ライフサイエンスコーパス: cathepsin G

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

2 ain pericellular proteolysis by inactivating cathepsin G.

3 sites that are susceptible to proteolysis by cathepsin G.

4 adation by the endolysosomal serine protease cathepsin G.

5 the regiospecific proteolysis of peptides by cathepsin G.

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

7 ies were confirmed with purified chymase and cathepsin G.

8 n introduced proteolytic cleavage sites into cathepsin G.

9 to inhibit and clear neutrophil elastase and cathepsin G.

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

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

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

13 in, chymotrypsin and the neutrophil protease cathepsin G.

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

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

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

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

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

19 cine pancreatic elastase or human neutrophil cathepsin G.

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

21 the P1 position, inhibited chymotrypsin and cathepsin G.

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

23 LPI is inhibition of neutrophil elastase and cathepsin G.

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

25 one inhibited cleavage of the dipeptide from cathepsin G.

26 honuclear leukocytes along with elastase and cathepsin G.

27 ing of proteinase 3 is distinct from that of cathepsin G.

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

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

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

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

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

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

34 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)

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

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

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

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

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

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

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

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

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

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

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

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

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

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

49 Cathepsin G addition to corn trypsin inhibitor-treated P

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

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

52 Cathepsin G and bactericidal-permeability-increasing pro

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

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

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

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

57 0- and 1,300-fold selective for chymase over cathepsin G and chymotrypsin, respectively.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

96 tochalasin B inhibited the ADP/epinephrine-, cathepsin G-, and TRAP-induced decrease in platelet surf

97 Neutrophil elastase and cathepsin G are abundant intracellular neutrophil protei

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

133 with neutral proteases (neutrophil elastase, cathepsin G, chymotrypsin, trypsin) generated fragments

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

151 rgeted mutation of the promyelocyte-specific cathepsin G gene (which lies just 3' to the granzyme gen

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

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

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

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

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

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

158 Cathepsin G had a small effect at 4 h.

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

160 Although cathepsin G has previously shown to have broad spectrum

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

176 Cathepsin G induced chemotaxis and production of proinfl

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

178 Cathepsin G-induced monocyte chemotaxis is partially per

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

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

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

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

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

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

185 Cathepsin G is a major secreted serine peptidase of neut

186 Cathepsin G is a neutral serine protease that is highly

187 Cathepsin G is a neutrophil-derived serine protease that

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

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

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

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

192 Cathepsin G is chemotactic rather than chemokinetic for

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

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

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

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

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

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

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

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

201 6 kb of regulatory sequences from the human cathepsin G locus, we hypothesized that sequences requir

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

203 Cathepsin G markedly activates phospholipase C and p38 M

204 Pretreatment with cathepsin G markedly increased susceptibility of macroph

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

226 Inhibitors of cathepsin G or elastase significantly delayed the burst

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

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

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

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

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

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

233 Similar elements occur in the elastase and cathepsin G promoters.

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

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

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

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

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

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

240 Cathepsin G proteolysed platelet surface GPIb alpha, but

241 Using the elastase and cathepsin G PU.1 and CG-like elements as probes results

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

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

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

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

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

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

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

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

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

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

252 Because some cathepsin G responses mimic cardiomyocyte activation by

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

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

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

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

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

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

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

260 Substituting preferred cathepsin G substrate sequences into sunflower trypsin i

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

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

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

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

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

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

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

268 tase proteolyse GPV, we show that neutrophil cathepsin G, thrombin receptor activating peptide (TRAP)

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

270 n of myeloperoxidase activity or increase in cathepsin G transcripts were detected.

271 First, flow cytometric studies showed that cathepsin G, TRAP, and ADP/epinephrine decreased the pla

272 Third, the cathepsin G-, TRAP-, and ADP/epinephrine-induced decreas

273 tin polymerization, completely inhibited the cathepsin G-, TRAP-, and ADP/epinephrine-induced decreas

274 50 min, massive fibrin could be observed on cathepsin G-treated platelets even at 35 min.

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

276 Cathepsin G triggered calcium mobilization in PAR4-trans

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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