ライフサイエンスコーパス: plasmin

1 e (an activator that converts plasminogen to plasmin).

2 XII either by kallikrein, thus formed, or by plasmin.

3 en and mediating the localized generation of plasmin.

4 inhibits plasma kallikrein, factor XIa, and plasmin.

5 dependent mechanism, to efficiently generate plasmin.

6 nolysis by virtue of its capacity to inhibit plasmin.

7 to its promise as an allosteric regulator of plasmin.

8 that these HAs are preferentially cleaved by plasmin.

9 arget-labeling indicator for the analysis of plasmin.

10 lisin, elastase, chymotrypsin, thrombin, and plasmin.

11 nism that does not require the generation of plasmin.

12 bundant precursor of the vertebrate protease plasmin.

13 rful inhibitor of plasminogen activators and plasmin.

14 uman plasminogen to form the plasma protease plasmin.

15 ic removal of the C terminus by thrombin and plasmin.

16 44 rendered TRPV5 resistant to the action of plasmin.

17 tease-inhibitory activity of IalphaI against plasmin.

18 ity via a mechanism similar to inhibition of plasmin.

19 NSGMs selectively inhibit human full-length plasmin.

20 logical inhibitor of the fibrinolytic enzyme plasmin.

21 -hairpin loop of trypsin, which is absent in plasmin.

22 ta-fibrinogen binding delays fibrinolysis by plasmin.

23 that are sensitive to enzymatic cleavage by plasmin.

24 E, in which FXII is cleaved and activated by plasmin.

25 ogen is the precursor of the serine protease plasmin, a central enzyme of the fibrinolytic system.

26 serine protease that converts plasminogen to plasmin, a general protease, which promotes fibrinolysis

27 d be discovered by exploiting allosterism in plasmin, a protease homologous to other allosteric serin

28 sub-pM concentration of plasminogen (but not plasmin) acting at the cell surface is sufficient to ind

29 The physical mechanism of plasmin action (crawling) and avoidance of inhibition is

30 Both kallikrein and plasmin activate factor XII; kallikrein is 20 times more

31 e importance of CHD4 in regulating embryonic plasmin activation after mid-gestation.

32 Similarly, pharmacologic inhibition of plasmin activation with tranexamic acid also delayed dis

33 ctivator (uPA)/uPA receptor (uPAR)-dependent plasmin activation.

34 ge mutagenesis and confirmed to lack surface plasmin activity after growth in human plasma or media s

35 sminogen in a cooperative manner to increase plasmin activity and reduce PAI-1 activity.

36 ding interactions with plasminogen increased plasmin activity and reduced PAI-1 antiproteolytic activ

37 PolyP70 did not modulate plasmin activity but stimulated activation of Glu and Ly

38 of the Pla subfamily can cause uncontrolled plasmin activity by converting plasminogen to plasmin an

39 nction by stimulating a 1.6-fold increase in plasmin activity compared with the saline-treated counte

40 Loss of surface plasmin activity left GAS unable to efficiently degrade

41 n many cancers and correlates with increased plasmin activity on the tumor cell surface, which mediat

42 in cells that might be important to restrict plasmin activity to specific sites and substrates.

43 The rPAI-1(23)-enhanced plasmin activity was achieved through a novel mechanism

44 upregulated in Chd4 mutant LYVE1+ cells, and plasmin activity was elevated near the LV valves.

45 Plasmin activity was not involved in promoting these cha

46 terolemic mice by stimulating an increase in plasmin activity.

47 ration in vitro and decreased membrane-bound plasmin activity.

48 ors play a central role in the regulation of plasmin activity.

49 the most recent in vitro study showing that plasmin acts on prey cells rather than on macrophages.

50 zae, and when converted to plasmin, PE-bound plasmin aids in immune evasion and contributes to bacter

51 ncreased ETP (121% vs 99%, overall P < .01), plasmin-alpha2-antiplasmin complex (520 vs 409 mug/L, ov

52 ential [ETP], thrombin-antithrombin complex, plasmin-alpha2-antiplasmin complex, plasminogen activato

53 Plasma levels of plasmin-alpha2-antiplasmin complexes increase with the e

54 s (assessed by tissue plasminogen activator, plasmin-alpha2-antiplasmin complexes, and plasminogen ac

55 Plasmin also cleaved C5 to products of 65, 50, 30, and 2

56 tides moderately affect the reaction between plasmin and alpha(2)-antiplasmin and accelerate the inac

57 (Ska), GAS activates human plasminogen into plasmin and binds it to the bacterial surface.

58 GaFK-Doxaz is hydrolyzable by the proteases plasmin and cathepsin B, both strongly linked with cance

59 Conversely, elevated plasmin and elastase were positively correlated with his

60 vation of plasminogen to the serine protease plasmin and facilitated cleavage of two disulfide bonds

61 lasmin activity by converting plasminogen to plasmin and inactivating the plasmin inhibitor alpha2-an

62 t potent bis-triazole derivative 10 inhibits plasmin and plasma kallikrein with K(i) of 0.77 and 2.4

63 well into the relatively open active site of plasmin and plasma kallikrein, while it is rejected from

64 OIR by enhancing perivascular activation of plasmin and remodeling of fibrin.

65 urokinase, which can convert plasminogen to plasmin and represents a possible source for plasmin gen

66 Notably, plasmin and tPA activities, as well as tPA-dependent gen

67 ase activity that inhibits the generation of plasmin, and a vitronectin-binding function that interfe

68 urokinase (uPA)-type plasminogen activators, plasmin, and plasminogen with submicromolar affinity.

69 d-dimer levels, greater than 5-fold elevated plasmin antiplasmin levels, and a complete absence of th

70 (thrombin-antithrombin [TAT]), fibrinolysis (plasmin-antiplasmin [PAP]), and complement (C3b, C5a, C5

71 D-dimer and plasmin-antiplasmin complex levels increased soon after

72 n, total homocysteine, D-dimer, factor VIII, plasmin-antiplasmin complex, and inflammation and coagul

73 (marker of coagulation activation), D-dimer, plasmin-antiplasmin complex, tissue plasminogen activato

74 fibrin clot or in the circulation by forming plasmin-antiplasmin complexes.

75 tPA and plasmin are upregulated after SCI and degrade the deglyc

76 pathway (urokinase plasminogen activator and plasmin) are elaborated in pleural injury and strongly i

77 yaluronic acid, and proteins that allow host plasmin assembly on the bacterial surface, viz. a high a

78 ssive generation of the fibrinolytic enzyme, plasmin, at the cell surface of the PML cells.

79 n of the fibrinogen alphaC domain removed by plasmin attenuates binding of heparin to fibrinogen and

80 l formation depended on conversion of Plg to plasmin, binding to the macrophage surface, and the cons

81 does not affect the rate of fibrinolysis by plasmin but increases by 4-5-fold the rate of fibrinolys

82 lots containing Abeta(42), and clot lysis by plasmin, but not trypsin, is delayed.

83 the human host where it can be converted to plasmin by host plasminogen activators or by endogenousl

84 d be activated to the potent serine protease plasmin by staphylokinase and tissue plasminogen activat

85 side of DCT, where it is cleaved into active plasmin by urokinase.

86 Here, we show that plasmin can cleave FXIIIa in purified systems and in blo

87 llectively, these findings show that the tPA/plasmin cascade may act downstream of ChABC to allow for

88 f degradation by three classes of proteases: plasmin, cathepsin L, and matrix metalloproteinases (MMP

89 We have identified plasmin cleavage sites, generated a truncated PlGF118 is

90 Chem158K was generated from chem163S by plasmin cleavage.

91 kinase-type plasminogen activator, generated plasmin cleaved complement protein C3b thus assisting in

92 The converted active plasmin cleaved the synthetic substrate S-2251, and the

93 nogen, when converted to the active protease plasmin, cleaved the chromogenic substrate S-2251 and th

94 evaluated by chromogenic, turbidimetric, and plasmin conversion assays, with surface plasmon resonanc

95 These results indicate that urinary plasmin could contribute to the downstream effects of pr

96 We show that direct allosteric inhibition of plasmin could led to new antifibrinolytic agent(s) that

97 d heparin binding to fragment X, a clottable plasmin degradation product of fibrinogen.

98 Bound plasminogen, upon conversion to active plasmin, degraded fibrinogen and complement C3b and cont

99 Cleavage products of plasmin-degraded LL-37 were analyzed by matrix-assisted

100 Similarly, plasmin degrades platelet-VWF complexes in platelet aggl

101 of tPA facilitated clot retraction through a plasmin-dependent mechanism.

102 The C3b fragments generated by plasmin differ in size from those generated by the compl

103 y, these activities were abrogated following plasmin digestion.

104 and when converted to proteolytically active plasmin dissolves preformed fibrin clots and extracellul

105 suggest that in vivo-generated thrombin and plasmin do not directly activate the complement in nonhu

106 alloproteinases, plasminogen activation, and plasmin downstream targets to influence invasion.

107 ght to potentiate anti-inflammatory and anti-plasmin effects that are inhibitory to leukocyte extrava

108 Similarly, plasmin either in the fluid phase or attached to surface

109 Coadministration of ChABC and plasmin enhanced the tPA(-/-) phenotype and supported re

110 inogen into its proteolytically active form, plasmin, enhances the ability of the bacteria to dissemi

111 I mutants rapidly activate after cleavage by plasmin, escape from inhibition through C1 esterase inhi

112 Plasmin exhibited a similar activity, but it was weaker

113 r binding to protein C, activated protein C, plasmin, factor VIIa (FVIIa), FIX, FIXa, and FXII.

114 This effect was dependent on plasmin formation and potentiated in the presence of pla

115 urface-associated enolase-1 (ENO-1) enhances plasmin formation and thus participates in the regulatio

116 plasminogen activator (TPA) as a source for plasmin formation.

117 Second, although SUPA did not protect plasmin from inactivation by alpha(2)-antiplasmin, fibri

118 man plasmin(ogen) and protected FBA-tb-bound plasmin from regulation by alpha(2)-antiplasmin, suggest

119 Here, we identify plasmin from the reactive brain stroma as a defense agai

120 pite inducing a strong burst of thrombin and plasmin, FXa/PCPS infusion did not produce measurable le

121 eas zymogen FXIII was not readily cleaved by plasmin, FXIIIa was rapidly cleaved and inactivated by p

122 nd subsequent hPg activation to the protease plasmin generate a proteolytic surface that GAS employs

123 Hence plasmin, generated on the cell surface selectively by t-

124 relatively hydrophobic fragments of protein (plasmin-generated protein fragments (PGPFs)) that are cy

125 l surface-translocated AnxA2 forms an active plasmin-generating complex, and this activity can be neu

126 ygen-primed Anxa2(-/-) retina and reinstates plasmin generation and directed migration in cultured An

127 of plasminogen to fibrin, which could impair plasmin generation and fibrin degradation.

128 luding neuroserpin and serpin B2, to prevent plasmin generation and its metastasis-suppressive effect

129 mainly related to decreased fibrin-dependent plasmin generation and reduced protease activity (Kcat/K

130 directly affects fibrinolysis by decreasing plasmin generation and reducing protein-specific activit

131 ctivation and the subsequent acceleration of plasmin generation by active matriptase reveals a feed-f

132 ion with annexin A2 with concomitant reduced plasmin generation by macrophages and OSCC cell lines.

133 Indeed, plasmin generation by tissue plasminogen activator (tPA)

134 plasmin and represents a possible source for plasmin generation in all types of hereditary angioedema

135 Pericellular plasmin generation, an important pathophysiological proc

136 injury by a mechanism that does not require plasmin generation, but instead is mediated by ERK1/2-re

137 ivation by a mechanism that does not require plasmin generation, but instead is mediated by extracell

138 play roles in cell proliferation, apoptosis, plasmin generation, exocytosis, endocytosis, and cytoske

139 vivo plasminogen glycation on fibrinolysis, plasmin generation, protein proteolytic activity, and pl

140 d E coli infusion led to robust thrombin and plasmin generation.

141 r (tPA), and plasminogen, thereby increasing plasmin generation.

142 nd returns to the cell surface to accelerate plasmin generation.

143 VDAC is also a substrate for plasmin; hence, it mimics fibrin activity.

144 which strongly binds host human plasminogen/plasmin (hPg/hPm) directly via an hPg/hPm surface recept

145 htly with human plasma plasminogen (hPg) and plasmin (hPm) via the kringle 2 (K2hPg) domain of hPg/hP

146 , SK is secreted by GAS and activates hPg to plasmin (hPm), thus generating a proteolytic surface on

147 y activating host human plasminogen (hPg) to plasmin (hPm), thus providing a proteolytic framework fo

148 h or without the participation of human host plasmin (hPm).

149 dy assigns a new function to plasminogen and plasmin in apoptotic cell clearance.

150 XIIIa was rapidly cleaved and inactivated by plasmin in solution (catalytic efficiency = 8.3 x 10(3)

151 ties, as well as tPA-dependent generation of plasmin in solution, are not decreased in the presence o

152 sminogen, was able to convert plasminogen to plasmin in the presence of plasminogen activators.

153 Several analogues inhibit plasmin in the subnanomolar range, and their potency aga

154 mplicating plasminogen (Plg), the zymogen of plasmin, in phagocytosis is extremely limited with the m

155 This cleavage is tPA-specific, plasmin-independent, and removes a predicted ~4-kDa frag

156 portantly rescue of both by in vivo supplied plasmin, indicated that plasmin is the crucial serine pr

157 tissue-type plasminogen activator-associated plasmin-induced fibrinolysis and/or a tissue-type plasmi

158 ibrin formation and fibrin susceptibility to plasmin-induced lysis were significantly impaired in BD

159 In summary, PAR-1 activation by plasmin induces PKC-mediated phosphorylation of TRPV5, t

160 Plasminogen when activated to plasmin inhibited complement as demonstrated by hemolyti

161 The plasminogen activation and plasmin inhibition system assembled at the site of acute

162 was fused to a sequence derived from alpha2-plasmin inhibitor (alpha2-PI1-8) that is a substrate for

163 thin the fibrinolytic pathway, including the plasmin inhibitor alpha2-antiplasmin (A2AP).

164 plasminogen to plasmin and inactivating the plasmin inhibitor alpha2-antiplasmin (alpha2-AP).

165 omoting these changes, as treatment with the plasmin inhibitor aprotinin had no effect.

166 ardiocytes with anti-uPAR or anti-uPA Abs or plasmin inhibitor aprotinin prior to coculturing with he

167 ith GAS were simultaneously treated with the plasmin inhibitor aprotinin, a significant reduction in

168 a2-antiplasmin (alpha2AP, also called alpha2-plasmin inhibitor) is the main physiological inhibitor o

169 Preincubation with a plasmin inhibitor, a PAR-1 antagonist, or a protein kina

170 plasmin(ogen) and is only a kinetically slow plasmin inhibitor.

171 New macrocyclic plasmin inhibitors based on our previously optimized P2-

172 Although plasmin inhibitors could be used in multiple disorders,

173 ategy for the design of potent and selective plasmin inhibitors was developed.

174 of our recently described substrate-analogue plasmin inhibitors, which were cyclized between their P3

175 lycan mimetics (NSGMs), as direct allosteric plasmin inhibitors.

176 Plasmin injection into the pleural cavity of BALB/c mice

177 ots, and subsequent degradation of fibrin by plasmin is a critical inflammatory mediator and essentia

178 The trypsin-like serine protease plasmin is a target for the development of antifibrinoly

179 lasminogen binds to cells, its activation to plasmin is markedly enhanced compared with the reaction

180 The insoluble aggregate-bound plasmin is shielded from inhibition by alpha2-antiplasmi

181 by in vivo supplied plasmin, indicated that plasmin is the crucial serine protease executing in vivo

182 duced when crosslinked fibrin is degraded by plasmin, is the most widely used clinical marker of acti

183 fold over other enzymes and proteins) toward plasmin; it also improved the reproducibility (<5%) of i

184 10 plays a crucial role in the generation of plasmin leading to fibrinolysis, thus providing a link t

185 Pretreatment of SF with plasmin led to a strongly reduced formation of aggregate

186 al structure of plasminogen, we propose that plasmin ligands such as phosphoglycerate kinase induce a

187 CUB domain-containing protein-1 (CDCP1), by plasmin-like serine proteases induces outside-in signal

188 or by inhibition of proteolytic activity of plasmin-like serine proteases with aprotinin prevented b

189 previously described prostasin (RKRK(178)), plasmin (Lys-189), and neutrophil elastase (Val-182 and

190 tion and structure, fibrin susceptibility to plasmin-lysis, plasma redox status, leukocyte oxidative

191 Ro binding to apoptotic cardiocytes enhances plasmin-mediated activation of TGF-beta, thereby promoti

192 omplement protease Factor I, suggesting that plasmin-mediated C3b cleavage fragments lack effector fu

193 Plasmin-mediated cleavage of beta(2)GPI prevented bindin

194 can be a source of activated plasminogen for plasmin-mediated cleavage of influenza virus HAs that co

195 nism of action of this probe is based on the plasmin-mediated cleavage of the Fib-Au NPs and the redu

196 RG fragment containing the HRR, released via plasmin-mediated cleavage, acts as a negative regulator

197 f LV thrombi and liver sinusoidal vessels to plasmin-mediated damage and demonstrate the importance o

198 platelet-derived FXIIIa were susceptible to plasmin-mediated degradation.

199 and prolonged embryonic survival by reducing plasmin-mediated extracellular matrix degradation around

200 Abeta binding to this alphaC region blocked plasmin-mediated fibrin cleavage at this site, resulting

201 her, these data suggest that plasminogen and plasmin-mediated fibrinolysis is a key modifier of the o

202 n and plasminogen at acidic pH and increased plasmin-mediated fibrinolysis.

203 inolysis-induced BBB leakage is dependent on plasmin-mediated generation of bradykinin and subsequent

204 suppresses elastin degradation by inhibiting plasmin-mediated matrix metalloproteinase 9 activation.

205 tissue plasminogen activator (tPA), reduced plasmin-mediated proteolysis of gamma'-Fn, and/or altere

206 by prohormone cleavage products formed from plasmin-mediated proteolysis.

207 r (uPA) and its receptor (uPAR) coordinate a plasmin-mediated proteolytic cascade that has been impli

208 and a reduced open probability accompany the plasmin-mediated reduction in Ca(2+) uptake.

209 Furthermore, our findings indicate that plasmin modulates disease activity in patients with FXII

210 e to conventional assays, this new probe for plasmin offers the advantages of high sensitivity and se

211 o longer bind to the lysine binding sites of plasmin(ogen) and is only a kinetically slow plasmin inh

212 FBA-tb bound human plasmin(ogen) and protected FBA-tb-bound plasmin from re

213 Additionally, upon activation plasmin(ogen) bound to PGK cleaved the central complemen

214 nd 557, sites involved in fibrin binding and plasmin(ogen) cleavage, respectively.

215 explanation why pathogenic microbes utilize plasmin(ogen) for immune evasion and tissue penetration.

216 Purified plasmin(ogen) from diabetic subjects had impaired fibrin

217 Plasma-purified plasmin(ogen) functional activity was evaluated by chrom

218 Here, we characterize the role of plasmin(ogen) in the complement cascade.

219 Thus, plasmin(ogen) regulates both complement and coagulation,

220 rp proteins include binding of host laminin, plasmin(ogen), and regulators of complement activation.

221 his C terminus contains the binding site for plasmin(ogen), the key component necessary for the rapid

222 hinner fibers, and (2) through inhibition of plasmin(ogen)-fibrin binding.

223 ly on recruitment of host proteases, such as plasmin(ogen).

224 ~50-residue-extended C-terminus, which binds plasmin(ogen).

225 Localization of plasmin on macrophages and activation of pro-MMP-9 play

226 catalyzes the conversion of plasminogen into plasmin on the cell surface.

227 catalyzes the conversion of plasminogen into plasmin on the cell surface.

228 alpha2AP inhibits plasmin on the fibrin clot or in the circulation by form

229 se C (PKC) inhibitor abolished the effect of plasmin on TRPV5.

230 prochemerin at position Lys-158, whether by plasmin or another serine protease, represents a major s

231 ble to dispersal by the fibrinolytic enzymes plasmin or nattokinase.

232 cemic rats, whereas injection of bradykinin, plasmin or tissue plasminogen activator did not elicit s

233 67)-His(368) is not able to inhibit trypsin, plasmin, or cathepsin G with or without heparin as a cof

234 vo incubation of baboon serum with thrombin, plasmin, or FXa did not show noticeable complement cleav

235 eased, but not when lysis was initiated with plasmin, or when only FPA was released.

236 cterium H. influenzae, and when converted to plasmin, PE-bound plasmin aids in immune evasion and con

237 The participation of the plasminogen (Plg)/plasmin (Pla) system in the productive phase of inflamma

238 The plasminogen (Plg)/plasmin (Pla) system is associated with a variety of bio

239 n-like serine proteases (thrombin, tPA, FXa, plasmin, plasma kallikrein, trypsin, FVIIa).

240 ytic cascade involving the components of the plasmin-plasminogen system.

241 Importantly, cleavage activation by plasmin/plasminogen was independent of the viral NA, sug

242 alpha(M)(-/-) myeloid cells showed impaired plasmin (Plm)-dependent extracellular matrix invasion, r

243 Plasmin (PLS) and thrombospondin-1 (TSP1) have been stud

244 a-domain were deleted to prevent cleavage by plasmin (Pm) and to disable Pg substrate binding to the

245 ved in PAI-1(-/-) mice that express inactive plasmin (Pm) but normal levels of zymogen Pg (PAI-1(-/-)

246 itation of the time courses of Pg depletion, plasmin (Pm) formation, transient formation of the confo

247 e plasminogen activator (uPA) and ultimately plasmin (Pm) generation.

248 binding to plasminogen (Pg), the zymogen of plasmin (Pm).

249 erated a truncated PlGF118 isoform mimicking plasmin-processed PlGF, and explored its biological func

250 Specifically, we show that plasmin processing of PlGF-2 yields a protease-resistant

251 uropilin-1 interaction and its regulation by plasmin processing.

252 lasminogen activator (tPA) thereby enhancing plasmin production, but whether CLEC3A contributes to pl

253 ring plasminogen, whose conversion to active plasmin promotes the invasion process.

254 The resulting surface plasmin protease activity has been proposed to play a ro

255 (ii) tPA/plasmin proteolysis impairs parallel fiber-PN synaptogen

256 does not, thus emphasizing the importance of plasmin proteolytic activity for ookinete invasion.

257 Cell-associated plasmin proteolytic activity is a key component of physi

258 cells by 3.5- to fivefold Plg receptors and plasmin proteolytic activity were required for phagocyto

259 in by the tissue plasminogen activator (tPA)/plasmin proteolytic system partially contributes to ChAB

260 asminogen activator (tPA), a part of the tPA/plasmin proteolytic system, influences several different

261 This complement-inhibitory activity of plasmin provides a new explanation why pathogenic microb

262 In this study, we found that plasmin purified from the urine of patients with nephrot

263 ing real-time microscopy, we determined that plasmin rapidly degrades platelet-VWF complexes on endot

264 No new rapid plasmin reagin (RPR) seroreactivity in young children is

265 T pallidum haemagglutination test and rapid plasmin reagin titre of >/=1:8) was higher in cases of y

266 rface, viz. a high affinity plasminogen (Pg)/plasmin receptor, Pg-binding group A streptococcal M pro

267 We found that plasmin regulates the local concentration of tPA through

268 owed hydrogel degradation by collagenase and plasmin relative to fibrin alone, and also decreased the

269 interacts with beta-amyloid (Abeta), forming plasmin-resistant abnormal blood clots, and increased fi

270 g in the generation of increased levels of a plasmin-resistant fibrin degradation fragment.

271 6)) and plasminogen, yielding active uPA and plasmin, respectively.

272 e demonstrate that plasminogen activation to plasmin restores PGE(2) sensitivity in fibrotic lung fib

273 ogen activator (uPA) converts plasminogen to plasmin, resulting in a proteolytic cascade that has bee

274 hrombin-activated fibrinolysis inhibitor and plasmin strongly correlated with the degree of renal fun

275 Plasmin suppresses brain metastasis in two ways: by conv

276 vage by activating the plasminogen activator/plasmin system.

277 nding mode in the widely open active site of plasmin that explains the strong potency and selectivity

278 ain blood fluidity by producing the protease plasmin that removes blood clots from the vasculature, a

279 We hypothesized that plasmin, the key enzyme of the fibrinolytic system, serv

280 ences for trypsin, chymotrypsin, matriptase, plasmin, thrombin, four kallikrein-related peptidases, a

281 In sum, excess tPA/plasmin, through separate downstream molecular mechanism

282 hown that C-terminal cleavage of chem163S by plasmin to chem158K, followed by a carboxypeptidase clea

283 cterial plasminogen (Pg) activators generate plasmin to degrade fibrin blood clots and other proteins

284 f NGF (proNGF) is cleaved extracellularly by plasmin to form mature NGF (mNGF) and that mNGF is degra

285 s use broad spectrum proteolytic activity of plasmin to invade tissue and form metastatic foci.

286 Direct high-affinity binding of hPg/plasmin to pattern D GAS is fully recapitulated by the h

287 lts in the rapid and localized generation of plasmin to the endothelial cell surface, thereby regulat

288 sminogen receptor, Plg-R(KT), and to fibrin, plasmin-treated fibrinogen, and Matrigel.

289 Furthermore, BBA70-bound plasmin was able to degrade the central complement prote

290 3 treated with either neutrophil elastase or plasmin was inhibited to a lesser extent, especially in

291 In contrast, Abeta degradation by plasmin was largely unaffected by phosphorylation.

292 okinase-type plasminogen activator to active plasmin was significantly augmented in the presence of C

293 activation of the fibrin-degrading protease plasmin, were upregulated in Chd4 mutant LYVE1+ cells, a

294 rmation of plasminogen into its active form (plasmin), which degrades fibrin and extracellular matrix

295 he zymogen plasminogen into the active form (plasmin), which then degrades the fibrin clots.

296 pha(2)-antiplasmin, fibrin did protect human plasmin, which formed a 31-fold higher avidity complex w

297 The most potent inhibitor 8 binds to plasmin with an inhibition constant of 0.2 nM, whereas K

298 trations (1.0-20 mug/ml), dsDNA competes for plasmin with fibrin and decreases the rate of fibrinolys

299 metry (LDI-MS) approach for the detection of plasmin with subnanomolar sensitivity through the analys

300 hage population and is dependent upon active plasmin, yet independent of known fibrinogen receptors.