ライフサイエンスコーパス: PAI

1 PAI can also effectively activate M2 receptors using two

2 PAI-039 reduced brain lesion volume by 26% at 24 hours a

3 PAI-1 expression is significantly increased in the epith

4 PAI-1 expression was significantly increased in epitheli

5 PAI-1 gain-of-function variants promote airway fibrosis

6 PAI-1 has been shown to play a role in a number of diver

7 PAI-1 inhibition restores tPA activity, rescues neurovas

8 PAI-1 inhibition significantly decreased baseline and TG

9 PAI-1 is an essential repressor of cardiac fibrosis in m

10 PAI-1 levels varied considerably, but a statistically si

11 PAI-1 levels varied from 0.1 to 4.5 ng/mL (mean, 2.4 ng/

12 PAI-1 mRNA was time-dependently upregulated, with a 305-

13 complex (520 vs 409 mug/L, overall P = .04), PAI-1 (10 vs 7 ng/mL, overall P = .02), and vWF (142% vs

14 or (tPA), plasminogen activator inhibitor 1 (PAI-1) and platelets.

15 inhibitor plasminogen activator inhibitor 1 (PAI-1) controlled both the extent of lysis propagation a

16 Plasminogen activator inhibitor 1 (PAI-1) is a serpin inhibitor of the plasminogen activato

17 (TF) and plasminogen activator inhibitor 1 (PAI-1) levels in venous endothelial cells in an AHR-depe

18 plexes of plasminogen-activator inhibitor 1 (PAI-1) with its target enzymes bind tightly to low-densi

19 ession of plasminogen activator inhibitor 1 (PAI-1), a key enzyme in the fibrinolytic cascade, was as

20 or (tPA), plasminogen activator inhibitor 1 (PAI-1), and platelets.

21 nhibitor, plasminogen activator inhibitor 1 (PAI-1), in Puumala hantavirus (PUUV)-infected patients a

22 bition of plasminogen activator inhibitor 1 (PAI-1), which was the most abundant ASC adipokine, led t

23 pair for plasminogen activator inhibitor 1 (PAI-1).

24 Plasminogen activator inhibitor 1 (PAI-1/serpinE1) can be induced by TGF-beta1, but its rol

25 d produce plasminogen activator inhibitor-1 (PAI-1) and stimulate the expression and secretion of the

26 ase (uPA):plasminogen activator inhibitor-1 (PAI-1) and uPA:plasminogen complexes.

27 Plasminogen activator inhibitor-1 (PAI-1) is a serine protease inhibitor (serpin) that regu

28 Plasminogen activator inhibitor-1 (PAI-1) is known to protect mice against cardiac fibrosis

29 Plasminogen activator inhibitor-1 (PAI-1) is the key endogenous inhibitor of fibrinolysis,

30 Plasminogen activator inhibitor-1 (PAI-1) is the main inhibitor of the tissue type and urok

31 d the tPA inhibitor plasminogen inhibitor-1 (PAI-1) was increased in male mice expressing the Swedish

32 rphism in plasminogen activator inhibitor-1 (PAI-1) with airway obstruction is modified by asthma sta

33 e protein plasminogen activator inhibitor-1 (PAI-1), an established regulator of these properties in

34 VEGF, plasminogen activator inhibitor-1 (PAI-1), and pigment epithelium-derived factor (PEDF) wer

35 or-alpha, plasminogen activator inhibitor-1 (PAI-1), and urinary oxidative stress marker 15-F2t-isopr

36 ubsequent plasminogen activator inhibitor-1 (PAI-1), connective tissue growth factor, fibronectin, an

37 erexpress plasminogen activator inhibitor-1 (PAI-1), S. aureusclfA expression and fibrin-encapsulated

38 n p53- or plasminogen activator inhibitor-1 (PAI-1)-deficient mice.

39 levels of plasminogen activator inhibitor-1 (PAI-1).

40 lpha) and plasminogen activator inhibitor-1 (PAI-1).

41 ndogenous inhibitor plasminogen inhibitor-1 (PAI-1).

42 e protein plasminogen activator inhibitor-1 (PAI-1).

43 lation of plasminogen activator inhibitor-1 (PAI-1).

44 dation by plasminogen activator inhibitor-1 (PAI-1).

45 ng [e.g., plasminogen activator inhibitor-1 (PAI-1; serine protease inhibitor, clade E, member 1), co

46 Plasminogen activator inhibitor type-1 (PAI-1) is a serine protease inhibitor (serpin) implicate

47 Plasminogen activator inhibitor type-1 (PAI-1; encoded by the SERPINE1 gene), a u-PA inhibitor a

48 lex, plasminogen activator inhibitor type 1 [PAI-1], D-dimer, and von Willebrand factor [vWF]) were m

49 The synthesized polyarylimide hybrid (2D-PAI@CNT) is featured with abundant pai-conjugated redox-

50 hly stable, crystalline 2D polyarylimide (2D-PAI) integrated with carbon nanotube (CNT) is demonstrat

51 on after 8000 cycles) are achieved in the 2D-PAI@CNT cathode, which far exceeds the state-of-the-art

52 ood ([Formula: see text]), we predict 34,797 PAIs which show strong overlap with the chromatin contac

53 HIF2alpha-dependent genes, including VEGF-A, PAI-1, and cyclin D1 in ccRCC cell lines and tumor xenog

54 t explained by elevated PAI-1 because active PAI-1 concentrations required to inhibit the PG assay we

55 f miR-30c and synthesize considerable active PAI-1.

56 ibutions incompatible with the high affinity PAI-1/LRP1 interaction.

57 pathway mediates the expressions of ET-1 and PAI-1 and migration and proliferation of contractile cel

58 of multiple genes, including HIF-1alpha and PAI-1, in AECs.

59 n molecule-1, fibrinogen-like protein 2, and PAI-1, the secretion of TNFalpha, IL-8, and monocyte che

60 The changes in miR-30c and PAI-1 levels were identified in platelets from healthy a

61 y biomarkers MMP-3, VE-cadherin, 6Ckine, and PAI-1 were correlated to each other in TMJOA patients an

62 xes to achieve combined CXCR4 antagonism and PAI-1 inhibition is a promising strategy for treatment o

63 ansforming growth factor-beta (TGF-beta) and PAI-1 regulated TGF-beta synthesis by cardiomyocytes in

64 eta-induced collagen accumulation, CTGF, and PAI-1 expression, but enhances Smad7 protein expression

65 agen I, alpha-smooth muscle actin, CTGF, and PAI-1, but decreased Smad7 expression.

66 atment with combined inhibition of CXCR4 and PAI-1 in ALI and various disease stages of IPF.

67 ture and elevated levels of plasma FXIII and PAI-1.

68 study demonstrates the potential of MRI and PAI for detecting the downstream cellular changes induce

69 p21 and PAI-1, which are two p53 downstream targets critical for

70 ted with reduced circulating VEGF, PEDF, and PAI-1, and could provide incentive for reducing weight a

71 bypassed by Rac1, p22(phox), p47(phox), and PAI-1 silencing.

72 , the perspectives and challenges of PTT and PAI for combating cancer, especially regarding their cli

73 We believe that PTT and PAI having noteworthy features would become promising ne

74 inhibition of AHR activity suppressed TF and PAI-1 expression in endothelial cells of the IVC and red

75 revealed nuclear AHR and upregulated TF and PAI-1 expression, telltale signs of an activated AHR-TF/

76 e and endothelial cells, cLDL induced TF and PAI-1 expression.

77 and tPA), and protease modulators (TIMP1 and PAI-1).

78 significantly associated with plasma tPA and PAI-1, suggesting endothelial cells as a potential sourc

79 significantly associated with plasma tPA and PAI-1, suggesting that endothelial cells could be a pote

80 Wild-type and PAI-1 knockout (KO) mice on a high-fat diet both became

81 tivator inhibitor 1 (Serpine1, also known as PAI-1), due in part to uncoupled TGF-beta-mediated suppr

82 ing even to closely related proteins such as PAI-2.

83 -1 levels did not mitigate this association, PAI-1 may contribute to airway obstruction in the contex

84 The interaction between PAI-1 and eNOS is a direct interaction as supported in e

85 strate a protein-protein interaction between PAI-1 and eNOS.

86 PAI-1 by TGF-beta1, the relationship between PAI-1 and esophageal fibrosis, and the role of PAI-1 in

87 g residues of uPA and the P3 residue of both PAI-1 and plasminogen.

88 sidues in PAI-1 for the interactions of both PAI-1 and uPA:PAI-1 complexes with LRP1.

89 s, potent activity against vitronectin-bound PAI-1 in vivo, and efficacy in a murine model of venous

90 d directly correlated with those measured by PAI.

91 ulatory mechanism for TGF-beta production by PAI-1, which explains the paradoxical effect of PAI-1 de

92 o understand how ImaA could be affecting cag PAI T4SS activity at the host cell interface, we utilize

93 containing the cag pathogenicity island (cag PAI) are associated with a higher risk of gastric adenoc

94 cells via its cag pathogenicity island (cag PAI) type IV secretion system (T4SS).

95 nocarcinoma or peptic ulcer disease than cag PAI-negative strains.

96 The cag PAI encodes a type IV secretion system (T4SS) that media

97 ein (HP0289) decreases the action of the cag PAI T4SS via tempering the bacterium's interaction with

98 atory response that was dependent on the cag PAI T4SS; here we extend those findings to show that the

99 in 2 otherwise healthy humans with complete PAI-1 deficiency because of a homozygous frameshift muta

100 s after AngII-Ald infusion, PAI-1-deficient (PAI-1(-/-)) mice developed severe cardiac fibrosis.

101 ate a major contribution by platelet-derived PAI-1 in the treatment of lenti-miR-30c to thrombus form

102 ysis, in part by decreasing platelet-derived PAI-1.

103 t high-throughput technologies for detecting PAIs, such as promoter capture Hi-C, are not scalable to

104 ably, a key marker of cardiovascular disease PAI-1 showed a difference in concentration between the o

105 es in PG were also not explained by elevated PAI-1 because active PAI-1 concentrations required to in

106 ts role in preventing fibrinolysis, elevated PAI-1 inhibits HGF's activation by u-PA and the resultan

107 y converting laser into ultrasound emission, PAI combines rich optical contrast, high ultrasonic spat

108 ve regulator of eNOS and disruptions in eNOS-PAI-1 binding promote increases in NO production and enh

109 CRR, FR, and FEV1 and increased FENO , EOS, PAI-1, FXIII, and CD in patients with asthma compared wi

110 Epithelial PAI-1 might serve as a marker of EoE severity and form p

111 Esophageal PAI-1 expression correlated with basal zone hyperplasia,

112 ETP, PAI-1, and vWF levels increased with increasing asthma s

113 We evaluated PAI-1 as a possible new target in a mouse controlled cor

114 cR2) and secretory phenotype (SASP) factors (PAI-1 and IL6).

115 Binding sites for PAI-1 within LRP1 have been localized to CR clusters II

116 the 1064 nm output of Nd-YAG lasers used for PAI.

117 this study, we examined the binding of free PAI-1 and complexes of PAI-1 with low-molecular-weight u

118 arding the nature of the interaction of free PAI-1 with LRP1.

119 st that, in addition to its other functions, PAI-mediated inhibition of HGF activation prohibits the

120 ma, FR negatively correlated with CD, FXIII, PAI-1, FENO , and EOS and positively with FEV1 .

121 esenchymal transition (EndoMT)-related genes PAI-1, collagen, and periostin expression in endothelial

122 The underlying mechanism of how PAI-1 expression is upregulated in DM2 is poorly underst

123 n a way not previously described for a human PAI-1 inhibitor.

124 hits and identified leads that inhibit human PAI-1 in the high-protein environments present in vivo U

125 and specificity to the active form of human PAI-1.

126 n umbilical vein endothelial cells (HUVECs), PAI-1 and eNOS colocalize and proximity ligation assays

127 s of plasminogen activator inhibitor type I (PAI-1) have been shown to promote fibrosis in multiple o

128 antly accelerates the process of identifying PAI-1 inhibitors that can be rapidly deployed in vivo, a

129 ential of DCNP@PDA NP as an efficient NIR-II/PAI dual-modal contrast agent for precision medicine.

130 e imaging approaches (photoacoustic imaging (PAI) and magnetic resonance imaging (MRI)) to detect mel

131 Photoacoustic imaging (PAI) combines laser technology with ultrasound in real t

132 Photoacoustic imaging (PAI) has ushered in a new era of observational biotechno

133 sed for high contrast photoacoustic imaging (PAI) in the second near-infrared window (NIR-II).

134 Photoacoustic imaging (PAI) is an attractive imaging modality that can volumetr

135 Photoacoustic imaging (PAI) is an emerging tool that bridges the traditional de

136 ence imaging (FI) and photoacoustic imaging (PAI) with the ultimate goal of improving diseases diagno

137 rticle imaging (MPI), photoacoustic imaging (PAI), and image-guided drug delivery with a tunable drug

138 and multi-wavelength photoacoustic imaging (PAI).

139 PTT) or sound energy (photoacoustic imaging, PAI) has been intensively investigated for the treatment

140 In PAI-1-deficient mice, the therapeutic effect of PAI-039

141 ith a 7.7% decrease (95% CI: -12.6, -2.5) in PAI-1.

142 contrast, there was a marked abnormality in PAI-2 levels in patients with HAE-N that is not seen in

143 ensin II-induced hypertension was blunted in PAI-1(-/-) mice, cardiac hypertrophy was accelerated.

144 gmentation induced a significant increase in PAI signals that are spectrally identifiable and shorten

145 ablation of cardiac fibrosis was observed in PAI-1(-/-) mice that express inactive plasmin (Pm) but n

146 eduction in cardiac fibrosis was observed in PAI-1(-/-)/uPA(-/-) double knockout mice that was associ

147 stically significantly greater reductions in PAI-1 at 12 months compared with controls (-19.3% vs. +3

148 with linear trends of greater reductions in PAI-1, PEDF, and VEGF.

149 essential requirement of lysine residues in PAI-1 for the interactions of both PAI-1 and uPA:PAI-1 c

150 examic acid, and we confirmed our results in PAI-1-deficient animals.

151 Genes whose promoters are involved in PAIs are more actively expressed, and gene pairs with pr

152 ted after exclusion of factors that increase PAI-1 including tobacco exposure and obesity.

153 ccounting for common exposures that increase PAI-1 level.

154 As exposures known to increase PAI-1 levels did not mitigate this association, PAI-1 ma

155 l cells with recombinant TGF-beta1 increased PAI-1 transcription, intracellular protein expression, a

156 emia-induced repression of miR-30c increases PAI-1 expression and thrombus formation in DM2.

157 ted collagen degradation regulators (induced PAI-1 and reduced Mmp3), collagen crosslinker (induced P

158 campal-dependent paired associate inference (PAI) paradigm, which afforded us the unique opportunity

159 Four weeks after AngII-Ald infusion, PAI-1-deficient (PAI-1(-/-)) mice developed severe cardi

160 protein 2, plasminogen activator inhibitor (PAI)-1), secretion of porcine cytokines and chemokines (

161 a levels of plasminogen activator inhibitor (PAI-1), and factor XIII (FXIII), NO in exhaled breath (F

162 min, active plasminogen activator inhibitor (PAI-1), and fibrin formation, but not fibrin crosslinkin

163 -1), tissue plasminogen activator inhibitor (PAI-1), and regulated on activation, normal T cell expre

164 (CTGF), and plasminogen activator inhibitor (PAI-1).

165 Plasminogen activator inhibitors (PAIs) 1 and 2 were also measured by means of ELISA.

166 In this study, peak area integration (PAI), Partial Least Squares Regression (PLSR), and Princ

167 Promoter-anchored chromatin interactions (PAIs) play a pivotal role in transcriptional regulation.

168 Interestingly, PAI-1 remained important even when its concentration was

169 Furthermore, the source of intracellular PAI-1 interacting with eNOS was shown to be endocytosis

170 r cagA-negative or cag pathogenicity island (PAI) mutant.

171 ocyte Effacement (LEE) pathogenicity island (PAI), which encodes genes that mediate the colonization

172 rmine distribution of pathogenicity islands (PAIs) across C. cellulans, which revealed 49 potential m

173 able in the NCBI database indicates that LAA PAI is exclusively present in a subset of emerging LEE-n

174 These associations have made PAI-1 an attractive pharmaceutical target.

175 h increased the PAI-1/TPA ratio, thus making PAI-1-induced inhibition relevant for the regulation of

176 These are highly conserved among mammalian PAI-1s.

177 ries of metallochromic sensors for molecular PAI.

178 cations and present challenges for molecular PAI.

179 over, the majority of current small-molecule PAI-1 inhibitors are poor pharmaceutical candidates.

180 Moreover, PAI-1 directly inhibits eNOS activity, reducing NO synth

181 Here we report a 86-kb mosaic PAI composed of four modules that encode 80 genes, inclu

182 The molecule, named PAI, was designed by introduction of a photoswitch into

183 d illustrate the potential of developing new PAI-1- and CCL5-targeting therapy for patients with TNBC

184 oncordance, hantaviruses induced tPA but not PAI-1 in microvascular endothelial cells, and the induct

185 In this study, we evaluated a novel PAI-1 inhibitor, annonacinone, a natural product from th

186 We have identified a novel PAI-1-dependent mechanism that regulates cardiomyocyte-d

187 s generating mice with selective ablation of PAI-1 demonstrate a major contribution by platelet-deriv

188 We tested the sensitivity and accuracy of PAI for analysis of placental and fetal oxygen saturatio

189 ynthesis, and the knockdown or antagonism of PAI-1 increases NO bioavailability.

190 -of-the-art developments and applications of PAI are described in this review.

191 Third, the emerging applications of PAI in cancer-related research are exemplified.

192 erpins, and the high-affinity association of PAI-1 with vitronectin in vivo have made it difficult to

193 d the binding of free PAI-1 and complexes of PAI-1 with low-molecular-weight urokinase-type plasminog

194 adoxically, homozygous genetic deficiency of PAI-1 is associated with spontaneous age-dependent, card

195 acological inhibition or genetic deletion of PAI-1 completely reversed the attenuation of the CBF inc

196 ion, with inhibition or genetic depletion of PAI-1 attenuating clot formation and lesion expansion af

197 -1-deficient mice, the therapeutic effect of PAI-039 was absent.

198 -1, which explains the paradoxical effect of PAI-1 deficiency in promoting cardiac-selective fibrosis

199 determine if the cardioprotective effect of PAI-1 is mediated through its ability to directly regula

200 ed to improve the pre-clinical efficiency of PAI and PTT.

201 We propose that the greater efficiency of PAI-1.uPA complex binding and clearance by LRP1, compare

202 ies (LCB) on the secretion and expression of PAI-1, IL-6, MCP-1 and leptin in mature 3T3-L1 adipocyte

203 yte chemotactic protein-1), and formation of PAI-1/tissue plasminogen activator complexes.

204 e chemotactic protein-1 and the formation of PAI-1/tissue plasminogen activator complexes.

205 wed that annonacinone inhibited formation of PAI-1/tPA complex via enhancement of the substrate pathw

206 y experiments to understand the induction of PAI-1 by TGF-beta1, the relationship between PAI-1 and e

207 ctivity also increased with the induction of PAI-1.

208 Pharmacological inhibition of PAI-1 increased tPA activity, prevented neurovascular un

209 performed the pharmacological inhibition of PAI-1 with PAI-039 and stimulation by tranexamic acid, a

210 and binding of a small-molecule inhibitor of PAI-1, CDE-096, confirming an important role for Lys-207

211 rtant role for Lys-207 in the interaction of PAI-1 with LRP1 and of the orientations of Lys-207, -88,

212 two charged residues for the interaction of PAI-1 with LRP1 and three charged residues for the inter

213 such is able to modulate the interaction of PAI-1 with tPA and uPA in a way not previously described

214 Knockdown of PAI-1 or eNOS eliminates the proximity ligation assay (P

215 High levels of PAI-1 are correlated with an increased risk of thromboti

216 The median levels of PAI-1 during the acute stage did not differ from those d

217 brain cancer suggest that elevated levels of PAI-1 may contribute to VTE.

218 Chemical modification of PAI-1 confirmed an essential requirement of lysine resid

219 as well as suppressed the overexpression of PAI-1 induced by H2O2.

220 to 76% of rt-PA activity in the presence of PAI-1, whereas only 24% activity was preserved for unenc

221 579 Fab to the reactive centre loop (RCL) of PAI-1 and at the same exosite used by both tissue and ur

222 al controlling process; although the role of PAI-1 concentration was much less in the presence of flo

223 I-1 and esophageal fibrosis, and the role of PAI-1 in fibrotic gene expression.

224 However, the in vivo role of PAI-1 in inactivating uPA and limiting the generation of

225 ght to understand the expression and role of PAI-1 in patients with EoE.

226 er the multiple patho-physiological roles of PAI-1, and understanding the relative contributions of t

227 in turn, accelerates TNBC cell secretion of PAI-1 and promotes TNBC cell metastasis, thus forming a

228 that miR-30c directly targeted the 3' UTR of PAI-1 and negatively regulated its expression.

229 of CR456 to arginine and lysine variants of PAI-1 and definitively identified the binding site as co

230 lts highlight the emergence and evolution of PAIs in the genus Cellulosimicrobium.

231 bacteria as a key factor in the evolution of PAIs.

232 PAIs and provides insights into the role of PAIs in complex trait variation.

233 esis studies to identify the binding site on PAI-1 for LRP1 have given conflicting results or implied

234 ent binding model in which multiple sites on PAI-1 and uPA:PAI-1 complexes interact with complementar

235 LRP1 with ~100-fold increased affinity over PAI-1 alone.

236 tions account quantitatively for the overall PAI-1/LRP1 affinity.

237 pression of precursor-miR-34a increased p53, PAI-1, and apoptosis in AECs of mice unexposed to bleomy

238 of miR-34a inhibited bleomycin-induced p53, PAI-1, and apoptosis and prevented PF, whereas overexpre

239 lasmin (Pm) but normal levels of zymogen Pg (PAI-1(-/-)/Pg(S743A/S743A)).

240 Taken together, these findings place PAI-1 as a negative regulator of eNOS and disruptions in

241 Plasma PAI-1 increased from the MHL to the MHO to the MUO group

242 tin, and matrix metalloproteases, and plasma PAI-1 levels correlated with plasma TGF-beta1 levels.

243 s to insulin resistance by increasing plasma PAI-1 concentrations and decreasing AT BCAA catabolism a

244 demonstrates the use of mQTL data to predict PAIs and provides insights into the role of PAIs in comp

245 tative trait locus (mQTL) studies to predict PAIs.

246 Integration of the predicted PAIs with GWAS data highlight interactions among 601 DNA

247 les that deliver miR-30c antagomiRs promoted PAI-1-dependent tumor growth and increased fibrin abunda

248 an emphasis on the potent fibrosis-promoting PAI-1 gene.

249 n ratio) (73%), and much lower prothrombotic PAI-1 levels (19%).

250 increase TSP-1 and decrease VEGF by reducing PAI-1 (plasminogen activator inhibitor-1/SERPINE1) level

251 ectin-3), tissue injury and repair (Serpine1/PAI-1) and growth factors (brain-derived neurotrophic fa

252 tic proteins including TGF-beta1, alpha-SMA, PAI-1, CTGF, FN and collagen-1.

253 In summary, PAI enables the detection of placental and fetal oxygena

254 Overexpression of eNOS and HA-tagged PAI-1 in COS7 cells confirmed the colocalization observa

255 aled that cLDL induced the expression of TF, PAI-1, and LOX-1 mRNA in vascular cells.

256 se metabolites and the control of the AHR-TF/PAI-1 axis and VTE in cancer.

257 ssion, telltale signs of an activated AHR-TF/PAI-1 axis.

258 fter Angiotensin II treatment confirmed that PAI-1 deficiency significantly enhanced multiple TGF-bet

259 is in multiple species, we hypothesized that PAI-1 also regulates fibrosis during cardiac injury.

260 In the present study, we hypothesized that PAI-1 mediates post-traumatic malfunction of coagulation

261 Our findings indicate that PAI-1 protects mice from hypertension-induced cardiac fi

262 In vitro assays revealed that PAI enables light-dependent activation of M2 mAChRs.

263 To validate the method, we show that PAI photoisomers display different cardiac effects in a

264 It has been speculated that PAI-1 may regulate cardiac fibrosis by inactivating urok

265 the GJA1 repression profile, suggesting that PAI-1 may mediate actions of ASC on transcriptional regu

266 tic secondary brain damage and suggests that PAI-1 may be a central endogenous inhibitor of the fibri

267 an interaction between asthma status and the PAI-1 polymorphism on FEV1 /FVC (P=.03).

268 by lenti-miR-30c significantly decreased the PAI-1 expression and prolonged the time to occlusion in

269 that the overlap between object pairs in the PAI paradigm results in a marked loss of episodic memory

270 x in the clotted vessel, which increased the PAI-1/TPA ratio, thus making PAI-1-induced inhibition re

271 its receptor, thereby making binding of the PAI-1 moiety to LRP1 a two-dimensional surface-localized

272 We estimated the relationship of the PAI-1 risk allele with FEV1/FVC by multivariate linear r

273 pport the possibility that modulation of the PAI-1-tPA pathway may be beneficial in diseases associat

274 Therefore, we named this PAI as Locus of Adhesion and Autoaggregation (LAA).

275 We suggest that the acquisition of this PAI is a recent evolutionary event, which may contribute

276 Thus, PAI-1 is a molecular switch that controls the cardiac TG

277 an accessible contrast agent for deep tissue PAI in the NIR-II window.

278 otein-protein interactions, we produced uPA, PAI-1, and plasminogen from human and zebrafish to repre

279 del in which multiple sites on PAI-1 and uPA:PAI-1 complexes interact with complementary sites on LRP

280 1 for the interactions of both PAI-1 and uPA:PAI-1 complexes with LRP1.

281 inding interfaces of uPA:plasminogen and uPA:PAI-1 may have coevolved to maintain tight interactions.

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

283 xplanation for the increased affinity of uPA:PAI-1 complexes for LRP1.

284 207, -88, and -80 for the interaction of uPA:PAI-1 complexes with LRP1.

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

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

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

288 r fibrin(ogen) had significantly upregulated PAI-1 expression in all cortical layers assessed (p < 0.

289 ation could be successfully quantified using PAI, PLSR and PCR techniques.

290 able dynamic sensing of divalent cations via PAI, we have engineered a new reversible near-infrared p

291 enhance EMT-induced TNBC cell metastasis via PAI-1 and CCL5 signaling and illustrate the potential of

292 e-negative breast cancer cell metastasis via PAI-1 and CCL5 signaling.

293 elial dysfunction orchestrated, in part, via PAI-1 up-regulation.

294 r-clock analysis performed on three virulent PAI proteins (Fic; D-alanyl-D-alanine-carboxypeptidase;

295 Facilitated by multi-wavelength PAI plus a spectral unmixing technique, the accuracy of

296 the pharmacological inhibition of PAI-1 with PAI-039 and stimulation by tranexamic acid, and we confi

297 binding and clearance by LRP1, compared with PAI-1 alone, is due solely to simultaneous binding of th

298 y inhibits serine protease interactions with PAI-1 while conserving vitronectin binding.

299 through 12 cm of chicken breast tissue with PAI.

300 Treatment of young PAI-1(-/-) mice with Angiotensin II induced extensive hy