ライフサイエンスコーパス: uPA

1 uPA (urokinase-type plasminogen activator) was related t

2 uPA induction of TGFbeta1-dependent Mf differentiation o

3 uPA regulates Lhx2 expression by suppressing expression

4 uPA-accelerated atherosclerosis and aortic dilation are

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

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

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

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

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

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

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

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

13 FTO/GNS/uPAR-Ab/uPA-Ag immunosensor displayed acceptable performance for

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

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

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

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

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

19 ion between urokinase plasminogen activator (uPA) and monoclonal uPAR antibody (Ab).

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

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

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

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

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

25 ion of urokinase-type plasminogen activator (uPA) and/or matrix metalloproteinases (MMPs) as well as

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

51 pression of urokinase plasminogen activator (uPA).

52 of SerpinB2-urokinase plasminogen activator (uPA).

53 xpress urokinase-type plasminogen activator (uPA).

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

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

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

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

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

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

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

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

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

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

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

65 Although uPA can be transiently upregulated by diverse extracellu

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

67 g model in which multiple sites on PAI-1 and uPA:PAI-1 complexes interact with complementary sites on

68 PAI-1 for the interactions of both PAI-1 and uPA:PAI-1 complexes with LRP1.

69 lasminogen activator inhibitor-1 (PAI-1) and uPA:plasminogen complexes.

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

71 injury also showed increased collagen-I and uPA.

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

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

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

75 ntal cortex of AD brains and 5xFAD mice, and uPA treatment abrogates the deleterious effects of Abeta

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

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

78 ; TGF-beta, Factor Xa, thrombin, plasmin and uPA all induced fibroblast/myofibroblast differentiation

79 he binding interfaces of uPA:plasminogen and uPA:PAI-1 may have coevolved to maintain tight interacti

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

81 dulate the interaction of PAI-1 with tPA and uPA in a way not previously described for a human PAI-1

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

83 nd urokinase plasminogen activators (tPA and uPA).

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

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

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

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

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

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

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

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

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

95 In the developing brain, uPA induces neuritogenesis and neuronal migration.

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

97 rk reveals that, following its activation by uPA/uPAR binding, pGAP-43 colocalizes with presynaptic v

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

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

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

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

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

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

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

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

108 oped sensor was profitably engaged to detect uPA in spiked serum samples up to 9.2 pM.

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

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

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

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

113 onsistent with a high turnover of endogenous uPA.

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

115 Macrophage-expressed uPA accelerates atherosclerosis by stimulation of lesion

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

117 Fish uPAs appear incapable of receptor binding in the manner

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

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

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

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

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

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

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

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

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

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

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

129 orm numerous polar interactions in the human uPA:PAI-1 Michaelis complex.

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

131 In liver-humanized uPA/severe combined immunodeficient (SCID)/beige mice ch

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

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

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

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

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

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

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

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

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

141 nds several extracellular ligands, including uPA and vitronectin.

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

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

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

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

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

147 3 inhibition abolished the rapamycin-induced uPA expression in TSC-compromised cells.

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

149 observed for the protein-protein interaction uPA.uPAR.

150 Intranuclear uPA modulates gene transcription by binding to a subset

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

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

153 ence comparable with that found in mammalian uPA.

154 criteria are the fish orthologs of mammalian uPA.

155 s made with appropriate side-chains to mimic uPA at this interface.

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

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

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

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

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

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

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

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

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

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

166 Here we show that neuronal uPA protects the synapse from the harmful effects of sol

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

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

169 nduced decrease in the synaptic abundance of uPA contributes to the development of synaptic damage in

170 hese observations, the synaptic abundance of uPA, but not uPAR, is decreased in the frontal cortex of

171 r 2alpha decreases the synaptic abundance of uPA, leaving unopposed the harmful effects of Abeta on t

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

173 an explanation for the increased affinity of uPA:PAI-1 complexes for LRP1.

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

175 Here we show that binding of uPA to uPAR induces not only the mobilization of GAP-43

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

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

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

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

180 ayed acceptable performance for detection of uPA and exhibited low detection limit with high reproduc

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

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

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

184 ese observations, the synaptic expression of uPA is decreased in the frontal cortex of AD brains and

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

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

187 In contrast, the expression and function of uPA in the mature brain are poorly understood.

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

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

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

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

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

193 Lys-207, -88, and -80 for the interaction of uPA:PAI-1 complexes with LRP1.

194 hree charged residues for the interaction of uPA:PAI-1 complexes with LRP1.

195 ins, we found that the binding interfaces of uPA:plasminogen and uPA:PAI-1 may have coevolved to main

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

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

198 3, and HT-1080) expressing various levels of uPA.

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

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

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

202 different forms of injury induce release of uPA and expression of uPAR in neurons and that uPA/uPAR

203 ion between the S3-pocket-lining residues of uPA and the P3 residue of both PAI-1 and plasminogen.

204 Together, these data reveal a novel role of uPA as an activator of the synaptic vesicle cycle in cer

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

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

207 ine resistance decrease after suppression of uPA.

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

209 ion factor 2alpha halts the transcription of uPA mRNA, leaving unopposed the deleterious effects of A

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

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

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

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

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

215 res of urokinase plasminogen activator (PLAU/uPA); subsequent plasmin-mediated degradation of diverse

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

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

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

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

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

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

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

223 on protein-protein interactions, we produced uPA, PAI-1, and plasminogen from human and zebrafish to

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

225 n AD patients, and indicate that recombinant uPA is a potential therapeutic strategy to protect the s

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

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

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

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

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

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

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

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

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

235 nt-membrane proteins were reduced in both SR-uPA(+/0) aortas and ruptured human plaques.

236 Collagens were minimally altered in SR-uPA(+/0) aortas and ruptured human plaques; however, sev

237 tic proteins were reproducibly altered in SR-uPA(+/0) aortas.

238 unctional categories that were altered in SR-uPA(+/0) aortas.

239 on of urokinase (SR-uPA(+/0) mice) and of SR-uPA(+/0) bone marrow transplant recipients, and we used

240 Parallel studies of SR-uPA(+/0) mouse aortas and human plaques identify mechani

241 age-specific overexpression of urokinase (SR-uPA(+/0) mice) and of SR-uPA(+/0) bone marrow transplant

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

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

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

245 reast tumorigenicity by regulating sustained uPA expression.

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

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

248 ated plasmin-independent mechanism, and that uPA-induced formation of NCAD dimers protects the synaps

249 A and expression of uPAR in neurons and that uPA/uPAR binding triggers axonal growth and synapse form

250 Our results confirmed that uPA:PAI-1 complexes bind LRP1 with ~100-fold increased a

251 We found that uPA treatment increases the synaptic expression of NCAD

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

273 from the interaction of three regions of the uPA:PAI-1 complex with LDLa repeats on LRP1 provided an

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

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

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

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 We found that neuronal urokinase-type (uPA) protects the synapse from the deleterious effects o

283 ators: tissue-type (tPA) and urokinase-type (uPA).

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

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

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

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

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

293 analyze the binding interfaces of urokinase (uPA):plasminogen activator inhibitor-1 (PAI-1) and uPA:p

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

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

296 In contrast, it is unknown whether uPA and its receptor (uPAR) contribute to the pathogenes

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