ライフサイエンスコーパス: proteinase 3

1 e monoclonal cytoplasmic staining ANCA (anti-proteinase 3).

2 city to myeloid leukemias (which overexpress proteinase 3).

3 luding neutrophil elastase, cathepsin G, and proteinase 3.

4 antineutrophil cytoplasmic antibody antigen proteinase 3.

5 All patients had ANCA reactive against proteinase 3.

6 serine proteases: cathepsin G, elastase, and proteinase 3.

7 when exposed to leukemia that overexpressed proteinase 3.

8 n of myeloid leukemia cells that overexpress proteinase 3.

9 f human leukocyte elastase, cathepsin G, and proteinase 3.

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

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

12 serine proteases: elastase, cathepsin G, and proteinase 3.

13 All had ANCA reacting with proteinase-3.

14 trophil proteases: elastase, cathepsin G and proteinase-3.

15 ue- and developmental-specific expression of proteinase-3.

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

17 tags to detect human autoantibodies against proteinase 3, a biomarker for the autoimmune disease Weg

18 ciation with autoantibodies directed against proteinase 3, a constituent of neutrophril azurophilic g

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

20 We screened proteinase 3 against the binding motif of HLA-A2.1.

21 Cathepsin G (but not proteinase-3) also enters tumor endosomes via the same m

22 sponsible for caseinolytic activity might be proteinase 3, an elastase-related enzyme whose physiolog

23 Reaction of MNEI with neutrophil proteinase-3, an elastase-like protease, and porcine pan

24 ents with myeloperoxidase ANCA (MPO-ANCA) or proteinase 3 ANCA (PR3-ANCA) and from controls.

25 Anti-proteinase 3 ANCA was associated with HLA-DP and the gen

26 nce relapses less frequently than those with proteinase 3 ANCA, suggesting greater immune regulation.

27 ide preliminary support for the concept that proteinase 3 ANCA-associated vasculitis and myeloperoxid

28 teinase 3 is a central pathogenic feature of proteinase 3 ANCA-associated vasculitis.

29 , combining urinary CD4 + T-cell counts with proteinase-3 ANCA levels suggested improved predictive p

30 ere younger, more frequently relapsing, PR3 (proteinase 3)-ANCA positive, and had lower serum creatin

31 nd that, among African Americans, those with proteinase 3-ANCA (PR3-ANCA) had 73.3-fold higher odds o

32 ients (59% men, median age 60), 60% had anti-proteinase 3-ANCA and 35% had anti-myeloperoxidase-ANCA,

33 al ANCAs isolated from patients and chimeric proteinase 3-ANCA induced the release of neutrophil micr

34 d 147 of 182 with data available (80.8%) had proteinase 3-ANCA positivity.

35 An animal model of proteinase 3-ANCA-induced vasculitis has not been found.

36 in both those with myeloperoxidase-ANCA and proteinase 3-ANCA.

37 ocalized on neutrophil plasma membranes with proteinase 3 and a complex of NB1 glycoprotein and prote

38 antibodies (ANCA) have been identified: anti-proteinase 3 and anti-myeloperoxidase antibodies.

39 with other serine proteinases (cathepsin G, proteinase 3 and azurocidin) at concentrations exceeding

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

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

42 ther granule constituents (ANCA targets anti-proteinase 3 and myeloperoxidase and elastase), was sign

43 ANCA bind to ANCA target, such as proteinase 3 and myeloperoxidase, and activate neutrophi

44 of markers, including the ANCA autoantigens proteinase 3 and myeloperoxidase.

45 addition to the more commonly known targets proteinase 3 and myeloperoxidase.

46 on of the myeloid leukemia-specific antigens proteinase 3 and neutrophil elastase found in the primar

47 ith the known association of autoimmunity to proteinase 3 and neutrophil elastase in Wegener's granul

48 substituting a cleavage site shared by human proteinase 3 and neutrophil elastase, yielded an agonist

49 ntigens in CML and AML, and in particular on proteinase 3 and other azurophil granule proteins as tar

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

51 ivation in aging neutrophils are mediated by proteinase-3 and caspase-3, leading to pyroptosis.

52 efinition of epitopes on the major antigens, proteinase-3 and myeloperoxidase, has been sought, and i

53 In vitro, the expression of proteinase-3 and other ANCA antigens on the surface of n

54 .g. CCL2, CCL7), neutrophil activation (e.g. proteinase-3), and epithelial injury (e.g. KRT19).

55 The adjacent neutrophil elastase, proteinase 3, and azurocidin genes encode serine proteas

56 rophil serine proteases, including elastase, proteinase 3, and cathepsin G, are closely related enzym

57 ony-stimulating factor receptor alpha chain, proteinase 3, and cathepsin G, were identified.

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

59 utrophil elastase, lactoferrin, cathepsin G, proteinase 3, and myeloperoxidase.

60 t leukemic CFU-GM based on overexpression of proteinase 3, and that proteinase 3-specific CTL could b

61 ine proteinases (NSPs): neutrophil elastase, proteinase-3, and cathepsin G degrade SP-D.

62 eatic and neutrophil elastases, cathepsin G, proteinase-3, and chymotrypsin, as previously shown for

63 ases: neutrophil elastase (NE), cathepsin G, proteinase-3, and MMPs-2, -8, -9, and -12.

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

65 antibodies to myeloperoxidase (anti-MPO) or proteinase 3 (anti-PR3) was recorded when available.

66 antibodies to myeloperoxidase (anti-MPO) and proteinase 3 (anti-PR3).

67 osphatidylserine, anti-myeloperoxidase, anti-proteinase 3, anti-dsDNA, anti-beta-2-glycoprotein I, an

68 unopathogenic effects of myeloperoxidase and proteinase 3 antibodies are well established, and good m

69 Titers of anti-myeloperoxidase and anti-proteinase 3 antibodies were 1500-fold and 10,000-fold h

70 ytoplasmic autoantibody immunoglobulin G and proteinase 3 antineutrophil cytoplasmic autoantibody imm

71 trophil cytoplasm autoantibodies rather than proteinase 3-antineutrophil cytoplasm autoantibodies.

72 could be explained by differing abilities of proteinase 3-antineutrophil cytoplasmic antibody (PR3-AN

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

74 Recombinant proteinase-3 applied to human brain microvascular endoth

75 neutrophil and monocyte myeloperoxidase and proteinase 3 are a feature of anti-neutrophil cytoplasmi

76 ntibodies directed toward myeloperoxidase or proteinase 3 are detected in sera of patients with small

77 al models of disease that is induced by anti-proteinase 3 are less robust.

78 d primarily toward myeloperoxidase (MPO) and proteinase 3, are detected in the majority of patients w

79 ligands unmasked by neutrophil elastase and proteinase-3, as well as synthetic peptides with sequenc

80 rent specificities (ie, neutrophil elastase, proteinase 3, azurocidin, and/or others) can substitute

81 was not caused by polymorphic differences in proteinase 3 between effectors and targets.

82 protein C/APC binding receptor, can bind to proteinase 3 bound to Mac-1 on leukocytes, potentially b

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

84 rs or after incubation with PMN elastase and proteinase-3, but not cathepsin G.

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

86 -1 is released from activated neutrophils by proteinase 3 cleavage and that endogenous sSIRL-1 protei

87 eport here that both neutrophil elastase and proteinase-3 cleave the human PAR1 N terminus at sites d

88 -Ile25 and Tyr28-Phe29, whereas elastase and proteinase 3 cleaved at Thr16-Ser17 and Thr31-Ser32.

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

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

91 ntimicrobial peptide, LL-37, is liberated by proteinase 3 coincident with degranulation and secretion

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

93 Elastin degraded by proteinase 3 could distinguish between COPD participants

94 e-antigen (HLA)-A2.1-restricted peptide from proteinase 3, could be used to elicit CTLs from normal i

95 proteases (NSPs; elastase, cathepsin G, and proteinase-3) directly kill invading microbes.

96 e action of the neutrophil serine proteases (proteinase 3, elastase, azurocidin, and cathepsin G) on

97 dest antifungal activity, and azurocidin and proteinase 3 exhibited no significant fungistasis agains

98 yeloid cells was proportional to cytoplasmic proteinase 3 expression.

99 Cytoplasmic proteinase-3 expression was one log greater in CML blast

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

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

102 ancer is located in the second intron of the proteinase-3 gene and so may regulate more than one gene

103 myelocytic cells results in an inhibition of proteinase-3 gene expression and a reduction in nuclear

104 Proteinase-3 gene expression is confined to the promyelo

105 t the CG element alone is not sufficient for proteinase-3 gene expression.

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

107 activity from wound fluid, and that purified proteinase 3 had a similar caseinolytic profile and inhi

108 hereas neutrophil elastase, cathepsin G, and proteinase 3 have been known as granule-associated serin

109 sociated with increased neutrophil elastase, proteinase-3, IL-1beta, and CXCL8.

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

111 te adipose tissue) or cancer (RAGE/leukocyte proteinase-3 in bone metastases).

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

113 serine proteases elastase, cathepsin G, and proteinase-3, increasingly recognized as regulators of i

114 PR1) derived from the primary granule enzyme proteinase 3 induced peptide specific cytotoxic T lympho

115 e found that SIRL-1 shedding is prevented by proteinase 3 inhibition and by extracellular adherence p

116 implicated in granulopoietic regulation: pro-proteinase 3 inhibits granulocyte macrophage-colony-form

117 ts that the response against the autoantigen proteinase 3 is a central pathogenic feature of proteina

118 Proteinase 3 is a human polymorphonuclear leukocyte seri

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

120 Proteinase 3 is also processed at the COOH-terminal exte

121 This indicates that processing of proteinase 3 is distinct from that of cathepsin G.

122 Proteinase 3 is initially identified as a 35-kDa precurs

123 e, indicating that the processing enzyme for proteinase 3 is not dipeptidyl peptidase I.

124 Proteinase 3 is present in high concentration in the pri

125 Human proteinase-3 is one of three serine proteinases present

126 emonstrated that PR1, a peptide derived from proteinase 3, is a potential target for CML-specific T c

127 n HLA-A2-restricted nonopeptide derived from proteinase 3, kill leukemia cells and may contribute to

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

129 nase 3 and a complex of NB1 glycoprotein and proteinase 3 may initiate the activation of neutrophils

130 Proteinase-3 might mediate vasogenic edema during diabet

131 erically activates CD177-associated membrane proteinase 3 (mPR3), and in conjugation with several pro

132 oantibodies and T cells with specificity for proteinase 3 or myeloperoxidase, expressed on the surfac

133 severe disease to have antibodies to either proteinase 3 or myeloperoxidase.

134 y pathogenic autoantibodies directed against proteinase 3 or myeloperoxidase.

135 lysozyme and were not killed by azurocidin, proteinase 3, or lactoferrin.

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

137 -restricted leukemia-associated peptide from proteinase 3 (P3) and neutrophil elastase (NE) that is r

138 erived from the neutrophil granule proteases proteinase 3 (P3) and neutrophil elastase (NE), which ar

139 trophil elastase (NE), cathepsin G (CG), and proteinase-3 (P3) have in vitro convertase activity.

140 which selectively inhibited proPO-activating proteinase-3 (PAP-3).

141 atic activity of prophenoloxidase activating proteinase 3 (PAP3).

142 beled HLE, CG, myeloperoxidase, lactoferrin, proteinase 3, phenylmethylsulfonyl fluoride (PMSF)-inact

143 amide in inducing remission in patients with proteinase 3-positive AAV.

144 's granulomatosis (WG), are directed against proteinase-3 (PR-3), a serine proteinase which is locate

145 c autoantibodies (ANCA) with specificity for proteinase-3 (PR-3).

146 (MPO ANCA) versus ANCA with specificity for proteinase 3 (PR3 ANCA).

147 odels of both myeloperoxidase (MPO) ANCA and proteinase 3 (PR3) ANCA associated vasculitis have been

148 -neutrophil cytoplasmic antibody autoanigens proteinase 3 (PR3) and elastase induce detachment and cy

149 eutrophilic and monocytic proteases, such as proteinase 3 (PR3) and human neutrophil elastase (HNE),

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

151 The ANCA autoantigens proteinase 3 (PR3) and myeloperoxidase (MPO) are exclusi

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

153 genes, including 2 that encode autoantigens: proteinase 3 (PR3) and myeloperoxidase (MPO).

154 NCA) binding to neutrophil elastase (NE) and proteinase 3 (PR3) are detectable in most patients with

155 toplasmic antibodies (ANCA) directed against proteinase 3 (PR3) are diagnostic markers for the small

156 Human neutrophil elastase (HNE) and proteinase 3 (PR3) are structurally and functionally rel

157 neutrophil-specific receptor presenting the proteinase 3 (PR3) autoantigen on the neutrophil surface

158 primary granule proteins elastase (ELA2) and proteinase 3 (PR3) both contain the nonapeptide PR1, whi

159 arbor antibodies not only to the autoantigen proteinase 3 (PR3) but also to complementary PR3 (cPR3(1

160 Elastase and proteinase 3 (PR3) cleave multimeric VWF and FRETS-VWF73

161 Longitudinal changes in proteinase 3 (PR3) gene expression were evaluated using

162 trophil elastase (NE), cathepsin G (CG), and proteinase 3 (PR3) have been identified in these short-l

163 Proteinase 3 (PR3) is a major autoantigen in patients wi

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

165 Proteinase 3 (PR3) is an abundant serine protease of neu

166 Although proteinase 3 (PR3) is known to have the potential to pro

167 Proteinase 3 (PR3) is the main target antigen of antineu

168 Proteinase 3 (PR3) is the target of anti-neutrophil cyto

169 ANCAs directed against proteinase 3 (PR3) or myeloperoxidase (MPO) bind their c

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

171 Membrane bound proteinase 3 (PR3) plays a key role in this microenviron

172 toplasmic antibodies (ANCA) directed against proteinase 3 (PR3) with a cytoplasmic immunofluorescence

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

174 face molecule that has been reported to bind proteinase 3 (PR3), a serine protease released from acti

175 We report here that expression of proteinase 3 (PR3), a serine protease, is down-regulated

176 The presence of anti-GBM, anti-proteinase 3 (PR3), and anti-myeloperoxidase (MPO) antib

177 vated neutrophils, neutrophil elastase (NE), proteinase 3 (PR3), and cathepsin G (Cat G).

178 ine proteases, neutrophil elastase (HNE) and proteinase 3 (PR3), are aberrantly expressed in human my

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

180 Proteinase 3 (PR3), the major target autoantigen in Wege

181 3 activation was mediated by serine protease proteinase 3 (PR3), which is present in the cytosol of a

182 To determine whether pro-proteinase 3 (PR3)-ANCA levels are a better measure of d

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

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

185 rophil cytoplasmic antibodies (ANCA) against proteinase 3 (PR3).

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

187 Neutrophil proteases, proteinase-3 (PR3) and elastase play key roles in glomer

188 cking for direct pathogenicity of human anti-proteinase-3 (PR3) antibodies in development of systemic

189 Anti-proteinase-3 (PR3) mAb and serum containing PR3-ANCA fro

190 Abs, it was found that soluble EPCR binds to proteinase-3 (PR3), a neutrophil granule proteinase.

191 As IL-32 is activated by proteinase-3 (PR3), we determined the effect of the seri

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

193 culitis and the positivity of ANCA targeting proteinase-3 (PR3-ANCA) or myeloperoxidase (MPO-ANCA).

194 hepsin G [CG], neutrophil elastase [NE], and proteinase 3 [PR3]) are expressed specifically in mature

195 We have determined whether granule proteins proteinase 3(PR3) and/or myeloperoxidase (MPO) are inter

196 cells, raised against a peptide contained in proteinase 3, preferentially lysed fresh human leukemic

197 Human neutrophil elastase (HNE) and proteinase 3 (PRO3) are myeloid tissue-restricted serine

198 However, the proteinase-3 promoter is not active in HeLa cells which

199 Within the first 200 base pairs of the proteinase-3 promoter, two elements were identified as i

200 DPPI or lacked both neutrophil elastase and proteinase 3 protected mice from NCGN induced by anti-MP

201 encoding alpha(1)-antitrypsin (SERPINA1) and proteinase 3 (PRTN3) (P=6.2x10(-89), P=5.6x10(-12,) and

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

203 al band-shift patterns to that obtained with proteinase-3 PU.1 and CG elements.

204 we found that monoclonal antibodies against proteinase 3 removed caseinolytic activity from wound fl

205 Neither bcr-abl nor proteinase 3 sequences were isolated.

206 on overexpression of proteinase 3, and that proteinase 3-specific CTL could be used for leukemia-spe

207 Proteinase 3-stimulated renal and lung MECs triggered CD

208 Proteinase 3, stored in the azurophilic granules, is exp

209 n the genes encoding neutrophil elastase and proteinase-3, target proteases inhibited by M/NEI.

210 a serine proteinase, nominally identified as proteinase-3, that hydrolyzed cell surface CD49e.

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

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

213 cy of T cells recognizing the PR1 epitope of proteinase 3 was not significantly different in allodepl

214 Analysis by flow cytometry showed that proteinase 3 was overexpressed in the leukemia targets c

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

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

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

218 rum, Azu-1 levels, but not total elastase or proteinase 3, were significantly reduced (P < .0001).

219 eases (neutrophil elastase, cathepsin G, and proteinase 3), which require cathepsin C activity for pr

220 (NSPs) cathepsin G, neutrophil elastase, and proteinase 3, which are enzymes that modulate inflammati

221 NH4Cl did not prevent the processing of the proteinase 3 zymogen into the mature form, suggesting th