ライフサイエンスコーパス: uPA

1 uPA induction of TGFbeta1-dependent Mf differentiation o

2 uPA regulates Lhx2 expression by suppressing expression

3 uPA-accelerated atherosclerosis and aortic dilation are

4 uPA-induced phosphorylation of eNOS was also inhibited b

5 uPA-induced phosphorylation of eNOS was decreased by ant

6 uPA-knock-out mice developed fewer and smaller TSC2-null

7 cardiac fibrosis was observed in PAI-1(-/-)/uPA(-/-) double knockout mice that was associated with r

8 Aortic wall PAI-1, uPA, and tPA concentrations were determined by western b

9 itor plasminogen activator inhibitor type 1, uPA receptor (uPAR), and beta1-integrin, which affect fo

10 propose that the greater efficiency of PAI-1.uPA complex binding and clearance by LRP1, compared with

11 Cord CRP, NT-proBNP, MMP-2, uPA, uPAR, and plasminogen levels were higher in cardiac

12 MMP-2, uPA, uPAR, and plasminogen were evaluated using ELISA.

13 PA and tPA levels in RGC-5 cells, and MMP-9, uPA, and tPA levels in the retinas and promoted the deat

14 creased their ability to degrade matrix in a uPA-dependent manner.

15 The first is that ILF3 activates uPA transcription by binding to the CTGTT sequence in th

16 (tPA), and urokinase plasminogen activator (uPA) activities were assessed by zymography assays.

17 elease urokinase-type plasminogen activator (uPA) and astrocytes recruit the uPA receptor (uPAR) to t

18 Urokinase plasminogen activator (uPA) and its receptor (uPAR) coordinate a plasmin-mediat

19 ity of urokinase-type plasminogen activator (uPA) and matrix metalloproteinase-2 (MMP-2).

20 Urokinase plasminogen activator (uPA) and PA inhibitor type 1 (PAI-1) are elevated in acu

21 pression of urokinase plasminogen activator (uPA) and plasminogen activator inhibitor (PAI)-1 in 2 mu

22 ges in urokinase-type plasminogen activator (uPA) and plasminogen activator inhibitor-1 (PAI-1) level

23 f both urokinase-type plasminogen activator (uPA) and the uPA receptor are elevated in FL-fibroblasts

24 ion of urokinase-type plasminogen activator (uPA) and the uPA receptor in AECs from the lungs of IPF

25 vators urokinase-type plasminogen activator (uPA) and tissue plasminogen activator, which binds tight

26 vating urokinase-type plasminogen activator (uPA) and ultimately plasmin (Pm) generation.

27 acking urokinase-type plasminogen activator (uPA) are highly susceptible, whereas those deficient in

28 PAI-1/urokinase-type plasminogen activator (uPA) balance as an important regulator of microribonucle

29 ses such as urokinase plasminogen activator (uPA) can be a hallmark of malignant transformation.

30 Urokinase plasminogen activator (uPA) converts plasminogen to plasmin, resulting in a pro

31 pression of urokinase plasminogen activator (uPA) drives signaling through the MAPK pathway, which re

32 tained urokinase-type plasminogen activator (uPA) expression is detected in aggressive breast tumors.

33 release of urokinase plasminogen activator (uPA) from injured brain leads to posttraumatic bleeding

34 Urokinase plasminogen activator (uPA) is a biomarker and therapeutic target for several c

35 Urokinase-type plasminogen activator (uPA) is a serine proteinase that upon binding to the uro

36 Urokinase-type plasminogen activator (uPA) is a serine proteinase that, upon binding to its re

37 Urokinase-type plasminogen activator (uPA) is expressed at elevated levels by macrophages in a

38 e-delivered urokinase plasminogen activator (uPA) is highly effective in preventing thrombosis, while

39 Urokinase plasminogen activator (uPA) is inhibited by PN-1.

40 ion of urokinase-type plasminogen activator (uPA) is sufficient for Mp to migrate into damaged muscle

41 zed by urokinase-type plasminogen activator (uPA) plays an important role in normal and pathological

42 of the urokinase-type plasminogen activator (uPA) reduces arthritis progression in the collagen-induc

43 Urokinase-type plasminogen activator (uPA) regulates angiogenesis and vascular permeability th

44 ion by urokinase-type plasminogen activator (uPA) was markedly inhibited (by 39%) by treatment with a

45 The urokinase plasminogen activator (uPA) was the first identified ligand for uPAR, but eluci

46 tease, urokinase-type plasminogen activator (uPA), is central in tissue remodeling processes and also

47 on, such as urokinase plasminogen activator (uPA), its inhibitor plasminogen activator inhibitor type

48 osis of the urokinase plasminogen activator (uPA), its receptor (uPAR), and plasminogen activator inh

49 amounts of urokinase plasminogen activator (uPA), we tested whether increased extracellular uPA prom

50 ing of urokinase-like plasminogen activator (uPA), which is a key protease involved in cancer invasio

51 ors of urokinase-type plasminogen activator (uPA), which is a prototypical target of cancer research.

52 lizing urokinase-type plasminogen activator (uPA)-mediated fibrinolysis to the pericellular micro-env

53 pression of urokinase plasminogen activator (uPA).

54 of SerpinB2-urokinase plasminogen activator (uPA).

55 xpress urokinase-type plasminogen activator (uPA).

56 of t-PA and urokinase plasminogen activator (uPA).

57 tif of urokinase-type plasminogen activator (uPA).

58 psin B/urokinase-type plasminogen activator (uPA)/matrix metalloproteinase-2 (MMP-2).

59 at the urokinase-type plasminogen activator (uPA)/uPA receptor (uPAR) complex is required for the loc

60 d increases urokinase plasminogen activator (uPA)/uPA receptor (uPAR)-dependent plasmin activation.

61 plicate the urokinase plasminogen activator (uPA)/uPA receptor (uPAR)/plasminogen system in the devel

62 se (MMP)-2; urokinase plasminogen activator (uPA); urokinase plasminogen activator receptor (uPAR); p

63 he protease urokinase plasminogen activator (uPA, PLAU).

64 es allowed us to noninvasively detect active uPA in prostate cancer xenograft models using optical an

65 In addition, U33 was able to image active uPA in small soft-tissue and osseous metastatic lesions

66 )-Lys(136)) and plasminogen, yielding active uPA and plasmin, respectively.

67 with BALB/c Rag2(-/-)Il2rg(-/-)Sirpa(NOD)Alb-uPA(tg/tg) mice, stably engrafted with human hepatocytes

68 HCV infection because HCV-infected SCID/Alb-uPA mice accumulated higher plasma ketones while fasting

69 transmission, we utilized chimeric SCID/Alb-uPA mice with transplanted human hepatocytes and infecte

70 Although uPA can be transiently upregulated by diverse extracellu

71 result of U33 IgG internalization through an uPA receptor-mediated mechanism in which U33 mimicked th

72 er treatment of wild-type mice with CSP, and uPA-deficient mice were unresponsive.

73 a suggest that increased uPAR expression and uPA activity induced by anti-Ro60 binding to the apoptot

74 injury also showed increased collagen-I and uPA.

75 nces transcriptional activation of LAMC2 and uPA by TCF4/beta-catenin.

76 ng a number of Wnt targets such as LAMC2 and uPA.

77 binding in the manner known from mammals and uPA-catalyzed plasminogen activation in fish may occur m

78 Two-chain uPA (1-20 nM) and uPA-PAI-1 induced phosphorylation of endothelial NOS-Ser

79 s of intact fibrin is initiated by t-PA, and uPA activates the remaining plasminogens.

80 ation of Glu- and Lys-plasminogen by tPA and uPA by 480- and 70-fold and 10.7- and 17-fold, respectiv

81 ction of dsDNA/oligonucleotides with tPA and uPA includes a fast bimolecular step, followed by two mo

82 inhibited plasminogen activation by tPA and uPA, attenuated ICH, lowered plasma d-dimers, lessened t

83 we found that ICH is reduced in tPA(-/-) and uPA(-/-) mice but increased in PAI-1(-/-) mice compared

84 oved neurologic outcome in WT, tPA(-/-), and uPA(-/-) mice.

85 Two-chain uPA and uPA-PAI-1 complexes (1-20 nM) increased the permeability

86 ade and inhibition of PKA prevented uPA- and uPA-PAI-1-induced permeability of PMVEC monolayers in vi

87 ermeability of PMVEC monolayers in vitro and uPA-induced lung permeability in vivo.

88 ion of VN binding or ablation of both VN and uPA binding specifically abrogates these activities of u

89 nt (muPAR(DeltaD1)) deficient in both VN and uPA binding.

90 In the CIA model, the impact of anti-uPA treatment was on par with the effect of blocking TNF

91 o-CHB-IgG cardiocytes with anti-uPAR or anti-uPA Abs or plasmin inhibitor aprotinin prior to cocultur

92 ed to be central to the functions of uPA, as uPA-catalyzed plasminogen activation activity appeared t

93 Upon systemic administration to mice bearing uPA-overexpressing breast tumors, FAM-labeled uCendR pep

94 teraction in vivo has been difficult because uPA has important physiologic functions that are indepen

95 By blocking uPA-stimulated cell adhesion, PAI-1R may be a useful age

96 activation and that astrocytes activated by uPA-uPAR binding promote synaptic recovery in neurons th

97 d accelerating the rate of its activation by uPA.

98 noparticles and showed that it is cleaved by uPA, and that the cleavage triggers binding to recombina

99 hage adhesion to vitronectin was enhanced by uPA and blocked by plasminogen activator inhibitor-1, th

100 L increases the rate of plasma clot lysis by uPA and single-chain tissue-type Pg activator approximat

101 ms: the alteration of collagen metabolism by uPA-mediated proteolytic processing of transforming grow

102 ate that regulation of gene transcription by uPA contributes to cancer stemness and clinical lethalit

103 s in immunodeficient BALB-DeltaRAG/gamma(c) -uPA (urokinase-type plasminogen activator) mice, freshly

104 Intranuclear single-chain uPA binds directly to and interferes with the function o

105 Here we report that wild type single-chain uPA, but not uPA variants incapable of nuclear transport

106 lerate the inactivation of tPA and two chain uPA by plasminogen activator inhibitor-1 (PAI-1), which

107 Two-chain uPA (1-20 nM) and uPA-PAI-1 induced phosphorylation of e

108 Two-chain uPA and uPA-PAI-1 complexes (1-20 nM) increased the perm

109 s in RAAA tissue (P = 0.01), with comparable uPA and decreased tPA levels (P = 0.02).

110 ctivator, severe combined immune deficiency (uPA-SCID) mice" (chimeric mice).

111 tion, by virtue of increasing uPAR-dependent uPA activity, thus initiating and amplifying a cascade o

112 In summary, Mp-derived uPA promotes muscle regeneration by inducing Mp migratio

113 nanofiber precursor (NIR-NFP) for detecting uPA activity.

114 ed male mice genetically deficient on either uPA (uPA(-/-)) or uPAR (uPAR(-/-)) or with a four-amino

115 asmic ILF3 staining correlates with elevated uPA level and higher grades of human breast tumor specim

116 Based on approaches employing uPA gene-deficient macrophages, plasminogen supplementat

117 onsistent with a high turnover of endogenous uPA.

118 the binding of recombinant uPA or endogenous uPA to uPAR induces membrane recruitment and activation

119 creased uPAR expression, as well as enhanced uPA activity.

120 Macrophage-expressed uPA accelerates atherosclerosis by stimulation of lesion

121 econd animal model that macrophage-expressed uPA stimulates atherosclerosis and aortic dilation.

122 We generated transgenic mice expressing uPA only in Mp, and we assessed the ability of these mic

123 ), we tested whether increased extracellular uPA promotes the persistence of Mfs on VN.

124 Fish uPAs appear incapable of receptor binding in the manner

125 dentification of fragments with affinity for uPA's S1 pocket.

126 smoke-induced lung injury were analyzed for uPA, PAI-1, and EMT markers.

127 r work unveils a new biological function for uPA-uPAR as mediator of a neuron-astrocyte cross talk th

128 Evidence for a unique role for uPA in the inverse relationship between macrophage adhes

129 The SAR for uPA inhibition around this scaffold is explored, and the

130 Matrigel-embedded aortic rings isolated from uPA knock-out (uPA(-/-)) mice was impaired compared with

131 Endothelial cells isolated from uPA(-/-) mice show less proliferation and migration in r

132 sure of wild-type macrophages to medium from uPA-overexpressing macrophages.

133 sed expression of p53-binding sequences from uPA, uPAR, and PAI-1 mRNA 3' untranslated regions in ATI

134 p53-binding sequences from uPA, uPAR, and PAI-1 mRNA 3' untranslated regions neithe

135 Furthermore, uPA or its aminoterminal fragment (ATF) can promote the

136 mouse embryonic fibroblasts expressed higher uPA levels than their WT counterparts, resulting from th

137 B virus (HBV) chronically infected humanized uPA/SCID mice were employed to establish a small animal

138 These studies identify uPA-dependent de-repression of vegfr1 and vegfr2 gene tr

139 imized preparation may be useful for imaging uPA activity in vivo.

140 To investigate whether changes in uPA and PAI-1 by ATII cells contribute to EMT, ATII cell

141 Tranexamic acid inhibited ICH expansion in uPA(-/-)mice but not in tPA(-/-) mice.

142 es not inhibit uPA prevented the increase in uPA-stimulated cell adhesion and reduced uPA-stimulated

143 e actions and implicate specific pathways in uPA/Plg-accelerated atherosclerosis and aneurysmal disea

144 rophages; up-regulation of S100A9 protein in uPA-overexpressing macrophages was confirmed by Western

145 ase-3 and PAI-1 with a parallel reduction in uPA expression.

146 the most highly up-regulated transcripts in uPA-overexpressing macrophages; up-regulation of S100A9

147 r, the in vivo role of PAI-1 in inactivating uPA and limiting the generation of Pm during cardiac fib

148 nds several extracellular ligands, including uPA and vitronectin.

149 Increased uPA levels and activity were present in supernatants gen

150 However, rapamycin further increased uPA expression in TSC2-null tumor cells and immortalized

151 ent to plaque caps and in aortas, increasing uPA expression at both sites.

152 with resected PDAC, we show that increasing uPA mRNA expression was significantly associated with po

153 scription failed to suppress PAI-1 or induce uPA mRNA in BLM-treated ATII cells.

154 PA shRNA in tumor cells or amiloride-induced uPA inhibition reduced tumorigenesis in vivo These findi

155 s in ATII cells suppressed PAI-1 and induced uPA after BLM treatment, leading to inhibition of ATII c

156 3 inhibition abolished the rapamycin-induced uPA expression in TSC-compromised cells.

157 Staurosporine induced uPA and tPA levels in RGC-5 cells, and MMP-9, uPA, and t

158 AI-1R) that binds to VN but does not inhibit uPA prevented the increase in uPA-stimulated cell adhesi

159 the reactive center loop, failed to inhibit uPA and to reduce Matrigel invasion.

160 Intranuclear uPA modulates gene transcription by binding to a subset

161 om transgenic mice with increased macrophage uPA expression or nontransgenic controls (all apolipopro

162 But zfuPA-a differs from mammalian uPA by lacking the exon encoding the uPAR-binding epider

163 -like domain; zfuPA-b differs from mammalian uPA by lacking two cysteines of the epidermal growth fac

164 ence comparable with that found in mammalian uPA.

165 criteria are the fish orthologs of mammalian uPA.

166 immunoprecipitate, suggesting a novel maspin-uPA-uPAR-beta1 integrin mega-complex that regulates mamm

167 nt-derived GBM cells and genetic GBM models, uPA is shown to suppress BIM levels through ERK1/2 phosp

168 A mAb that neutralizes mouse uPA significantly reduced arthritis progression in the C

169 tumorigenesis we fed wild-type (WT) and MUP-uPA mice, in which hepatocyte ER stress is induced by pl

170 atory macrophages that accumulate in the MUP-uPA liver in response to hepatocyte ER stress.

171 ains were equally insulin resistant, the MUP-uPA mice exhibited more liver damage, more immune infilt

172 lved five X-ray crystal structures of murine uPA (muPA) in the absence and presence of allosteric mol

173 best compounds in the series have nanomolar uPA affinity and selectivity with respect to the related

174 in and that astrocytes activated by neuronal uPA promote synaptic recovery in neurons that have suffe

175 hypoxic injury and that binding of neuronal uPA to astrocytic uPAR induces astrocytic activation by

176 We found that binding of neuronal uPA to astrocytic uPAR promotes astrocytic activation an

177 ort that wild type single-chain uPA, but not uPA variants incapable of nuclear transport, increases t

178 tPA(-/-), but not uPA(-/-), mice developed a systemic coagulopathy post-TB

179 In the absence of uPA overexpression, however, uPAR contributes modestly t

180 However, addition of uPA to cells on VN increased Mf differentiation (9.7-fol

181 onal injury express uPAR and that binding of uPA to this uPAR promotes axonal recovery by a mechanism

182 ined to cell surfaces through the binding of uPA to uPAR.

183 n Ab that blocks the proteolytic capacity of uPA in the CIA model and the delayed-type hypersensitivi

184 gments are transformed into a novel class of uPA inhibitors with an imidazo[1,2-a]pyridine scaffold.

185 refore propose that the current consensus of uPA-catalyzed plasminogen activation taking place on cel

186 ubstitution into the growth factor domain of uPA that abrogates its binding to uPAR (Plat(GFDhu/GFDhu

187 by the isolated growth factor-like domain of uPA.

188 croarray data suggest significant effects of uPA overexpression on cell migration and cell-matrix int

189 The effects of uPA-PAI-1 were abrogated by the nitric-oxide synthase (N

190 onstruct (Ad-PAI-1) suppressed expression of uPA and collagen-I and attenuated proliferation in FL-fi

191 t mechanisms for PAR-dependent expression of uPA and PAI-1.

192 The arthritic synovium showed expression of uPA and uPAR in neutrophils, macrophages, and a fraction

193 Furthermore, Mp expression of uPA regulated the level of active hepatocyte growth fact

194 mechanisms and conformational flexibility of uPA and trypsin-like serine proteases in general.

195 n believed to be central to the functions of uPA, as uPA-catalyzed plasminogen activation activity ap

196 minibolus of t-PA followed by an infusion of uPA was administered to 101 patients with acute myocardi

197 ow that induction of PAI-1 and inhibition of uPA during fibrosing lung injury lead to EMT in ATII cel

198 Inhibition of uPA expression in Tsc2-null cells reduced the growth and

199 the function of the endogenous inhibitor of uPA to gain entry into the cancer cell.

200 r TSC2-null lung tumors, and introduction of uPA shRNA in tumor cells or amiloride-induced uPA inhibi

201 n be reversed by siRNA-mediated knockdown of uPA.

202 3, and HT-1080) expressing various levels of uPA.

203 regeneration were unaffected by the loss of uPA binding to uPAR.

204 deficient in uPAR to elucidate mechanisms of uPA/uPAR/plasminogen-accelerated atherosclerosis and ane

205 aim was to determine the cellular origins of uPA and the uPA receptor (uPAR) in joint tissue from pat

206 The cellular expression patterns of uPA and uPAR were characterized by double immunofluoresc

207 cond is that ILF3 inhibits the processing of uPA mRNA-targeting primary microRNAs (pri-miRNAs).

208 In the present study we examine the role of uPA in the generation of PDAC CSC.

209 ts the hypothesis that elevated secretion of uPA in fibrotic tissue may promote cell adhesion and the

210 ine resistance decrease after suppression of uPA.

211 nic for human alphaIIb compared with that of uPA-T, and prevents clot formation in a microfluidic sys

212 Transplantation of uPA-overexpressing macrophages increased aortic matrix m

213 MVEC permeability and suggest the utility of uPA-based approaches that attenuate untoward permeabilit

214 On uPA activation, NIR-NFP releases peptide fragments (PEG(

215 Mp-only uPA expression was sufficient to induce wild-type levels

216 /-) mdx mice, could be reversed by miR-21 or uPA-selective interference, whereas forced miR-21 overex

217 to VEGF than their wild type counterparts or uPA(-/-) endothelial cells in which expression of wild t

218 ed aortic rings isolated from uPA knock-out (uPA(-/-)) mice was impaired compared with vessels emanat

219 PLT/uPA-T recognizes human alphaIIbbeta3 on both quiescent a

220 mportantly, in two murine injury models, PLT/uPA-T did not lyse preexisting clots, even when administ

221 Thus, PLT/uPA-T represents the prototype of a platelet-targeted th

222 tivatable, low-molecular-weight pro-uPA (PLT/uPA-T).

223 LRP blockade and inhibition of PKA prevented uPA- and uPA-PAI-1-induced permeability of PMVEC monolay

224 rombin-activatable, low-molecular-weight pro-uPA (PLT/uPA-T).

225 p complex cleaves the inactive zymogens, pro-uPA (at consensus sites Lys(158)-Ile(159) and Lys(135)-L

226 ata indicate that the binding of recombinant uPA or endogenous uPA to uPAR induces membrane recruitme

227 ith a parallel increase in PAI-1 and reduced uPA expression.

228 in uPA-stimulated cell adhesion and reduced uPA-stimulated integrin alphavbeta3/alphavbeta5 binding

229 l molecular pathway in which MMP-9 regulates uPA activity and tumor cell invasion through cleavage of

230 We found that neurons release uPA and astrocytes recruit uPAR to their plasma membrane

231 g cancer cells via a mechanism that requires uPA-initiated cell signaling.

232 ive cigarette smoke-induced EMT and restored uPA expression while suppressing PAI-1.

233 nd approximately 95% of the circulating scFv/uPA-T remained bound to RBCs.

234 roximately 70% and approximately 35% of scFv/uPA-T was retained in the blood, respectively, and appro

235 NIR-NFP was able to detect cell-secreted uPA from human cancer cells (SKBR-3, PANC-1, MCF-7, SKOV

236 omal remodelling and highlights the SerpinB2/uPA axis for further investigation as a potential therap

237 We found that macrophage-specific uPA overexpression accelerates atherosclerosis and cause

238 ice, including mice with macrophage-specific uPA overexpression and mice genetically deficient in uPA

239 Specifically, uPA cleaves the zymogen plasminogen into the active form

240 ng factor 3 (ILF3) is required for sustained uPA expression.

241 Unfortunately, how sustained uPA expression is achieved in invasive/metastatic breast

242 LF3 highlights the role of ILF3 in sustained uPA expression as a transcription activator and pri-miRN

243 reast tumorigenicity by regulating sustained uPA expression.

244 reast tumorigenicity by regulating sustained uPA expression.Oncogene advance online publication, 17 S

245 phase from an acute ischemic injury and that uPA binding to uPAR promotes neurological recovery after

246 In vitro studies demonstrated that uPA promotes Mp migration through proteolytic and nonpro

247 NS axonal injury to test the hypothesis that uPA binding to uPAR promotes axonal regeneration in the

248 Our previous studies indicate that uPA and uPAR expression increase in the ischemic brain d

249 We observe that uPA interacts directly with transcription factors LIM ho

250 We reported previously that uPA is transported from cell surface receptors to nuclei

251 It is therefore proposed that uPA can have a key role in the inflammatory response at

252 We report that uPA/uPAR binding is necessary and sufficient to induce a

253 In summary, we show that uPA/uPAR-induced astrocytic activation mediates a cross

254 nhibitors, it is reported in this study that uPA activity is a central component of the invasion of m

255 etermine the cellular origins of uPA and the uPA receptor (uPAR) in joint tissue from patients with r

256 ase-type plasminogen activator (uPA) and the uPA receptor are elevated in FL-fibroblasts from the lun

257 ase-type plasminogen activator (uPA) and the uPA receptor in AECs from the lungs of IPF patients, and

258 MMP-2 and the uPA/uPAR/plasminogen cascade provide therapeutic targets

259 Because the uPA/uPAR system plays a role in TGF-beta activation, we

260 A link between the uPA-uPAR-ERK1/2 pathway and BIM has not been previously

261 tion of TSC2-null cells was inhibited by the uPA inhibitor UK122, dexamethasone, and a FOXO inhibitor

262 Knockout of the uPA gene, but not the t-PA gene, inhibited fibrinolysis.

263 is due solely to simultaneous binding of the uPA moiety in the complex to its receptor, thereby makin

264 nucleotides -1004 approximately -1000 of the uPA promoter; the second is that ILF3 inhibits the proce

265 ndings are consistent with activation of the uPA proteolytic cascade by P. gingivalis being required

266 h is required for endosomal recycling of the uPA receptor to the plasmalemma, remained abnormally ass

267 ltered expression of major components of the uPA system on ATII cell EMT during lung injury is not we

268 increased the total cellular content of the uPA-PAI-1 protein complex.

269 y identifies a principal in vivo role of the uPA-uPAR interaction in cell-associated fibrinolysis cri

270 ) mice revealed an unanticipated role of the uPA-uPAR interaction in suppressing inflammation seconda

271 elucidation of the specific functions of the uPA-uPAR interaction in vivo has been difficult because

272 ting that these mutations do not perturb the uPA binding properties of uPAR.

273 n activator (uPA) and astrocytes recruit the uPA receptor (uPAR) to their plasma membrane during the

274 ention studies have focused on targeting the uPA.uPAR interaction in vivo.

275 Our results show that the uPA/uPAR/LRP1 system is a potential target for the devel

276 iated protein (RAP), and when binding to the uPA receptor was blocked by the isolated growth factor-l

277 findings suggest that interference with the uPA-dependent pathway, when used along with rapamycin, m

278 activity was found to be required for these uPA-mediated effects.

279 LM injury showed augmented binding of p53 to uPA, uPA receptor (uPAR), and PAI-1 mRNA.

280 elial cells in which expression of wild type uPA had been restored.

281 In mice with wild-type uPA expression, Mp-specific overexpression further incre

282 le mice genetically deficient on either uPA (uPA(-/-)) or uPAR (uPAR(-/-)) or with a four-amino acid

283 e urokinase-type plasminogen activator (uPA)/uPA receptor (uPAR) complex is required for the localiza

284 reases urokinase plasminogen activator (uPA)/uPA receptor (uPAR)-dependent plasmin activation.

285 te the urokinase plasminogen activator (uPA)/uPA receptor (uPAR)/plasminogen system in the developmen

286 jury showed augmented binding of p53 to uPA, uPA receptor (uPAR), and PAI-1 mRNA.

287 This antibody and one of the uPAR/uPA antagonist antibodies shows a significant combined e

288 w that sustained and transiently upregulated uPA expression are regulated by distinct mechanisms.

289 , sustained, but not transiently upregulated uPA expression contributes to breast cancer invasion/met

290 Urokinase (uPA, urinary plasminogen activator) is a serine protease

291 nucleotides bind tissue-(tPA) and urokinase (uPA)-type plasminogen activators, plasmin, and plasminog

292 nces the activation of [Glu]Pg by urokinase (uPA) approximately 20-fold, to a maximum rate indistingu

293 interact with FPRs and to mediate urokinase (uPA) or fMLF-dependent cell migration.

294 reclinical proof-of-principle that validates uPA as a novel therapeutic target in rheumatic diseases.

295 Fluorescence changes were uPA dependent, as confirmed with both Western blot analy

296 GFDhu)) to investigate the mechanism whereby uPA promotes neurorepair in the ischemic brain.

297 However, it is yet unknown whether uPA binding to uPAR has an effect on axonal recovery in

298 ng to HHEX/PRH as a novel mechanism by which uPA mediates the pro-angiogenic effects of VEGF and iden

299 we describe an additional mechanism by which uPA regulates angiogenesis.

300 However, the mechanisms through which uPA/uPAR/plasminogen stimulate these diseases are not ye

301 also up-regulated in the aortae of mice with uPA-overexpressing macrophages, and macrophage S100A9 mR