ライフサイエンスコーパス: proteinase

1 d by Virgibacillus halodenitrificans SK1-3-7 proteinase.

2 stants when it is a zymogen in comparison to proteinase.

3 reby enforcing zymogen-like character in the proteinase.

4 ece to enforce zymogen-like character in the proteinase.

5 olled activation of a specific plasma serine proteinase.

6 ns are well-known inhibitors of C1A cysteine proteinases.

7 ed receptor activated by trypsin-like serine proteinases.

8 rendering it unable to interact with target proteinases.

9 stallites is assisted by enamel proteins and proteinases.

10 er of a family of multi-domain, zinc-binding proteinases.

11 protein-coupled receptor activated by serine proteinases.

12 Mannan-binding lectin-associated serine proteinase 2 (MASP-2) is essential for LP activation, an

13 specific inhibitors of the coxsackievirus B proteinase 2A activity for acute and chronic cardiac inf

14 nctions by the proteolytic activity of viral proteinase 2A in cases of unexplained dilated cardiomyop

15 d production of proteolytically active viral proteinase 2A in human cardiomyocytes.

16 Neutrophil serine proteases, proteinase 3 (PR3) and human neutrophil elastase (HNE),

17 Proteinase 3 (PR3) and myeloperoxidase (MPO) are two maj

18 Proteinase 3 (PR3) is a myeloid serine protease expresse

19 GN or vasculitis, ANCAs are directed against proteinase 3 (PR3) or myeloperoxidase (MPO).

20 gnant cells in advanced prostate cancer, and proteinase 3 (PR3), a serine protease present in inflamm

21 Proteinase 3 (PR3), the autoantigen in granulomatosis wi

22 3 activation was mediated by serine protease proteinase 3 (PR3), which is present in the cytosol of a

23 A-associated vasculitis, positive for either proteinase 3 (PR3)-ANCA or myeloperoxidase (MPO)-ANCA, w

24 oplasmic antibodies (ANCAs) directed against proteinase 3 (PR3).

25 ibodies to the neutrophil proteins leukocyte proteinase 3 (PR3-ANCA) or myeloperoxidase (MPO-ANCA).

26 autoantigen genes myeloperoxidase (MPO) and proteinase 3 (PRTN3) in leukocytes of patients with ANCA

27 unders, plasma levels of elastin degraded by proteinase 3 and cathepsin G were independently associat

28 ANCAs directed to proteinase 3 and myeloperoxidase (MPO) in particular are

29 -mediated release of neutrophil elastase and proteinase 3 and subsequent down-regulation of the compl

30 hepsin G (CG), neutrophil elastase (NE), and proteinase 3 cleaved C5aR to a 26- to 27-kDa membrane-bo

31 Elastin degraded by proteinase 3 could distinguish between COPD participants

32 r caspase alone or of elastase or neutrophil proteinase 3 failed to prevent inflammatory disease.

33 ADAM8, neutrophil elastase, cathepsin G, and proteinase 3 from contributing to circulating sIL-6R.

34 llateral involvement of cathepsin G, NE, and proteinase 3 in cigarette smoke-induced tissue damage an

35 cific regulators of the immune response, and proteinase 3 is a major target antigen in antineutrophil

36 P = 0.027) lower ratios of baseline 12-month proteinase 3 titers than patients who did not have CYP.

37 ir response to inflammatory cytokines and to proteinase 3, a major autoantigen in GPA, and analyzed t

38 proteases (NSPs): neutrophil elastase (NE), proteinase 3, and cathepsin G.

39 lear (neutrophil) elastase, cathepsin G, and proteinase 3, but not neutrophil motility.

40 egradation products generated by the enzymes proteinase 3, cathepsin G, neutrophil elastase, MMP7 or

41 hil serine proteases (NSPs), cathepsin G and proteinase 3, coexist with NE in humans and mice, but th

42 serine proteases, elastase, cathepsin G, and proteinase 3, were absent.

43 Proteinase 3-stimulated renal and lung MECs triggered CD

44 antineutrophil cytoplasmic antibody antigen proteinase 3.

45 arget antigens are myeloperoxidase (MPO) and proteinase 3.

46 luding human leukocyte elastase (p < 0.001), proteinase-3 (p < 0.01), and myeloperoxidase (p < 0.001)

47 on, we examined the role of ADAM17 in active proteinase-3 (PR3)-positive ANCA-associated vasculitis (

48 during diabetic ketoacidosis, and selective proteinase-3 antagonists may offer future vascular- and

49 cell monolayers was increased by recombinant proteinase-3 application (p = 0.010).

50 Recombinant proteinase-3 applied to human brain microvascular endoth

51 eutrophil azurophilic enzymes examined, only proteinase-3 correlated with diabetic ketoacidosis sever

52 ocyte origin of human leukocyte elastase and proteinase-3 in diabetic ketoacidosis was confirmed with

53 the three azurophilic enzymes elevated, only proteinase-3 levels correlated with diabetic ketoacidosi

54 Proteinase-3 might mediate vasogenic edema during diabet

55 Circulating elastase and proteinase-3 were associated with infection, and serum e

56 trophil gelatinase-associated lipocalin, and proteinase-3) were elevated in the blood of patients wit

57 neutrophil proteases including elastase and proteinase-3, generating the 33-kDa isoform that is larg

58 stricted peptides of TAA WT1-RMF, RHAMM-ILS, proteinase-3-VLQ, PRAME-VLD, and NY-eso-1-SLL were isola

59 (NSPs) neutrophil elastase, cathepsin-G, and proteinase-3.

60 It has been shown that the viral proteinase 3CD cleaves PCBP2 and contributes to viral tr

61 BP2 is cleaved in its linker region by viral proteinase 3CD, translation initiation ceases allowing t

62 rmation of vasculature, we hypothesized that proteinase-activated receptor (Par)-2 (official name F2r

63 e use genetic epistasis analysis to identify proteinase-activated receptor (PAR)-2-dependent inflamma

64 Proteinase-activated receptor (PAR)-4 is a member of the

65 cardiomyocytes, and cardiac fibroblasts via proteinase-activated receptor 1 (PAR-1) and mammalian ta

66 f the major high-affinity thrombin receptor, proteinase-activated receptor 1 (PAR-1), during the deve

67 er integrity following the activation of the proteinase-activated receptor 1 (PAR1) by thrombin.

68 cantly increased, together with those of the proteinase-activated receptor 1 (PAR1), an inflammation-

69 The high-affinity thrombin receptor, proteinase-activated receptor 1 (PAR1), has been implica

70 Thrombin-induced and proteinase-activated receptor 1 (PAR1)-mediated signalin

71 Proteinase-activated receptor 2 (PAR2 ) is a G protein-c

72 ulation signaling via tissue factor (TF) and proteinase-activated receptor 2 (PAR2) in obesity-mediat

73 ta), serine proteinases such as trypsin, and proteinase-activated receptor 2 (PAR2) promote tumor dev

74 1 (TRPA1)-deficient mice but not in c-kit or proteinase-activated receptor 2 mice.

75 ucts), which likely led to the initiation of proteinase-activated receptor 2-mediated pruritus and My

76 aggregation induced by low concentrations of proteinase-activated receptor 4-activating peptide, U466

77 Proteinase-Activated Receptor-2 (PAR2 ) is a G protein-c

78 Proteinase-activated receptor-2 (PAR2), a G protein-coup

79 of the following key proinflammatory genes: proteinase-activated receptor-2 (PAR2), tumor necrosis f

80 ed 5,6-EET via a mechanism that involved the proteinase-activated receptor-2 and cytochrome epoxygena

81 trated markedly reduced capacity to activate proteinase-activated receptor-2.

82 ning GTPase activating protein 2) and F2rl2 (proteinase-activated receptor-3), 2 genes that were also

83 A role for proteinase-activated receptor-4 (PAR-4) was recently sug

84 telet aggregation by coordinately activating proteinase-activated receptors (PARs) 1 and 4.

85 Proteinase-activated receptors (PARs) are a four-member

86 ing/activating a G-protein-coupled family of proteinase-activated receptors (PARs).

87 nicity and airway inflammation by activating proteinase-activated receptors (PARs).

88 V1, and that DE lowers the threshold for the proteinase activation.

89 ultures showing a reduction in extracellular proteinase activity as demonstrated by the reduction, or

90 study revealed that the preservatives reduce proteinase activity by 50% (EC50) at a much lower concen

91 Serine proteinase activity in liquid cultures was reduced in 83

92 We show evidence of increased neutrophil proteinase activity in older adults, namely, raised leve

93 The proteinase activity was analysed with a bioluminescent m

94 Each of the three serine proteinase activity-based probe-labelled enzymes isolate

95 We find that the proteinase ADAM17 activates the extracellular signal-reg

96 (ADAMTS7 and 12), the von-Willebrand Factor proteinase (ADAMTS13) and a group of orphan enzymes (ADA

97 oteolytically processed by the procollagen N-proteinases ADAMTS2 and ADAMTS14 between Asp-218 and Tyr

98 am was prepared using Virgibacillus sp. SK33 proteinase and fractionated using sequential ultrafiltra

99 vity toward PAPP-A2, but not selected serine proteinases and metalloproteinases.

100 psin S is one of the most important cysteine proteinases and plays key roles in nematodes and many ot

101 ically target a class of cartilage-degrading proteinases and to minimize adverse effects on bone and

102 factors Streptolysin S, PrtS (IL-8 degrading proteinase), and SpeB (cysteine protease).

103 ted activities by inactivating their cognate proteinases, and are involved in multiple physiological

104 y of a series of mitochondrial translocases, proteinases, and chaperones.

105 H prepared from V. halodenitrificans SK1-3-7 proteinase are potential functional food ingredients wit

106 These proteinases are termed sheddases because they have a tra

107 factors of periodontal pathogens implicated proteinases as major determinants of remarkable pathogen

108 New opportunities exist to exploit proteinases as therapeutic targets in plaque rupture.

109 m of the central, structural pilins involves proteinase-assisted removal of their N-terminal beta str

110 uring assembly, activation of the adenovirus proteinase (AVP) during maturation and endosome escape f

111 Recently, mutations in the gene for the proteinase bone morphogenetic 1 (BMP1) were reported in

112 n procollagen processing by the C-propeptide proteinase bone morphogenetic protein 1 (BMP-1).

113 teins (eg, MPO [myeloperoxidase] and various proteinases) but can gather other proteins found in bloo

114 leading to the activation of Cathepsin-like proteinases, but it is unknown how this process is trigg

115 and IL-18 through activation of the cysteine proteinase caspase-1.

116 Several serine proteinases clearly influence vascular remodelling and a

117 G3BP1, which differs from the poliovirus 3C proteinase cleavage site previously identified.

118 We previously showed that poliovirus 3C proteinase cleaves the SG-nucleating protein G3BP1, bloc

119 in receptor-related protein 1 (LRP1) in both proteinase-complexed and uncomplexed forms.

120 ogenetic protein-1 (BMP1)/Tolloid (TLD)-like proteinases confine Na(+) channel clustering to these si

121 pia mince hydrolyzed by V. halodenitrificans proteinases contained ACE inhibitory peptides that are p

122 Enhanced binding to zymogen versus proteinase correlates with the ability of the propiece t

123 the activity of MMP-25, suggesting that this proteinase could be a potential therapeutic target for i

124 indicate that current paradigms relevant to proteinase-dependent morphogenesis need be revisited, bu

125 Both proteins were sensitive to proteinase digestion.

126 P-9 expression, suggesting that the observed proteinase expression was regulated by the synthesis of

127 s represent a novel mechanism whereby serine proteinases facilitate epithelial cell survival and may

128 esults show that matrix localization of this proteinase facilitates the initiation of collagen assemb

129 n that irreversibly inactivates the clotting proteinases factor Xa and thrombin by forming covalent c

130 d by Virgibacillus halodenitrificans SK1-3-7 proteinases for up to 24h.

131 We have identified three different serine proteinases from the German cockroach that may, via PAR2

132 Recognition of the strategic importance of proteinase function should inspire more work harnessing

133 les in regulating prothrombin activation and proteinase function.

134 Aspartic proteinases, which include HIV-1 proteinase, function with two aspartate carboxy groups a

135 hrills of discovery as we uncovered specific proteinase genes and defined specialized activities in d

136 ed under osmotic stress, along with the ClpP proteinase genes.

137 The helper component proteinase (HCPro) is an indispensable, multifunctional

138 al RNA silencing suppressor helper-component proteinase (HCpro), presumably in association with virus

139 MC/B mediators or receptors, such as serine proteinases, histamine 4-receptor, 5-lipoxygenase-activa

140 the region of AT that makes contact with the proteinase in the final acyl-enzyme complex.

141 depth analyses of in vivo roles of BMP1-like proteinases in bone and other tissues, and for their rol

142 human organs suggests a direct role of these proteinases in e.g., heart infection and myocardial inju

143 y, isolate and characterize the trypsin-like proteinases in German cockroach allergen extracts used f

144 WSSV probably inhibits the activity of some proteinases in the proPO cascade.

145 Increasing evidence implicates serine proteinases in the proteolytic cascades leading to the p

146 ases (MMPs), particularly macrophage-derived proteinases, in COPD pathogenesis.

147 he conformational rearrangement required for proteinase inactivation, increase the risk of venous thr

148 Remarkably, proteinases including matrix metalloproteinase-9 (Mmp9)

149 , we observed no discernible effects of each proteinase individually to E2-mediated TMJ matrix loss b

150 The efficacy of alpha1 proteinase inhibitor (A1PI) augmentation treatment for a

151 Purified alpha1 proteinase inhibitor (A1PI) slowed emphysema progression

152 itors I and II were identified to be alpha-1-proteinase inhibitor (alpha1-PI) based on LC-MS/MS.

153 8-OHdG) and human neutrophil elastase/alpha1-proteinase inhibitor (HNE/alpha1-PI) complex have been r

154 evels of kallistatin, a member of the serine proteinase inhibitor (SERPIN) superfamily with antiangio

155 of the substrate-like Schistocerca gregaria proteinase inhibitor 2 (SGPI-2) to select reversible hig

156 The proteinase inhibitor activity and expression of JA-relat

157 Our work identifies STC2 as a novel proteinase inhibitor and a previously unrecognized extra

158 pression of a biosafe, anti-feedant cysteine proteinase inhibitor and an anti-root invasion, non-leth

159 atrix, is composed of the light-chain serine proteinase inhibitor bikunin and two homologous heavy ch

160 titors, T. forsythia possesses a serpin-type proteinase inhibitor called miropin.

161 samples was impaired using a broad-spectrum proteinase inhibitor cocktail, but not the pan-specific

162 pressed multifunctional member of the serine proteinase inhibitor family.

163 Purification of proteinase inhibitor from common carp (Cyprinus carpio)

164 covalent complexation between PR3 and alpha1-proteinase inhibitor was delayed in the presence of MCPR

165 Serine proteinase inhibitor, clade E, member 2 (SERPINE2), is a

166 Our data are the first to identify STC1 as a proteinase inhibitor, suggesting a previously unrecogniz

167 Serine proteinase inhibitors (serpins), typically fold to a met

168 e volatile (E)-alpha-bergamotene and trypsin proteinase inhibitors (TPIs), which are also found in he

169 ncy of one of the most important circulating proteinase inhibitors and predisposes to early-onset emp

170 spermiogenesis (metalloproteinase and serine proteinase inhibitors), and steroidogenesis (CYP21A2 and

171 njunction with an up-regulation of genes for proteinase inhibitors, in particular those containing th

172 reconfigurations to produce toxic compounds, proteinase inhibitors, oxidative enzymes, and behavior-m

173 We therefore conclude that the STCs are proteinase inhibitors, probably restricted in specificit

174 evolution of two unrelated canonical serine proteinase inhibitors.

175 Coincidentally, proteinases inside the endosome cleave the EGF and insul

176 Recently, we showed the adenovirus proteinase interacts productively with its protein subst

177 Meizothrombin, the proteinase intermediate in thrombin formation, cleaves f

178 with thrombospondin motifs-4) is a secreted proteinase involved in inflammation and matrix degradati

179 the cleavage of PCBP2 by the poliovirus 3CD proteinase is a necessary step for efficient viral RNA r

180 Although neither proteinase is required for branching morphogenesis, tran

181 tion with receptors, and cleavage by tolloid proteinases is thought to relieve this inhibition.

182 ndopeptidase (AEP), a pH-controlled cysteine proteinase, is activated during ageing and mediates APP

183 ne endopeptidase (AEP), a lysosomal cysteine proteinase, is activated during aging and proteolyticall

184 ed receptor activated by trypsin-like serine proteinases, is expressed on intestinal epithelial cells

185 ononucleotide coacervate droplets containing proteinase K (2), and proteinosome-adhered pH-resistant

186 could be cleaved by extracellularly applied proteinase K (PK), an N-terminal truncation up to amino

187 rm passage, the mutant cells stably produced proteinase K (PK)-resistant, insoluble, and aggregated a

188 This was true for samples containing both proteinase K (PK)-sensitive and PK-resistant PrP(Sc) and

189 selectively cleaved by the serine protease, proteinase K (PK).

190 ion, 'cracking', second fixation, (optional) Proteinase K (Pro-K) or sonication treatment, antibody s

191 PrP(Sc) resistance to proteinase K (PrP(res)), residual infectivity by mouse b

192 Proteinase K accessibility assays and whole-cell partiti

193 e comparisons between the structures using a proteinase K assay.

194 proves the number of identified proteins for proteinase K by 731%.

195 pore linker of hERG is the target domain for proteinase K cleavage.

196 In the absence of cholesterol, trypsin or proteinase K cleaved cytosolic loop 4, generating a prot

197 duced by DeltapgfS was highly susceptible to proteinase K degradation, in contrast to the high-molecu

198 Synaptic and fine granular proteinase K digestion (PrPres) immunoreactivity is foun

199 seq is a modified protocol that replaces the proteinase K digestion applied in FiT-seq with extended

200 Limited proteinase K digestion revealed strain-specific PrP(Sc)

201 Spx1 was resistant to limited proteinase K digestion, but was unrelated to the express

202 TM domain to assess membrane insertion using proteinase K digestion.

203 f the alpha-synuclein fibrils was studied by proteinase K digestion.

204 ctive ingredients, we devised a method using proteinase K followed by heating to deactivate proteins

205 s for improved DNA recovery as compared with proteinase K for forensic, biochemical research, genetic

206 nsing platform to detect the presence of the proteinase K in human wound fluid, highlighting the pote

207 However, AspN, GluC, chymotrypsin, and proteinase K largely benefited from being paired with tr

208 ting the need for the cumbersome spheroplast-proteinase K method for topology determinations.

209 Our data suggest that relative proteinase K resistance does not significantly influence

210 human brain display a distinct intermediate proteinase K resistance, suggesting the detection of a c

211 of hyperphosphorylated and abnormally folded proteinase K resistant tau.

212 ilm was selectively degraded by cutinase and proteinase K to form a porous material.

213 background uninfected PBMC counts increased; proteinase K treatment demonstrated some benefit in rest

214 ferred motility upon a pagM null mutant, and proteinase K treatment eliminated motility.

215 a disappeared in parallel with SpoVAD during proteinase K treatment of germinated spores.

216 fugation, size-exclusion chromatography, and proteinase K treatment of plant extracts suggest this RN

217 The insensitivity of Fe(0) corrosion to proteinase K treatment suggests that electron uptake fro

218 Notably, proteinase K treatment uncoupled electron uptake from bi

219 as a soluble complex that was insensitive to proteinase K treatment, consistent with MIR2911 being st

220 Upon incubation with proteinase K, a conspicuous blue shift of the EOT is obs

221 developed as a biosensing platform to detect proteinase K, an enzyme which is a readily available mod

222 d showed resistance to low concentrations of proteinase K, it was not overtly detrimental to the flie

223 Treatment of target cells with proteases (proteinase K, papain, alpha-chymotrypsin, and trypsin) a

224 to proteolytic digestion in vitro by either Proteinase K, pepsin or pancreatin.

225 The microaggregate species were resistant to proteinase K, phosphorylated at serine-129, oxidized, an

226 was largely accessible to exogenously added proteinase K, suggesting that this protease can access t

227 Secreted into the plasma by the liver, the proteinase K-like serine protease PCSK9 binds the low-de

228 the plasma membrane upon reculture following proteinase K-mediated clearance of cell-surface proteins

229 linker and made it no longer susceptible to proteinase K-mediated cleavage.

230 propagated prions differed in conversion and proteinase K-resistance levels in these astrocytes.

231 ns of clinically sick mice accumulate longer proteinase K-resistant (PrP(res)) fragments of approxima

232 In addition, larger proteinase K-resistant aggregates developed, along with

233 hat NPT100-18A decreased the accumulation of proteinase K-resistant alpha-synuclein aggregates in the

234 T-QuIC product indicated the generation of a proteinase K-resistant and fibrillary alpha-synuclein sp

235 triatum led to decrease in the levels of the proteinase K-resistant fraction of alpha-synuclein, amel

236 also increased alphaS tetramers and reduced proteinase K-resistant lipid-rich aggregates.

237 ce again resulted in significantly augmented proteinase K-resistant prion protein deposition and acce

238 f PrP(C), leading to increased generation of proteinase K-resistant prion protein.

239 induced conversion of PrP(C) to the abnormal proteinase K-resistant state, referred to as atypical Pr

240 gregated alpha-synuclein within Lewy bodies (proteinase K-resistant).

241 t extracts suggest this RNA resides within a proteinase K-sensitive complex.

242 Here we show a linear increase of proteinase K-sensitive PrP isoforms distinct from classi

243 physiological, presynaptic alpha-synuclein (proteinase K-sensitive) and highly aggregated alpha-synu

244 In contrast, proteinase K-treated AD homogenates and Sarkosyl-soluble

245 ubstrates and/or immunoblot band profiles of proteinase K-treated RT-QuIC reaction products indicated

246 ophobic and more resistant to proteolysis by proteinase K.

247 erminal tail from proteolytic degradation by proteinase K.

248 degradation even in the presence of protease proteinase K.

249 bit excellent proteolytic resistance against proteinase K.

250 lysis when intact bacteria were treated with proteinase K.

251 ophores by means of enzymatic digestion with proteinase K.

252 Progressive aggregation of proteinase-K resistant and Ser129-phosphorylated alpha-s

253 ecombinant PrP amyloid fibrils with extended proteinase-K resistant beta-sheet cores and infrared spe

254 d4 as a result of decreased MMP2, a secreted proteinase key for brain tumor invasion.

255 through the deregulation of kallikrein-like proteinase (KLK) family members.

256 viral proteins, one of them being the leader proteinase L.

257 trix metalloproteinase 3, a matrix-degrading proteinase linked to pulmonary fibrosis.

258 n foot-and-mouth disease virus (FMDV) leader proteinase (Lpro) (W105) that is involved in the interac

259 Foot-and-mouth disease virus (FMDV) leader proteinase (Lpro) affects several pathways of the host i

260 BMP1 and the closely related proteinase mammalian tolloid-like 1 (mTLL1) are co-expre

261 size that several membrane-associated serine proteinases (MASPs), in synergy with or in place of TMPR

262 OA cartilage such that we hypothesized this proteinase may also contribute to matrix turnover.

263 nduction of MMP9 and MMP13 suggests that the proteinases may together contribute to E2-mediated TMJ f

264 valent complex between the inhibitor and the proteinase, mediated by Cys-120 of STC2.

265 ed expression of PD-L1 and of matrix metallo-proteinases (MMPs) and CD-10 in those cells.

266 ng the nucleating factor G3BP1 via the viral proteinase NS6(Pro) This work provides new insights into

267 BP1), which is mediated by the viral 3C-like proteinase NS6(Pro) Using mutational analysis, we identi

268 olysin with karilysin, as well as a cysteine proteinase of another periodontal pathogen, Prevotella i

269 hydrolysis with a non-commercially available proteinase of fig-leaf gourd fruit (Cucurbita ficifolia)

270 The secreted aspartyl proteinases of Candida albicans have long been implicate

271 represents a prime target for 3C or 3C-like proteinases of different viruses.

272 d that NEMO is also cleaved by 3C or 3C-like proteinases of picornavirus and artertivirus.

273 t characteristic of emphysema, extracellular proteinases, particularly those with elastolytic ability

274 However, the roles that these proteinases play during mammary gland development in viv

275 A Ficus carica L. latex proteinase preparation was investigated for its ability

276 es showed a 57%-71% sequence identity with a proteinase previously cloned from the American cockroach

277 is a readily available model system for the proteinase produced by Pseudomonas aeruginosa.

278 heighten inflammation as a result of excess proteinase release during inaccurate chemotaxis, as well

279 endent conformations of PrP(Sc), we purified proteinase-resistant PrP(Sc) (PrP(RES)) from mouse brain

280 subunit of fimbriae and an arginine-specific proteinase, respectively, was downregulated in the pgn_1

281 rances, mating competency, secreted aspartyl proteinase (Sap) activities, and virulence.

282 The A. bisporus serine proteinase SPR1 is induced by humic acids and is highly

283 proteaseStreptococcus pyogenescell envelope proteinase (SpyCEP), thus blunting neutrophil-mediated k

284 adults, namely, raised levels of neutrophil proteinase substrate-derived peptides and evidence of pr

285 dentification of metalloproteinase and other proteinase substrates and their respective cleavage site

286 The propeptides of subtilisin-like serine proteinases (subtilases, SBTs) serve dual functions as i

287 mily that is cleaved and activated by serine proteinases such as thrombin, trypsin, and cathepsin-G.

288 orming growth factor-beta (TGF-beta), serine proteinases such as trypsin, and proteinase-activated re

289 tance1 (mir1) gene product, a cysteine (Cys) proteinase that is a key defensive protein against chewi

290 type plasminogen activator (uPA) is a serine proteinase that upon binding to the urokinase-type plasm

291 type plasminogen activator (uPA) is a serine proteinase that, upon binding to its receptor (uPAR), ca

292 type plasminogen activator (uPA) is a serine proteinase that, upon binding to its receptor (uPAR), ca

293 teinase with thrombospondin) are a family of proteinases that are structurally similar to the family

294 like elastases (CELAs) are pancreatic serine proteinases that digest dietary proteins.

295 ent increased the activity of matrix metallo-proteinases that initiate degradation of the BBB-associa

296 es inhibit the central blood-clotting serine proteinase thrombin that is also the target of several c

297 r the past 5 years in relating extracellular proteinases to plaque rupture, the cause of most myocard

298 trated that the type II transmembrane serine proteinase (TTSP) matriptase acts as a novel initiator o

299 ccal CXC protease, S. pyogenes cell envelope proteinase, we developed a combination vaccine that is h

300 Aspartic proteinases, which include HIV-1 proteinase, function wi