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 All patients had ANCA reactive against proteinase 3.

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

5 when exposed to leukemia that overexpressed proteinase 3.

6 n of myeloid leukemia cells that overexpress proteinase 3.

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

8 antineutrophil cytoplasmic antibody antigen proteinase 3.

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

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

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

12 All had ANCA reacting with proteinase-3.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

62 Recombinant proteinase-3 applied to human brain microvascular endoth

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

81 yeloid cells was proportional to cytoplasmic proteinase 3 expression.

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

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

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

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

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

87 Proteinase-3 gene expression is confined to the promyelo

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

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

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

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

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

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

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

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

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

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

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

99 Proteinase 3 is a human polymorphonuclear leukocyte seri

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

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

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

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

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

105 Proteinase 3 is present in high concentration in the pri

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

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

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

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

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

111 Proteinase-3 might mediate vasogenic edema during diabet

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

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

114 y pathogenic autoantibodies directed against proteinase 3 or myeloperoxidase.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

155 3 activation was mediated by serine protease proteinase 3 (PR3), which is present in the cytosol of a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

179 Proteinase 3-stimulated renal and lung MECs triggered CD

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

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

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

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

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

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

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

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

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

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

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

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