ライフサイエンスコーパス: PAI

1 PAI and T2-weighted spin-echo-based BOLD MR imaging were

2 PAI results correlated well with the corresponding PET i

3 PAI-039 treatment failed to improve angiogenesis in the

4 PAI-1 expression is significantly increased in the epith

5 PAI-1 expression was significantly increased in epitheli

6 PAI-1 expression was significantly less in RAAA tissue (

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

8 PAI-1 inhibition had no effect on dermal collagen levels

9 PAI-1 inhibition significantly decreased baseline and TG

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

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

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

13 PAI-1 was found to comparably relocate with a subset of

14 PAI-2 levels varied from 25 to 87 ng/mL (mean, 53.8 ng/m

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

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

17 line, and plasminogen activator inhibitor 1 (PAI-1) levels were significantly elevated at the end of

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

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

20 levels of plasminogen activator inhibitor 1 (PAI-1), regardless of their glycemic control.

21 encoding plasminogen activator inhibitor 1 (PAI-1).

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

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

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

25 TAFI) and plasminogen activator inhibitor-1 (PAI-1) are causal factors for thrombolytic failure.

26 y in 4, a plasminogen-activator inhibitor-1 (PAI-1) deficiency in 2, and 1 patient each with protein

27 plasminogen activator (PA), PA inhibitor-1 (PAI-1) has a paradoxical protumorigenic role in cancer,

28 ession of plasminogen activator inhibitor-1 (PAI-1) in human and murine FL-fibroblasts was reduced, w

29 Levels of plasminogen activator inhibitor-1 (PAI-1) increased significantly with increasing severity

30 PAR), and plasminogen activator inhibitor-1 (PAI-1) into the early and late endosomes by 4- to 5-fold

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

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

33 (uPA) and plasminogen activator inhibitor-1 (PAI-1) levels in the regulation of alveolar epithelial i

34 ic factor plasminogen activator inhibitor-1 (PAI-1) observed in humans is driven by an endogenous mec

35 d using a plasminogen activator inhibitor-1 (PAI-1) reporter transfected in HGFs.

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

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

38 markers, plasminogen activator inhibitor-1 (PAI-1), and fibronectin, when compared to contralateral

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

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

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

42 Plasminogen activator inhibitor-1 (PAI-1), which inhibits fibrinolysis, is a key circulatin

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

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

45 he serpin plasminogen activator inhibitor-1 (PAI-1).

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

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

48 2 or plasminogen activator inhibitor type 2 (PAI-2) is highly induced in macrophages in response to i

49 n of plasminogen activator inhibitor type 2 (PAI-2), a serine protease inhibitor, resulted in NLRP3-

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

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

52 ced accelerated latency transition of active PAI-1 may, together with supporting x-ray data, provide

53 y enhancing the latency transition of active PAI-1.

54 a small fraction in equilibrium with active PAI-1, a latent-like prelatent form, from which latent P

55 on of an adenovirus PAI-1 cDNA construct (Ad-PAI-1) suppressed expression of uPA and collagen-I and a

56 which were reversed by transduction with Ad-PAI-1.

57 Transduction of an adenovirus PAI-1 cDNA construct (Ad-PAI-1) suppressed expression of

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

59 9), whereas PAI-1 expression (P = 0.022) and PAI-1/tPA complexes in plasma (P = 0.015) were lower aft

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

61 inhibitors of metalloproteinases, TIMP-1 and PAI-1 protein levels, increased at MOI 25.

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

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

64 showed increased activation of caspase-3 and PAI-1 with a parallel reduction in uPA expression.

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

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

67 fibrosis genes (CCN2, Col1a2, TGF-beta1, and PAI-1) seen in placebo-treated diabetic mice.

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

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

70 odels for prognosticating graft failure, and PAI-1 mRNA level was the only independent predictor (odd

71 ase expression and increased fibronectin and PAI-1 expression.

72 sangial cell hypertrophy and fibronectin and PAI-1 expression.

73 pertrophy, and expression of fibronectin and PAI-1.

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

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

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

77 TGFbeta signaling through p-SMAD2 and PAI-1 was highly active in all chondrosarcoma subtypes,

78 neered bispecific inhibitor against TAFI and PAI-1 (heterodimer diabody, Db-TCK26D6x33H1F7) in severa

79 n of a bispecific inhibitor against TAFI and PAI-1 results in a prominent profibrinolytic effect in m

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

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

82 To investigate whether changes in uPA and PAI-1 by ATII cells contribute to EMT, ATII cells from p

83 ding of p53 to uPA, uPA receptor (uPAR), and PAI-1 mRNA.

84 of p53-binding sequences from uPA, uPAR, and PAI-1 mRNA 3' untranslated regions in ATII cells suppres

85 p53-binding sequences from uPA, uPAR, and PAI-1 mRNA 3' untranslated regions neither interfered wi

86 l markers such as fibronectin, vimentin, and PAI-1, together with the repression of epithelial marker

87 expression of inflammatory mediators such as PAI-1 (plasminogen activator inhibitor 1), suggesting th

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

89 -1 levels did not mitigate this association, PAI-1 may contribute to airway obstruction in the contex

90 he tumor hemodynamic response to carbogen at PAI (P = .030).

91 On the contrary, inhibition of basal PAI-1 in NL-fibroblasts increased collagen-I and alpha-s

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

93 d directly correlated with those measured by PAI.

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

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

96 with the fact that infections with both cag PAI-positive and -negative strains are associated with g

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

98 These results define a set of cag PAI genes that are required for both pilus biogenesis an

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

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

101 n this study, we selected 7 genes in the cag PAI that are known to be required for T4SS function and

102 k is higher in individuals infected with cag PAI-positive strains.

103 ins, but the effect was more robust with cag PAI-positive strains.

104 ory SASP components (i.e., IL-6, IL-8, CCL2, PAI-1) was also highest in PSC cholangiocytes.

105 ted a robust circadian rhythm in circulating PAI-1 with a peak corresponding to approximately 6:30 am

106 Collectively, PAI holds great promise to drive biomedical applications

107 le oxygenation conditions (n = 6) to compare PAI measurements and BOLD MR imaging measurements.

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

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

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

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

112 the transcriptional regulation of endogenous PAI-1 expression.

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

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

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

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

117 Besides the notable PTT and an excellent PAI effect, the NIR-absorbing GBFs may also find applica

118 Excessive PAI-1 activity is associated with human disease, making

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

120 on (P </= .05 for all comparisons except for PAI level).

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

122 Fibroblasts isolated from PAI-1-deficient mice without lung injury also showed inc

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

124 the promoter of the TGFbeta-responsive gene PAI-1.

125 promoter, using the TGFbeta-responsive gene PAI-1.

126 lic steatohepatitis had significantly higher PAI-1 values than those with normal liver (P < 0.001).

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

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

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

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

131 Photoacoustic imaging (PAI) has the potential for real-time molecular imaging a

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

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

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

135 interface system, for photoacoustic imaging (PAI)-guided photothermal therapy (PTT).

136 st agents for in vivo photoacoustic imaging (PAI).

137 and multi-wavelength photoacoustic imaging (PAI).

138 essfully utilized for photoacoustic imaging (PAI)/magnetic resonance imaging (MRI) dual-modal imaging

139 Importantly, PAI-039 treatment significantly improved epidermal cellu

140 Likewise, overexpressing Beclin 1 in PAI-2-deficient cells rescued the suppression of NLRP3 a

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 Changes in PAI and BOLD signal intensity before and after VDA treat

145 in PAI-1 was 8-times larger than changes in PAI-1 induced by standardized behavioral stressors, incl

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

147 ge at sampling, there were no differences in PAI-1 to PAI-2 or MMA ratios between trial arms, but the

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

149 = 0.002) and a 27.9% (p = 0.001) increase in PAI-1 and plasminogen, respectively, and a 12.5% (p = 0.

150 were associated with a parallel increase in PAI-1 and reduced uPA expression.

151 independently contributes to the increase in PAI-1 levels, whereas other coagulation factors are unal

152 tPA(-/-) and uPA(-/-) mice but increased in PAI-1(-/-) mice compared with wild-type (WT) mice.

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

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

155 We tested whether this morning peak in PAI-1 is caused by the internal circadian system or by b

156 If this large endogenous morning peak in PAI-1 persists in vulnerable individuals, it could help

157 The excellent performance in PAI and PTT is mainly attributed to the unique features

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

159 hat pharmacologically mediated reductions in PAI-1 using PAI-039 would normalize cutaneous wound heal

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

161 This rhythm in PAI-1 was 8-times larger than changes in PAI-1 induced b

162 waist circumference, 21% of the variance in PAI-1.

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

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

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

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

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

168 TLR2 or TLR4 agonist induced PAI-2 expression, which subsequently stabilized the auto

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

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

171 e experiments revealed that AZ3976 inhibited PAI-1 by enhancing the latency transition of active PAI-

172 n [ratio of plasminogen-activator inhibitor (PAI) 1 to PAI-2 and mean uterine-artery resistance index

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

174 of mRNA for plasminogen activator inhibitor (PAI)-1, vimentin, tissue inhibitor of metalloproteinase-

175 (tPA), and plasminogen activator inhibitor (PAI)-1.

176 eficient in plasminogen activator inhibitor (PAI-1) are resistant to lung injury and pulmonary fibros

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

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

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

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

181 Following cutaneous injury, PAI-039 was orally administered twice daily for 10 days.

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

183 smid harboring a 21-kb pathogenicity island (PAI) for growth in host macrophages.

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

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

186 nfection with both cag pathogenicity island (PAI)-positive and -negative strains, but the effect was

187 he presence of the cag pathogenicity island (PAI).

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

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

190 3976 only had measurable affinity for latent PAI-1, we propose that its mechanism of inhibition is ba

191 atent-like prelatent form, from which latent PAI-1 is then generated more rapidly.

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

193 cations and present challenges for molecular PAI.

194 ries of metallochromic sensors for molecular PAI.

195 hat has led to the testing of small-molecule PAI-1 inhibitors, initially developed as antithrombotic

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

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

198 the development of efficacious and nontoxic PAI-1 inhibitors as anticancer agents.

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

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

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

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

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

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

205 In this review, we describe the basics of PAI and its recent advances in biomedical research, foll

206 by logistic regression) and a combination of PAI-1 mRNA and creatinine levels (P = 0.001) were the be

207 0.80-1.0; P < 0.001) for the combination of PAI-1 mRNA and creatinine.

208 A combination of PAI-1 mRNA level, BKVN biopsy stage, and creatinine leve

209 area under the curve for the combination of PAI-1 mRNA, biopsy, and creatinine was 0.92 (95% CI, 0.8

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

211 -1, which explains the paradoxical effect of PAI-1 deficiency in promoting cardiac-selective fibrosis

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

213 tent state; correctly predict the effects of PAI-1 mutations on the kinetics; and provide a potential

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

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

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

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

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

219 in support of the protumorigenic function of PAI-1 that has led to the testing of small-molecule PAI-

220 terization of a high affinity inactivator of PAI-1.

221 These studies show that induction of PAI-1 and inhibition of uPA during fibrosing lung injury

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

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

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

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

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

227 eatosis remained an independent predictor of PAI-1 levels, explaining, together with fasting C-peptid

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

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

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

231 This study defines a new role of PAI-1 in the control of fibroblast activation and expans

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

233 with that of tPA and inversely with that of PAI-1 in rTx-TMA.

234 These findings support the use of PAI-039 as a novel therapeutic agent to improve diabetic

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

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

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

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

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

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

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

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

243 Further, partial PAI-1 deficiency, attributable to a polymorphism in huma

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

245 Plasma PAI-1/tPA complex was assessed by enzyme-linked immuosor

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

247 By targeting extracellular airway proteases, PAI-1 inhibits IAV glycoprotein cleavage, thereby reduci

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

249 essment Inventory Borderline Features Scale (PAI-BOR) collected in two Dutch cohorts (N=7125), the Ne

250 However, like other serpins, PAI-1 has a labile structure, making it a difficult targ

251 -tripods) to U87MG tumor-bearing mice showed PAI contrasts in tumors almost 3-fold higher than for th

252 Interestingly, although all of the simulated PAI-1 variants readily access the prelatent intermediate

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

254 induced p53 activation (>95%) and subsequent PAI-1, fibronectin, connective tissue growth factor, and

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

256 ntranslated regions in ATII cells suppressed PAI-1 and induced uPA after BLM treatment, leading to in

257 nd restored uPA expression while suppressing PAI-1.

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

259 t improved cutaneous wound healing, and that PAI-1 inhibition improves skeletal muscle repair in mice

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

261 It has been demonstrated that PAI-1-deficient mice exhibit improved cutaneous wound he

262 The fact that PAI systems can be made portable and compatible with exi

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

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

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

266 The PAI encodes a family of 6 virulence-associated proteins

267 The PAI signals were linearly correlated with their concentr

268 The PAI-1/tPA complexes, D-dimers, and prothrombin fragment

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

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

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

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

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

274 mpared with the other three subscales of the PAI-BOR (42.7% vs non-significant estimates for self-har

275 nd Anxiety, we show that heritability of the PAI-BOR total score using genome-wide single-nucleotide

276 ers substantially across the 24 items of the PAI-BOR.

277 ance components in the four subscales of the PAI-BOR.

278 t only in subjects with higher scores on the PAI-BOR.

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

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

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

282 f plasminogen-activator inhibitor (PAI) 1 to PAI-2 and mean uterine-artery resistance index (UtARI)]

283 pling, there were no differences in PAI-1 to PAI-2 or MMA ratios between trial arms, but there was a

284 de a single vap family member, vapA, and two PAI-located transcriptional regulators, virR and virS.

285 e-induced lung injury were analyzed for uPA, PAI-1, and EMT markers.

286 reased the total cellular content of the uPA-PAI-1 protein complex.

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

288 esign in the hunt for therapeutically useful PAI-1 inhibitors.

289 logically mediated reductions in PAI-1 using PAI-039 would normalize cutaneous wound healing in strep

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

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

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

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

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

295 Aortic wall PAI-1, uPA, and tPA concentrations were determined by we

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

297 as significantly higher (P = 0.009), whereas PAI-1 expression (P = 0.022) and PAI-1/tPA complexes in

298 malemma, remained abnormally associated with PAI-1 in early and late endosomes.

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

300 Carbogen-based functional imaging with PAI and BOLD MR imaging enables monitoring of early chan

301 elation between the parameters measured with PAI and BOLD MR imaging in vitro.

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