulated the expression of urokinase-type plasminogen activator (uPA) and/or matrix metalloprotein

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

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

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

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

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

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

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

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

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

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

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

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

69 rement of nitric oxide, endothelin-1, tissue plasminogen activator and plasminogen activator inhibito

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

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

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

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

74 lasminogen, which after activation by tissue plasminogen activator cleaved the bound histone.

75 Intravenous tissue plasminogen activator did not impact outcomes.

76 Combined delivery of plasminogen and tissue plasminogen activator during NMP lysed the plugs leading

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

78 d increase in cerebral tissue-type/urokinase plasminogen activator expression.

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

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

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

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

83 novel Ter119-polymeric NP containing tissue plasminogen activator for on-demand targeting of GPA rec

84 Intravenous tissue plasminogen activator has been a cornerstone for treatme

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

86 inogen activator, alpha2-antiplasmin, active plasminogen activator inhibitor (PAI-1), and fibrin form

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

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

89 D-dimer, tissue plasminogen activator (tPA), plasminogen activator inhibitor 1 (PAI-1) and platelets.

90 The concentration of the main TPA inhibitor plasminogen activator inhibitor 1 (PAI-1) controlled bot

91 pathway and augmented tissue factor (TF) and plasminogen activator inhibitor 1 (PAI-1) levels in veno

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

93 D-dimer, tissue plasminogen activator (tPA), plasminogen activator inhibitor 1 (PAI-1), and platelets

94 Furthermore, inhibition of plasminogen activator inhibitor 1 (PAI-1), which was the

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

96 led to upregulate the fibrinolysis inhibitor plasminogen activator inhibitor 1 (Serpine1, also known

97 protein M130, Fatty acid binding protein 4, Plasminogen activator inhibitor 1 and Insulin-like growt

98 Increased activated plasminogen activator inhibitor 1 had a strong associati

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

100 asminogen activators, a relatively decreased plasminogen activator inhibitor 1, and decreased levels

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

102 ptor annexin 2A as well as downregulation of plasminogen activator inhibitor serpine1 in myocardium a

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

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

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

106 Plasminogen activator inhibitor type-1 (PAI-1) is a seri

107 Plasminogen activator inhibitor type-1 (PAI-1; encoded b

108 ones emerging (collagen-I, thrombospondin-I, plasminogen activator inhibitor, MMP1, 9, ADAMTS4, TIMP1

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

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

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

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

113 ze the binding interfaces of urokinase (uPA):plasminogen activator inhibitor-1 (PAI-1) and uPA:plasmi

114 Plasminogen activator inhibitor-1 (PAI-1) is a serine pr

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

116 Plasminogen activator inhibitor-1 (PAI-1) is the key end

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

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

119 factor receptor (EGFR), p53] and subsequent plasminogen activator inhibitor-1 (PAI-1), connective ti

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

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

122 receptor type 4 (CXCR4) and upregulation of plasminogen activator inhibitor-1 (PAI-1).

123 e agent shields rt-PA against degradation by plasminogen activator inhibitor-1 (PAI-1).

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

125 eral eNOS interactors, including the protein plasminogen activator inhibitor-1 (PAI-1).

126 l and extracellular matrix remodeling [e.g., plasminogen activator inhibitor-1 (PAI-1; serine proteas

127 Falpha, leptin, adiponectin, fibrinogen, and plasminogen activator inhibitor-1 were determined.

128 ines, including migration inhibitory factor, plasminogen activator inhibitor-1, and C-C motif chemoki

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

130 ded natriuretic peptides, cardiac troponins, plasminogen activator inhibitor-1, D-dimer, fibrinogen,

131 3, high urokinase-type plasminogen activator/plasminogen activator inhibitor-1, hormone receptor (HR)

132 (+/+) mice contained plasminogen activators, plasminogen activator inhibitor-1, plasminogen, and alph

133 dothelin-1, tissue plasminogen activator and plasminogen activator inhibitor-1, was depressed by expo

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

135 e TSP-1 and decrease VEGF by reducing PAI-1 (plasminogen activator inhibitor-1/SERPINE1) levels.

136 These patients have low tissue plasminogen activator levels and are not detectable by R

137 erfibrinolytic biomarker profile, low tissue plasminogen activator levels but high plasma levels of S

138 s This study demonstrated that the Y. pestis plasminogen activator Pla, a protease that promotes fibr

139 Activating MMP gelatinases with tissue plasminogen activator potentiated cue-induced reinstatem

140 The plasminogen activator protease (Pla) is a critical Y. pe

141 gression of infection is the activity of the plasminogen activator protease Pla.

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

143 nity, and coagulation, and soluble urokinase plasminogen activator receptor (suPAR) has been identifi

144 The role of the soluble urokinase plasminogen activator receptor (suPAR) in focal segmenta

145 Soluble urokinase plasminogen activator receptor (suPAR) independently pre

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

147 Soluble urokinase plasminogen activator receptor (suPAR) is a signaling gl

148 Soluble urokinase plasminogen activator receptor (suPAR) is an immune-deri

149 e demonstrated that a soluble urokinase-type plasminogen activator receptor (suPAR) plays an essentia

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

151 y) and serum levels of the soluble urokinase plasminogen activator receptor (suPAR), a proposed patho

152 Levels of soluble urokinase plasminogen activator receptor (suPAR), an inflammation

153 Soluble urokinase plasminogen activator receptor (suPAR), lipopolysacchari

154 eloped for rapid detection of urokinase type plasminogen activator receptor (uPAR) - a biomarker for

155 , we used a monoclonal antibody to urokinase plasminogen activator receptor (uPAR) as a therapeutic s

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

157 The role of urokinase-type plasminogen activator receptor (uPAR) in kidney physiolo

158 models, the wild type (WT) and the urokinase plasminogen activator receptor (uPAR) KO (uPAR), in an a

159 We identify the urokinase-type plasminogen activator receptor (uPAR)(11) as a cell-surf

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

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

162 )Ga-NOTA-AE105, targeting the urokinase-type plasminogen activator receptor (uPAR), and Gleason score

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

164 ntified, we discovered that a urokinase-type plasminogen activator receptor (uPAR)/integrin beta1/Src

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

166 x [IGFBP7]), and the soluble urokinase-type plasminogen activator receptor are of diagnostic value f

167 IMP-2] x [IGFBP7] and soluble urokinase-type plasminogen activator receptor are promising biomarker c

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

169 Soluble urokinase-type plasminogen activator receptor levels at inclusion showe

170 s over time and serum soluble urokinase-type plasminogen activator receptor levels once at inclusion

171 Soluble urokinase-type plasminogen activator receptor performed best by using a

172 tudy the ability of suPAR (soluble urokinase plasminogen activator receptor), a potential biomarker o

173 necrosis factor receptor 1), UPAR (urokinase plasminogen activator receptor), IGFBP7 (insulin-like gr

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

175 an endocytic mechanism governed by urokinase plasminogen activator receptor-associated protein (uPARA

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

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

178 I-1 with low-molecular-weight urokinase-type plasminogen activator to LRP1.

179 The plasminogen activator tPA was lower in HA-NCI while neur

180 ivities of the fibrinolysis protease, tissue plasminogen activator tPA, without effects on hemostasis

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

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

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

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

185 Accelerated tPA (tissue-type plasminogen activator) dosing regimens for ultrasound-fa

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

187 mic stroke with intravenous tPA (tissue-type plasminogen activator) may increase the risk of administ

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

189 scores after accounting for tPA (tissue-type plasminogen activator) treatment.

190 te Ischemic Stroke network: tPA (tissue-type plasminogen activator) use, complications related to tPA

191 total dose of r-tPA (recombinant tissue-type plasminogen activator) was 14 mgs in bilateral PE and 12

192 uPA (urokinase-type plasminogen activator) was related to systolic blood pre

193 al thrombus to alteplase (recombinant tissue plasminogen activator), potentially facilitating early r

194 thrombolytic treatment with tPA (tissue-type plasminogen activator).

195 for mouse plasma that is sensitive to tissue plasminogen activator, alpha2-antiplasmin, active plasmi

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

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

198 IV recombinant tissue plasminogen activator, endovascular treatment, IV albumi

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

200 After intravenous tissue plasminogen activator, intra-arterial mechanical thrombe

201 A or glycine) and the serine protease tissue plasminogen activator, previously shown to potentiate NM

202 ischemic stroke who were treated with tissue plasminogen activator, shorter door-to-needle times were

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

204 ction of blood mediates resistance to tissue plasminogen activator.

205 the aminoterminal fragment of urokinase-type plasminogen activator.

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

207 rrelated significantly with levels of tissue plasminogen activator.

208 ecreting enzymatic factors, including tissue plasminogen activator.

209 pecific protein ligands, such as tissue-type plasminogen activator.

210 rotease plasmin by staphylokinase and tissue plasminogen activator.

211 ke was strictly dependent on plasminogen and plasminogen activator.

212 bolytic and proteolytic properties of tissue plasminogen activator.

213 vated alpha(2)-macroglobulin and tissue-type plasminogen activator.

214 intermediate phenotype in response to tissue plasminogen activator.

215 er than 2, grade 2 to 3, high urokinase-type plasminogen activator/plasminogen activator inhibitor-1,

216 inst the use of intravenous tPA (tissue-type plasminogen activator; IV tPA) in acute ischemic stroke

217 It is well-established that complexes of plasminogen-activator inhibitor 1 (PAI-1) with its targe

218 me exosite used by both tissue and urokinase plasminogen activators (tPA and uPA).

219 and cell motility via its interactions with plasminogen activators and vitronectin.

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

221 is, increased tissue-type and urokinase-type plasminogen activators, a relatively decreased plasminog

222 us thrombi from alpha2AP(+/+) mice contained plasminogen activators, plasminogen activator inhibitor-

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

224 n activator (tPA; residues gamma312-324) and plasminogen (alpha148-160) binding sites, thus interferi

225 FD-fed mice was not due to altered levels of plasminogen, alpha2-antiplasmin, or fibrinogen.

226 antiplasmin are counterbalanced by decreased plasminogen and a decreased fibrin clot permeability.

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

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

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

230 Plasminogen and its active form, plasmin, have diverse f

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

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

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

234 Combined delivery of plasminogen and tissue plasminogen activator during NMP

235 we found that the binding interfaces of uPA:plasminogen and uPA:PAI-1 may have coevolved to maintain

236 tivators, plasminogen activator inhibitor-1, plasminogen, and alpha2AP, which changed with thrombus a

237 ressive disease (PD) upregulated kynurenine, plasminogen, and gap-junction pathways.

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

239 Plasminogen binding did not to occur by the same mechani

240 tly to the cells through a surface receptor, plasminogen-binding group A streptococcal M-protein (PAM

241 XII-W268R variant leads to the exposure of a plasminogen-binding site that is cryptic in FXII-WT.

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

243 ls of Plg-R(KT) and bound significantly more plasminogen compared with the other respective subsets.

244 inogen activator inhibitor-1 (PAI-1) and uPA:plasminogen complexes.

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

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

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

248 after ligation; thrombi were even larger in plasminogen-deficient mice (P < .001).

249 tingly, macrophage migration was restored in plasminogen-deficient mice by simultaneous imposition of

250 significant increase in fibrin(ogen) in the plasminogen-deficient mice.

251 in interactions, we produced uPA, PAI-1, and plasminogen from human and zebrafish to represent mammal

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

253 Due to these roles in inflammation, plasminogen has been implicated in the progression of a

254 genes [GAS]) recruit host single-chain human plasminogen (hPg) to the cell surface-where in the case

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

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

257 In this review, we discuss the functions of plasminogen in inflammatory regulation and how this syst

258 activity was reduced, and the tPA inhibitor plasminogen inhibitor-1 (PAI-1) was increased in male mi

259 by upregulation of its endogenous inhibitor plasminogen inhibitor-1 (PAI-1).

260 60) binding sites, thus interfering with tPA-plasminogen interaction and representing 1 potential mec

261 receptor (uPAR), catalyzes the conversion of plasminogen into plasmin and activates signaling pathway

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

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

264 the other kringle domains tested, including plasminogen kringle 1.

265 was higher in MCI and AD brain tissue, with plasminogen mRNA not likewise elevated, suggesting dimin

266 ProNGF levels correlated with plasminogen, neuroserpin, and VAChT while NGF correlated

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

268 Urinary plasminogen/plasmin, or plasmin (ogen) uria, has been de

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

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

271 Plasminogen (Plg)-binding M protein (PAM) is a group A s

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

273 , due to mutations in factor XII (FXII-HAE), plasminogen (PLG-HAE), angiopoietin 1 (ANGPT1-HAE), kini

274 Plasminogen protein was higher in MCI and AD brain tissu

275 33-fold in human hepatoma cells in which the plasminogen receptor (KT) was knocked out.

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

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

278 of the fibrin degradation pathway, including plasminogen receptor annexin 2A as well as downregulatio

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

280 The plasminogen receptor Plg-R(KT) is expressed by immune ce

281 of ccRCC cells through the regulation of the plasminogen receptor S100A10.

282 S100A10 is a cell surface plasminogen receptor which may drive the hyperfibrinolys

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

284 tients and exposure of cultured podocytes to plasminogen results in injury via oxidative stress pathw

285 nolytic targets, the lysine binding sites on plasminogen's kringle domains, and plasmin's serine prot

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

287 Plasminogen, the primary fibrinolytic enzyme, also modif

288 bacterial membrane and simultaneously binds plasminogen, thereby promoting its conversion to plasmin

289 The ability of plasminogen to induce matriptase zymogen activation and

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

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

292 In cultured human podocytes, plasminogen treatment was associated with decreased foca

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

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

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

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

297 largest glomerular disease cohorts to study plasminogen, we validated previous findings while sugges

298 hatidylcholines, and the coagulation protein plasminogen were altered between the control and PEs gro

299 FnBPB bound simultaneously to H3 and plasminogen, which after activation by tissue plasminoge

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