ライフサイエンスコーパス: plasmin

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

2 NSGMs selectively inhibit human full-length plasmin.

3 logical inhibitor of the fibrinolytic enzyme plasmin.

4 both, primed and nonprimed binding sites of plasmin.

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

6 ta-fibrinogen binding delays fibrinolysis by plasmin.

7 that are sensitive to enzymatic cleavage by plasmin.

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

9 en and mediating the localized generation of plasmin.

10 inhibits plasma kallikrein, factor XIa, and plasmin.

11 inished activation of the proNGF convertase, plasmin.

12 nolysis by virtue of its capacity to inhibit plasmin.

13 that these HAs are preferentially cleaved by plasmin.

14 arget-labeling indicator for the analysis of plasmin.

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

16 bundant precursor of the vertebrate protease plasmin.

17 rful inhibitor of plasminogen activators and plasmin.

18 uman plasminogen to form the plasma protease plasmin.

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

20 e or primed by limited selective cleavage by plasmin.

21 milar TG, but swine plasmas did not generate plasmin.

22 rface-associated miropin, strongly inhibited plasmin.

23 the primary serine protease in fibrinolysis, plasmin.

24 hibit plasma kallikrein, activated FXII, and plasmin.

25 plasmin (alpha2AP), the primary inhibitor of plasmin.

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

27 dependent mechanism, to efficiently generate plasmin.

28 to its promise as an allosteric regulator of plasmin.

29 nism that does not require the generation of plasmin.

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

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

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

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

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

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

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

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

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

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

40 Plasmin activity was not involved in promoting these cha

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

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

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

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

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

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

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

48 catalyzes the conversion of plasminogen into plasmin and activates signaling pathways that promote ce

49 After plasmin and ADAMTS3, KLK3 is the third protease shown to

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

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

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

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

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

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

56 ibrosis (PF); TGF-beta, Factor Xa, thrombin, plasmin and uPA all induced fibroblast/myofibroblast dif

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

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

59 olytic changes were present in AKI, a higher plasmin-antiplasmin complex indicated a hyperfibrinolyti

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

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

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

63 assessment included fibrinolytic factors and plasmin-antiplasmin complex.

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

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

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

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

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

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

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

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

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

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

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

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

76 The fibrils generated via plasmin cleavage were more stable than those prepared at

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

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

79 omains, an A1A2A3 tridomain fragment of VWF, plasmin-cleaved dimers of VWF, multimeric recombinant VW

80 itive to activation by plasma kallikrein and plasmin, compared with FXII-WT or FXII-T309R.

81 The thrombin and plasmin concentration peak heights (PH) and production r

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

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

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

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

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

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

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

89 ointed to EFV effects at the synaptic level, plasmin-depended amyloid clearance, inflammation and mic

90 l migration of proinflammatory monocytes was plasmin dependent and was abolished by anti-Plg-R(KT) mo

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

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

93 y, these activities were abrogated following plasmin digestion.

94 In culture, plasmin directly, and in synergy with high-mobility grou

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

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

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

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

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

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

101 Plasmin exhibited a similar activity, but it was weaker

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

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

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

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

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

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

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

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

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

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

112 ecific fluorogenic substrate, we developed a plasmin generation (PG) assay for mouse plasma that is s

113 AR has dual functions: as a key regulator of plasmin generation and a component of the innate immune

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

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

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

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

118 Affimer F5 reduced fibrin-dependent plasmin generation and was predicted to bind fibrinogen

119 deling identified interaction sites, whereas plasmin generation assays determined effects on plasmino

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

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

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

123 Pericellular plasmin generation, an important pathophysiological proc

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

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

126 thological properties, such as inhibition of plasmin generation, have been attributed to its main str

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

128 aptic N-methyl-d-aspartate receptors but not plasmin generation.

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

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

131 types of promising active site inhibitors of plasmin have been developed: tranexamic acid conjugates

132 Plasminogen and its active form, plasmin, have diverse functions related to the inflammat

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

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

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

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

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

138 e disulfide-linked two-chain protease, human plasmin (hPm).

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

140 In these studies, inhibition of plasmin in mice with tranexamic acid delayed up-regulati

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

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

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

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

145 Inhibition of plasmin in vivo also prevented trafficking of monocyte-d

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

147 naptic expression of NCAD by a uPAR-mediated plasmin-independent mechanism, and that uPA-induced form

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

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

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

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

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

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

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

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

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

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

158 Inhibition of fibrinolysis by the indirect plasmin inhibitor epsilon-aminocaproic acid or by alpha2

159 thus, it represents the first proteinaceous plasmin inhibitor of prokaryotic origin described to dat

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

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

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

163 applicability was demonstrated by screening plasmin inhibitors and fibrinolytic bioactives from mixt

164 Furthermore, several allosteric plasmin inhibitors based on heparin mimetics have been d

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

166 Although plasmin inhibitors could be used in multiple disorders,

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

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

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

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

171 Collectively, these studies demonstrate that plasmin is an important regulator of macrophage function

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

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

174 Membrane-bound plasmin is used by immune cells to degrade extracellular

175 the hypothesis that the fibrinolytic enzyme, plasmin, is a key regulator of macrophage function after

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

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

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

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

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

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

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

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

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

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

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

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

188 plasminogen activator (PLAU/uPA); subsequent plasmin-mediated degradation of diverse alpha-granule pr

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

190 y of miropin protects envelope proteins from plasmin-mediated degradation.

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

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

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

194 The macrophage requirement for plasmin-mediated fibrinolysis, both in vivo and in vitro

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

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

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

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

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

200 techniques to purify the catalytic domain of plasmin, micro-plasmin (uPlm), which can be used for an

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

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

203 A causative role for plasmin (ogen) as a "second hit" in kidney disease progr

204 Together, these findings suggest a role for plasmin (ogen) in mediating glomerular injury and as a v

205 In patients, we found associations between plasmin (ogen) uria and edema status as well as eGFR.

206 ing a potentially novel relationship between plasmin (ogen) uria and estimated glomerular filtration

207 Additionally, association between plasmin (ogen) uria and kidney function in glomerular di

208 nephropathy was associated with increases in plasmin (ogen) uria and proteinuria.

209 time-of-biopsy albuminuria, proteinuria, and plasmin (ogen) uria for correlations with kidney outcome

210 Urinary plasminogen/plasmin, or plasmin (ogen) uria, has been demonstrated in proteinuri

211 sminogen activation, and measured changes in plasmin (ogen) uria.

212 Increased glomerular plasmin (ogen) was found in PAN rats and focal segmental

213 Our study demonstrates a role for plasmin (ogen)-induced podocyte injury in the PAN nephro

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

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

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

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

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

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

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

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

222 n and clearance, including (pro)thrombin and plasmin(ogen), have powerful roles in driving acute and

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

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

225 ed the mechanisms underlying the deficits of plasmin(ogen)-mediated macrophage migration in 2 models:

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

227 of inflammation requires cell surface-bound plasmin(ogen).

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

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

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

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

232 y furin-like proteases or extracellularly by plasmin or matrix metalloproteinases.

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

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

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

236 Urinary plasminogen/plasmin, or plasmin (ogen) uria, has been demonstrated i

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

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

239 Simultaneous thrombin (TG) and plasmin (PG) generation is useful to assessing coagulati

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

255 expression of S100A10 through SRC to promote plasmin production, endothelial cell invasion, and angio

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

271 sites on plasminogen's kringle domains, and plasmin's serine protease domain greatly contributed to

272 VEGFC) and VEGFD are cleaved by thrombin and plasmin, serine proteases generated during hemostasis an

273 Using a plasmin-specific fluorogenic substrate, we developed a p

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 A dysfunctional tPA-plasmin system causes defective proteolytic degradation

277 vage by activating the plasminogen activator/plasmin system.

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

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 Miropin inhibits plasmin through the formation of a stable covalent compl

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

283 s also a specific and efficient inhibitor of plasmin; thus, it represents the first proteinaceous pla

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

285 minogen, thereby promoting its conversion to plasmin to destroy the bound histone.

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

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

288 urify the catalytic domain of plasmin, micro-plasmin (uPlm), which can be used for an Abeta-clearance

289 tion (PA) system catalyzes the generation of plasmin via two activators: tissue-type (tPA) and urokin

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

291 3 treated with either neutrophil elastase or plasmin was inhibited to a lesser extent, especially in

292 AMC) from substrates specific to thrombin or plasmin was monitored.

293 e inhibition of the fibrinolytic activity of plasmin was nearly as effective as that exerted by alpha

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

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

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

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

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

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.