ライフサイエンスコーパス: cathepsin G

1 with PMN elastase and proteinase-3, but not cathepsin G.

2 sins B, K, V, and S with no activity against cathepsin G.

3 r of the serine peptidases, chymotrypsin and cathepsin G.

4 ain pericellular proteolysis by inactivating cathepsin G.

5 sites that are susceptible to proteolysis by cathepsin G.

6 the regiospecific proteolysis of peptides by cathepsin G.

7 es, specifically elastase, chymotrypsin, and cathepsin G.

8 ies were confirmed with purified chymase and cathepsin G.

9 n introduced proteolytic cleavage sites into cathepsin G.

10 to inhibit and clear neutrophil elastase and cathepsin G.

11 r the homologous neutrophil serine protease, cathepsin G.

12 nhibits chymotrypsin, trypsin, elastase, and cathepsin G.

13 motrypsin-like enzymes mast cell chymase and cathepsin G.

14 NEI, whereas EIB was only able to do so with cathepsin G.

15 in, chymotrypsin and the neutrophil protease cathepsin G.

16 cathepsin G, had effects similar to purified cathepsin G.

17 ction had no effect on platelet responses to cathepsin G.

18 reate a loss-of-function mutation for murine cathepsin G.

19 cine pancreatic elastase or human neutrophil cathepsin G.

20 the P1 position, inhibited chymotrypsin and cathepsin G.

21 the protein revealed this to be identical to cathepsin G.

22 LPI is inhibition of neutrophil elastase and cathepsin G.

23 roteins, such as elastase, glucuronidase and cathepsin G.

24 one inhibited cleavage of the dipeptide from cathepsin G.

25 adation by the endolysosomal serine protease cathepsin G.

26 neutrophil elastase (NE), proteinase 3, and cathepsin G.

27 ases, including neutrophil elastase (NE) and cathepsin G.

28 ophil extracellular traps, which bind NE and cathepsin G.

29 ue to serine protease cleavage, primarily by cathepsin G.

30 trix metalloproteinase-2 (MMP-2), MMP-9, and cathepsin G.

31 e proteinases such as thrombin, trypsin, and cathepsin-G.

32 us by enzymes such as thrombin, trypsin, and cathepsin-G.

33 SPs, we studied here the effects of EapH1 on cathepsin-G.

34 crystal structures of 1 complexed with human cathepsin G (1.85 A) and human chymase (1.90 A) reveal t

35 The addition of cathepsin G (425 nm) or convulxin (10 nm) to PRP dramati

36 to 8.6 +/- 2.3 (+/-SD) x 10(-18) mol of free cathepsin G (5.2 +/- 1.4 x 10(6) molecules)/cell; and 3)

37 In contrast, we find that cathepsin G, a granule enzyme found in NB4 cells, cleave

38 t SPI-1 forms a stable complex in vitro with cathepsin G, a member of the chymotrypsin family of seri

39 They also secrete cathepsin G, a serine protease implicated in cytokine re

40 We report that cathepsin G, a serine protease, plays a vital role in th

41 en to examine further the gene expression of cathepsin G, acid phosphatase, and alpha 1-PI in keratoc

42 Ala(226)Glu mutants of mouse cathepsin G acquire tryptic activity and human ability t

43 activated receptor-4 (PAR4), indicating that cathepsin G activates platelets through PAR4.

44 tive in reducing the neutrophil elastase and cathepsin G activities in an in vivo model of lung infla

45 Together, our data indicate that cathepsin G activity at the tumor-bone interface plays a

46 We found that activated neutrophils lost cathepsin G activity by a pathway requiring myeloperoxid

47 ted than in uninfected B cells, induction of cathepsin G activity by EBV led to total degradation of

48 generated by myeloperoxidase might regulate cathepsin G activity in vivo.

49 and its effectiveness against membrane-bound cathepsin G activity.

50 biosensor to detect the presence of HNE and Cathepsin-G activity in situ.

51 Cathepsin G addition to corn trypsin inhibitor-treated P

52 Furthermore, 50 nM human cathepsin G and 50 nM trypsin also activated the recepto

53 lease of neutrophil granule proteins such as cathepsin G and azurocidin/CAP37.

54 Cathepsin G and bactericidal-permeability-increasing pro

55 he fungistatic activities of combinations of cathepsin G and BPI were additive, as were those of comb

56 and 1 occupies the S(1) and S(2) subsites of cathepsin G and chymase similarly, with the 2-naphthyl i

57 onstrate that it is possible to inhibit both cathepsin G and chymase with a single molecule and sugge

58 red with other chymotryptic enzymes, such as cathepsin G and chymotrypsin, it is much more slowly inh

59 0- and 1,300-fold selective for chymase over cathepsin G and chymotrypsin, respectively.

60 imal cleavage by the chymotryptic peptidases cathepsin G and chymotrypsin.

61 demonstrate that neutrophil serine proteases cathepsin G and elastase can cleave full-length human IL

62 Human neutrophil proteases cathepsin G and elastase can directly alter platelet fun

63 ated previously that monocyte-bound forms of cathepsin G and elastase cleave and activate factor V, s

64 Murine IL-33 is also cleaved by neutrophil cathepsin G and elastase, and both full-length and cleav

65 eukocytes release several mediators, such as cathepsin G and elastase, which can activate both the co

66 ties of the neutrophil degranulation markers cathepsin G and elastase.

67 ition was observed for both human neutrophil cathepsin G and human mast cell chymase.

68 hibit enzymatic activity of human neutrophil cathepsin G and human neutrophil elastase, but not a ran

69 s-1 and approximately 3 x 10(4) M-1 s-1 for cathepsin G and mast cell chymase, respectively.

70 We found that cathepsin G and matrix metallopeptidase 9 directly inhib

71 1 interferon-associated genes, but increased cathepsin G and matrix metallopeptidase 9 expression.

72 S-VWF73 at the V(1607)-T(1608) peptide bond; cathepsin G and matrix metalloprotease 9 cleave VWF subs

73 eutrophils deficient in the serine proteases cathepsin G and neutrophil elastase (CG/NE neutrophils)

74 The neutrophil-derived serine proteases cathepsin G and neutrophil elastase are implicated in th

75 Mast cell/neutrophil cathepsin G and neutrophil elastase generate similar fra

76 similar neutrophil serine proteases (NSPs), cathepsin G and proteinase 3, coexist with NE in humans

77 ivity of the neutrophil proteases: elastase, cathepsin G and proteinase-3.

78 how that PAR4 mediates platelet responses to cathepsin G and support the hypothesis that cathepsin G

79 inhibitor that was >100-fold selective over cathepsin G and that mitigated a number of liabilities a

80 t from other chymotryptic enzymes, including cathepsin G and the stratum corneum chymotryptic enzyme.

81 a uniform tryptase(+), chymase(+), CPA3(+), cathepsin G(+), and granzyme B(+) phenotype.

82 ownstream proteases (neutrophil elastase and cathepsin G) and serum levels of IL-1beta, IL-6, IL-12p4

83 Thus, defensins, cathepsin G, and BPI are the major anti-H. capsulatum ef

84 the human serine proteinases, chymotrypsin, cathepsin G, and elastase, showed that jellypin inhibite

85 atrix metalloproteinase-12, cathepsin K, and cathepsin G, and enhanced proliferation and migration of

86 ers such as PRTN3, MPO, Neutrophil elastase, Cathepsin G, and Eosinophil peroxidase in Cited2-/- feta

87 hat inhibits plasmin, trypsin, chymotrypsin, cathepsin G, and plasma kallikrein but not urokinase-typ

88 Thus, cathepsin G, and possibly other neutrophil-derived serin

89 excluded ADAM10, ADAM8, neutrophil elastase, cathepsin G, and proteinase 3 from contributing to circu

90 Whereas neutrophil elastase, cathepsin G, and proteinase 3 have been known as granule

91 three serine proteases (neutrophil elastase, cathepsin G, and proteinase 3), which require cathepsin

92 ses polymorphonuclear (neutrophil) elastase, cathepsin G, and proteinase 3, but not neutrophil motili

93 luding the major serine proteases, elastase, cathepsin G, and proteinase 3, were absent.

94 ne proteases, including neutrophil elastase, cathepsin G, and proteinase 3.

95 ible inhibitors of human leukocyte elastase, cathepsin G, and proteinase 3.

96 major neutrophil serine proteases: elastase, cathepsin G, and proteinase 3.

97 Neutrophil serine proteases (NSPs; elastase, cathepsin G, and proteinase-3) directly kill invading mi

98 inhibitor of the serine proteases elastase, cathepsin G, and proteinase-3, increasingly recognized a

99 elastase, those with aromatic side chains of cathepsin G, and those with a basic side chain of bovine

100 serine proteases (NSPs) neutrophil elastase, cathepsin-G, and proteinase-3.

101 Here, we show that IC-activated cathepsin G- and neutrophil elastase-deficient (CG/NE) P

102 Neutrophil elastase and cathepsin G are abundant intracellular neutrophil protei

103 The actions of cathepsin G are reported to be mediated by protease-acti

104 eases, including elastase, proteinase 3, and cathepsin G, are closely related enzymes stored in simil

105 These data identify cathepsin G as a critical component sustaining neutrophi

106 ignaling in osteoclast precursors as well as cathepsin G at the tumor-bone interface has the potentia

107 The major source of cathepsin G at the tumor-bone interface seems to be oste

108 icidin antimicrobial peptide (hCAP18/LL-37), cathepsin G, bactericidal/permeability-increasing protei

109 and in the Golgi complex in untreated cells, cathepsin G becomes diffusely distributed during apoptos

110 In addition, a peptide inhibitor of cathepsin G blocks hbrm cleavage during apoptosis but do

111 ributions from the inhibitor backbone in the cathepsin-G-bound form.

112 cleavage site blocked platelet activation by cathepsin G but not other agonists.

113 ased controls, the labeling was enhanced for cathepsin G but was diminished for alpha 1-PI in the epi

114 Cathepsin G (but not proteinase-3) also enters tumor end

115 nzymatic conversion of the protease studied (cathepsin G), but its presence decreased the observed ra

116 Mucins caused leukocytes to release cathepsin G, but only if platelets were present.

117 llows the control of neutrophil elastase and cathepsin G by their natural inhibitors.

118 d proinflammatory neutrophil granule protein cathepsin G (CaG) has been reported as a chemoattractant

119 The chemotactic activity of cathepsin G can also be completely blocked by alpha1 ant

120 ophil elastase (NE), proteinase 3 (PR3), and cathepsin G (Cat G).

121 The neutrophil-derived serine protease cathepsin G (Cat.G) has been shown to induce neonatal ra

122 Cathepsin G (Cat.G), a neutrophil-derived serine proteas

123 The neutrophil-derived serine protease, cathepsin G (Cat.G), has been shown to induce myocyte de

124 Here we establish the importance of the cathepsin G (CatG) in the context of arterial myeloid ce

125 Cathepsin G (CatG) is a serine protease found in the azu

126 ancer-induced bone metastases, we identified cathepsin G, cathepsin K, matrix metalloproteinase (MMP)

127 duction by human mast cells with chymase and cathepsin G cells may be grossly underestimated.

128 The neutrophil serine proteases cathepsin G (CG) and neutrophil elastase (NE) are involv

129 Neutrophil serine proteases, such as cathepsin G (CG) and neutrophil elastase (NE), have been

130 Human leukocyte elastase (HLE) and cathepsin G (CG) are expressed at high levels on the sur

131 utrophil proteases such as elastase (NE) and cathepsin G (CG) attach to NETs and contribute to the di

132 We hypothesized that the protease cathepsin G (CG) may participate in degrading lubricin i

133 ates with elevated neutrophil elastase (NE), cathepsin G (CG), and MMP-9 levels within marrow and is

134 serine proteases, neutrophil elastase (NE), cathepsin G (CG), and proteinase 3 (PR3) have been ident

135 proteinases, human neutrophil elastase (NE), cathepsin G (CG), and proteinase-3 (P3) have in vitro co

136 Purified NSPs cathepsin G (CG), neutrophil elastase (NE), and proteina

137 mice lacking the neutrophil serine protease cathepsin G (CG)-induced hapten-reactive CD4 and CD8 T c

138 e (CG 117-136) derived from human neutrophil cathepsin G (CG).

139 erine proteases neutrophil elastase (NE) and cathepsin G (CG).

140 Neutrophil-derived serine proteases (cathepsin G [CG], neutrophil elastase [NE], and proteina

141 Ala-Ala-Pro-Val-CH(2)Cl), but not mice given cathepsin G/chymase inhibitors (alpha1-antichymotrypsin

142 ino-terminal sequence analyses revealed that cathepsin G cleaves factor V at several sites (Phe1031,

143 s lost in the absence of NE, and NE (but not Cathepsin G) deficient animals were protected from APL d

144 In contrast, ischemic kidneys from cathepsin G-deficient mice had a 70% decrease in tubular

145 ce within 4 days of reperfusion, whereas all cathepsin G-deficient mice survived.

146 Mucins failed to generate microthrombi in cathepsin G-deficient mice.

147 were decreased more than 50% in kidneys from cathepsin G-deficient versus wild-type mice.

148 SPs): neutrophil elastase, proteinase-3, and cathepsin G degrade SP-D.

149 rmolecular interactions formed by EapH1 with cathepsin-G differed considerably from that with neutrop

150 The G:C --> A:T transition at cathepsin G dinucleotides commonly reported in p53 mutat

151 The serine protease cathepsin G (EC 3.4.21.20; Cat G), which is stored in th

152 ntibodies directed against antigens, such as cathepsin G, elastase, and anticardiolipin, may also be

153 by the neutrophil-derived serine proteases: cathepsin G, elastase, and proteinase 3.

154 The inhibition of plasmin, subtilisin A, cathepsin G, elastase, and trypsin by rLEKTI occurred th

155 activation inhibition studies indicated that cathepsin G enhances fibrin deposition under flow condit

156 These data indicate that membrane-bound cathepsin G expressed on neutrophils is an inducible and

157 Purified syndecan-1 ectodomain protects cathepsin G from inhibition by alpha1-antichymotrypsin a

158 chymotrypsin-like proteases were also rapid: cathepsin G from neutrophils (>10(6) M(-1) s(-1)), mast

159 nic granule proteins, including elastase and cathepsin G, from the anionic sulphated proteoglycan mat

160 promyelocytic leukemia (APL) by using human cathepsin G gene regulatory elements to direct the expre

161 to the 5' untranslated region of the murine cathepsin G gene, using homologous recombination in embr

162 anzyme is located between the granzyme B and cathepsin G genes on human chromosome 14q11.2.

163 G also lie between the murine granzyme B and cathepsin G genes on murine chromosome 14; murine granzy

164 ntified by mass spectroscopy, five proteins, cathepsin G, glutaredoxin-1, thioredoxin, GP1b, and fibr

165 expression of chymase, carboxypeptidase A3, cathepsin G, granzyme B, and the tryptases derived from

166 Cathepsin G had a small effect at 4 h.

167 ants from neutrophil cultures, which contain cathepsin G, had effects similar to purified cathepsin G

168 Although cathepsin G has previously shown to have broad spectrum

169 te-specific targeting sequences of the human cathepsin G (hCG) gene to direct the expression of a PML

170 ne is expressed under the control of a human Cathepsin G (hCG) minigene.

171 sgenic mice under the direction of the human cathepsin G (hCG) promoter.

172 mast cell chymase (HC) and human neutrophil cathepsin G (hCG) show relatively similar cleavage speci

173 sis are, we crossed PML(-/-) mice with human cathepsin G (hCG)-PMLRARalpha or mammary tumor virus (MM

174 racerebral injection of neutrophil elastase, cathepsin G, heparatinase and plasmin.

175 he serine proteinases plasmin, subtilisin A, cathepsin G, human neutrophil elastase, and trypsin, but

176 teoclastogenesis is reduced by inhibition of cathepsin G in a coculture model and that in vivo inhibi

177 e that PAR-1 does not mediate the actions of cathepsin G in cardiomyocytes, and neither PAR-1 nor PAR

178 ther PAR-1 nor PAR-4 mediates the actions of cathepsin G in fibroblasts.

179 s injury remains poorly defined, the role of cathepsin G in renal ischemia/reperfusion injury was tes

180 ecific and quantitative detection of HNE and Cathepsin-G in solution and in spiked saliva samples wit

181 he role of neutrophil products, particularly cathepsin G, in HIV infection.

182 ial proteins, elastase, myeloperoxidase, and cathepsin G, in response to these species was measured u

183 Thus, oxidation of Met110 may contribute to cathepsin G inactivation by at least two distinct mechan

184 Cathepsin G induced chemotaxis and production of proinfl

185 Our data show that cathepsin G-induced chemotaxis of monocytes is mediated

186 Cathepsin G-induced monocyte chemotaxis is partially per

187 The application of the related cathepsin G inhibitor (CGI), benzyloxycarbonyl-glycine-l

188 ypsin inhibitor-1 (SFTI-1) produced a potent cathepsin G inhibitor (Ki = 0.89 nM).

189 eutrophil protease inhibitors Sivelestat and cathepsin G inhibitor I or by intraperitoneal injection

190 the most selective (>/=360-fold) engineered cathepsin G inhibitor reported to date.

191 a promising lead for further development of cathepsin G inhibitors targeting chronic inflammatory di

192 motactic activity, subcutaneous injection of cathepsin G into BALB/c mice led to infiltration of both

193 Cathepsin G is a major secreted serine peptidase of neut

194 Cathepsin G is a neutral serine protease that is highly

195 Cathepsin G is a neutrophil-derived serine protease that

196 ry tumor-induced osteolysis and suggest that cathepsin G is a potentially novel therapeutic target in

197 In addition, cathepsin G is also a potent chemoattractant for neutrop

198 Enzymatic activity of cathepsin G is associated with its monocyte chemotactic

199 Moreover, we showed that cathepsin G is capable of shedding the extracellular dom

200 Cathepsin G is chemotactic rather than chemokinetic for

201 We now report that this action of cathepsin G is mediated by PAR4.

202 have no obvious defects in function; either cathepsin G is not required for any of these normal neut

203 The neutrophil granule protease, cathepsin G, is known to cause platelet secretion and ag

204 a novel, potent dual inhibitor of neutrophil cathepsin G (K(i) = 38 nm) and mast cell chymase (K(i) =

205 reover, purified syndecan-1 ectodomain binds cathepsin G (Kd = 56 nM) and elastase (Kd = 35 nM) tight

206 ffinity for angiotensin I compared with free cathepsin G (Km = 5.9 x 10(-4) and 4.6 x 10(-4) M; k(cat

207 g PML (promyelocytic leukemia)-RARA from the cathepsin G locus (mCG-PR).

208 transgene might be located elsewhere in the cathepsin G locus and that a knock-in model might yield

209 6 kb of regulatory sequences from the human cathepsin G locus, we hypothesized that sequences requir

210 ing PML-RARalpha under control of the murine cathepsin G locus.

211 Cathepsin G markedly activates phospholipase C and p38 M

212 Pretreatment with cathepsin G markedly increased susceptibility of macroph

213 suggest that proteolytic cleavage of PLTP by cathepsin G may enhance the injurious inflammatory respo

214 is toxin prior to cathepsin G treatment, the cathepsin G-mediated effect was almost abrogated, sugges

215 Attenuation of PAR-1 activation abrogates cathepsin G-mediated induction of monocyte chemotaxis.

216 In marked contrast to soluble cathepsin G, membrane-bound enzyme was substantially res

217 Neutrophils derived from cathepsin G-/- mice have normal morphology and azurophil

218 Hematopoiesis in cathepsin G-/- mice is normal, and the mice have no over

219 cathepsin G and support the hypothesis that cathepsin G might mediate neutrophil-platelet interactio

220 ng evidence of the collateral involvement of cathepsin G, NE, and proteinase 3 in cigarette smoke-ind

221 vation of neutrophil serine proteases (NSPs) cathepsin G, neutrophil elastase, and proteinase 3, whic

222 ducts generated by the enzymes proteinase 3, cathepsin G, neutrophil elastase, MMP7 or MMP9/12 were p

223 In sum, cathepsin G-/- neutrophils have no obvious defects in fu

224 tic activity, since DFP- or PMSF-inactivated cathepsin G no longer induced monocyte migration.

225 By using protease inhibitors, chymase and cathepsin G, not tryptase, were identified in the mast c

226 Membrane-bound cathepsin G on activated neutrophils 1) converts both hu

227 Herein, we report that membrane-bound cathepsin G on intact neutrophils has potent angiotensin

228 hils express inducible, catalytically active cathepsin G on their cell surface.

229 ses (proteinase 3, elastase, azurocidin, and cathepsin G) on granulopoiesis in vitro.

230 the sequestration of neutrophil elastase and cathepsin G onto surfaces.

231 n sections using a tritium-labeled probe for cathepsin G or alpha 1-PI.

232 e additive, as were those of combinations of cathepsin G or BPI with HNP-1, HNP-2, and HNP-3.

233 peptides MOG35-55 and MOG1-20 Inhibition of cathepsin G or citrullination of the arginine residue wi

234 Incubation of FVaIIa with either cathepsin G or elastase resulted in cleavage within the

235 Inhibitors of cathepsin G or elastase significantly delayed the burst

236 ctivate platelets in blood from mice lacking cathepsin G or protease-activated receptor-4 (PAR4), ind

237 sis, treatment of neutrophils with elastase, cathepsin G, or plasmin increased their plasminogen bind

238 rine protease activity in BALF (elastase and cathepsin G), plasma elastase footprint (Aalpha-Val(360)

239 APL cells from a murine cathepsin G-PML-RARalpha knockin mouse were genetically

240 ates with individual proteases revealed that cathepsin G preferentially cleaved at Phe24-Ile25 and Ty

241 but not selective inhibition of elastase or cathepsin G, prevented the fall in TER induced by PMN co

242 Expression of PML/RARalpha from the cathepsin G promoter in transgenic mice causes a nonfata

243 This study provides the first evidence that cathepsin G promotes inositol 1,4,5-trisphosphate accumu

244 mozygous for this mutation had no detectable cathepsin G protein or activity, indicating that no othe

245 ranules along with other serine proteinases (cathepsin G, proteinase 3 and azurocidin) at concentrati

246 including neutrophil elastase, lactoferrin, cathepsin G, proteinase 3, and myeloperoxidase.

247 es with pancreatic and neutrophil elastases, cathepsin G, proteinase-3, and chymotrypsin, as previous

248 rophage proteases: neutrophil elastase (NE), cathepsin G, proteinase-3, and MMPs-2, -8, -9, and -12.

249 Cathepsin G proteolysed platelet surface GPIb alpha, but

250 The serine protease cathepsin G recapitulated the effects of MET-1 on DRG ne

251 culture model and that in vivo inhibition of cathepsin G reduces mammary tumor-induced osteolysis.

252 We also show that in vivo inhibition of cathepsin G reduces the number of CD11b(+) osteoclast pr

253 n early myeloid cells under control of human cathepsin G regulatory sequences all develop a myeloprol

254 ng antibodies, we found that mucin-triggered cathepsin G release requires L-selectin and PSGL-1 on ne

255 tion and fibrinolytic cascades, elastase and cathepsin G released from activated neutrophil granules

256 Cleavage by cathepsin G removes a 20-kDa fragment containing a bromo

257 ing that enhancement of HIV-1 replication by cathepsin G requires Gi protein-mediated signal transduc

258 tested against 1 nM membrane-bound and free cathepsin G, respectively).

259 n limit of 1 pg/mL and 100 fg/mL for HNE and Cathepsin-G, respectively.

260 Because some cathepsin G responses mimic cardiomyocyte activation by

261 l serine proteinases neutrophil elastase and cathepsin G resulted in loss of the biological activity

262 s to release the Ser proteases, elastase and cathepsin G, resulting in the proteolytic destruction of

263 prolonged incubation of cardiomyocytes with cathepsin G results in the activation of caspase-3, clea

264 ndem mass spectrometric analysis of oxidized cathepsin G revealed that loss of a peptide containing A

265 Cathepsin G's P2' preference was determined by screening

266 levels of the platelet aggregation agonist, cathepsin G stored in the azurophilic granules of promye

267 High levels of cathepsin G subsequently may increase the risk of VTE.

268 Substituting preferred cathepsin G substrate sequences into sunflower trypsin i

269 teases (neutrophil and pancreatic elastases, cathepsin G, subtilisin, and trypsin) with a stoichiomet

270 Studies in Ctsg-null mice suggest that cathepsin G supports antimicrobial defenses but can inju

271 Although prolonged exposure to cathepsin G suppressed HIV infection of macrophages, ser

272 ing, and specific inhibitors of elastase and cathepsin G suppressed the up-regulation that occurred d

273 ggest that methionine oxidation could render cathepsin G susceptible to autolytic cleavage.

274 se studies describe novel cardiac actions of cathepsin G that do not require PARs and are predicted t

275 ealed a protease-binding mode for EapH1 with cathepsin-G that was globally similar to that seen in th

276 In cathepsin G, this group occupies the hydrophobic S(3)/S(

277 rate constants that ranged from 2.7 x 10(4) (cathepsin G) to 7.1 x 10(5) m(-1)s(-1) (subtilisin).

278 50 min, massive fibrin could be observed on cathepsin G-treated platelets even at 35 min.

279 ges were exposed to pertussis toxin prior to cathepsin G treatment, the cathepsin G-mediated effect w

280 Cathepsin G triggered calcium mobilization in PAR4-trans

281 ded substrate specificity (P4-P1) of the NSP cathepsin G using a peptide substrate library.

282 e osteoclasts that up-regulate production of cathepsin G via interaction with tumor cells.

283 In flow assays, purified cathepsin G was a far more potent activator of platelet-

284 To test this hypothesis, human cathepsin G was compared with mouse wild-type and humani

285 onic peptide (CG 117-136) of human lysosomal cathepsin G was determined by using a single amino acid

286 The monocyte chemotactic activity of human cathepsin G was dose dependent with optimal concentratio

287 Isolated cathepsin G was inactivated by HOCl but not by hydrogen

288 activation by tissue kallikrein, trypsin, or cathepsin G was not affected.

289 markers, Human Neutrophil Elastase (HNE) and Cathepsin-G, was constructed as proof of concept to pote

290 the physical basis for EapH1's inhibition of cathepsin-G, we crystallized EapH1 bound to this proteas

291 ally deficient in neutrophil elastase and/or cathepsin G were impaired in their ability to degrade SP

292 vels of elastin degraded by proteinase 3 and cathepsin G were independently associated with mortality

293 Additionally, purified elastase and cathepsin G were sufficient to kill S. pneumoniae in a s

294 ctor receptor alpha chain, proteinase 3, and cathepsin G, were identified.

295 Cathepsin G, which disables thrombin receptors, had no e

296 y is not an attribute of ancestral mammalian cathepsin G, which was primarily chymotryptic, and that

297 is not able to inhibit trypsin, plasmin, or cathepsin G with or without heparin as a cofactor.

298 e of this peptide was blocked by pretreating cathepsin G with phenylmethylsulfonyl fluoride, strongly

299 We found that EapH1 inhibits cathepsin-G with a K(i) of 9.8 +/- 4.7 nm Although this

300 city is markedly narrower than that of human cathepsin G, with much greater Tyr activity and selectiv