ライフサイエンスコーパス: convertase

1 , via formation of C3-activating enzymes (C3 convertases).

2 cell surface by accelerating the decay of C3 convertase.

3 cal for the interaction of C3 with the AP C3 convertase.

4 block formation and/or activity of the AP C3-convertase.

5 1 and MASP-2 cleave C4 and C2 to generate C3 convertase.

6 cleavage by the nephritic factor-stabilized convertase.

7 y corresponding to a functional form of this convertase.

8 pting components and regulators of the AP C3-convertase.

9 nd promoted formation of an overactive C3/C5 convertase.

10 evented assembly of the classical pathway C3-convertase.

11 o C3b and subsequent inhibition of the AP C3 convertase.

12 ulted from the formation of a hyperactive C3 convertase.

13 se, C3 products and partially stabilizes the convertase.

14 mably preventing the formation of the C4bC2a convertase.

15 comparably to wild-type (WT) C3 to form a C3 convertase.

16 hrough the activity of furin-like proprotein convertases.

17 0.7 mum but did not bind to other proprotein convertases.

18 cell surface by accelerating the decay of C3 convertases.

19 d by a series of steps involving fluid-phase convertases.

20 thepsin D and K, kallikrein 4 and proprotein convertases.

21 ysis by metalloproteinase N-arginine dibasic convertase 1 (NRD1) and leads to the significant inducti

22 e linked to reduced expression of prohormone convertase 1 (PC1).

23 p-FLCs were neuroendocrine genes: prohormone convertase 1 (PCSK1); neurotensin; delta/notch-like EGF

24 otein convertases (PCs) furin and proprotein convertase 1/3 (PC1) cleave substrates at dibasic residu

25 Proprotein convertase 1/3 (PC1/3) deficiency, an autosomal-recessiv

26 tor 15, and unexpectedly Tgr5 and prohormone convertase 1/3 gene expression in the ileum.

27 pKa of the conserved histidine in proprotein convertase 1/3 is acid-shifted compared with furin and i

28 The proprotein convertase 1/3 is expressed in the regulated secretory p

29 thin the propeptides of furin and proprotein convertase 1/3 using a histidine hydrogen-deuterium exch

30 k at a pH of 6.5 while a paralog, proprotein convertase 1/3, activates in secretory vesicles at a pH

31 ype 1 gene (PCSK1), which encodes proprotein convertase 1/3, causes a severe multihormonal disorder m

32 n of two members of the family of prohormone convertases 1 and 2 (PC1 and PC2).

33 he eukaryotic proteases furin and proprotein convertase-1/3.

34 for the productive maturation of proprotein convertase 2 (proPC2) to an active enzyme form; this act

35 immortalized human hepatocytes inhibited C3 convertase activity and complement-dependent cytolysis o

36 hrombin-mediated complement component 5 (C5) convertase activity leads to the generation of C5a (anap

37 rmed on a properdin surface and inhibits the convertase activity of a reconstituted C3bBb complex in

38 cally HCV-infected patient sera inhibited C3 convertase activity, further implicating HCV-specific im

39 l culture-conditioned medium and inhibits C3 convertase activity.

40 d medium, suggesting that CD55/sCD55 impairs convertase activity.

41 nts with anti-FB Abs selectively enhanced C3 convertase activity; IgG from patients with anti-C3b/ant

42 ce of Thr(373) in either the C3 substrate or convertase-affiliated C3b impaired C3 activation and ops

43 In contrast to other zymogen proprotein convertases, all incompletely matured intermediates of S

44 development and/or in adulthood, but certain convertases also exhibit complementary, redundant, or op

45 reorganization increases stability of the C3 convertase and facilitates recruitment of fluid-phase C3

46 P activation, although assembly of active C5 convertase and formation of the terminal complement prod

47 form or regulate the alternative pathway C3 convertase and has opened the door to new therapeutic ap

48 in cluster 3 had prevalent activation of C3 convertase and highly electron-dense intramembranous dep

49 recombinant hybrid protein stabilized the C3 convertase and reduced factor H-mediated convertase deca

50 ons caused by severe dysregulation of the C3 convertase and, in particular, those that involve nephri

51 the assembly of the classical pathway C3/C5 convertases and C4b binding to regulators.

52 ow that MERS-S is a substrate for proprotein convertases and demonstrate that processing by these enz

53 by sterically preventing C5 from binding to convertases and explain the exquisite selectivity of ecu

54 ivation and provides insights into how other convertases and proteases may regulate their precise spa

55 ively, attenuating the activity of the C3/C5 convertases and, consequently, avoiding serious damage t

56 xes of the pathways, C3 proconvertase and C3 convertase, as well as the unbound zymogen C2 obtained b

57 intracellularly and by all three proprotein convertases at the cell surface.

58 clusively dependent on prior cleavage by the convertases, because both R198A and R221A lack protein C

59 AP) providing stabilization of the C3 and C5 convertases, but its oligomeric nature challenges struct

60 did not inhibit regulation of solid-phase C3 convertase by FH and did not inhibit terminal complement

61 nzymatic complex, the alternative pathway C3 convertase, by targeting a functional "hot spot" on the

62 r frequency of rare and novel variants in C3 convertase (C3 and CFB) and complement regulator (CFH, C

63 H2O) to form C3b,Bb or a novel cell-bound C3 convertase [C3(H2O),Bb], which normally is present only

64 eriolysis but binds the AP proconvertase, C3 convertase, C3 products and partially stabilizes the con

65 stal structure of the alternative pathway C3 convertase C3bBb, which is in accordance with their iden

66 ated by autoantibodies that stabilize the C3 convertase C3bBb.

67 e (C3bB), which is cleaved by factor D to C3 convertase (C3bBb).

68 Both Abs also bind the preformed convertase, C3bBb, and provide powerful inhibition of co

69 properdin; stabilization of the alternative convertase, C3bBb, is well accepted, whereas the role of

70 of a stabilized form of the active CP/LP C3 convertase C4b2a is strikingly similar to the crystal st

71 component C2 within C4b2 resulting in the C3 convertase C4b2a.

72 ts specifically at the level of the CP/LP C3 convertase (C4b2a).

73 both C4 and C2, allowing formation of the C3 convertase, C4bC2a.

74 and GF monomer are linked before proprotein convertase cleavage and how much conformational change o

75 s still cleaved by these PCs, revealing that convertase cleavage can precede thrombin activation.

76 We conclude that prior convertase cleavage of protein C in hepatocytes is criti

77 f basic residues at the predicted proprotein convertase cleavage site blocks proprotein processing, r

78 ructure of pro-TGF-beta1 with the proprotein convertase cleavage site mutated to mimic the structure

79 in mediates the assembly of stabilized C3/C5-convertase clusters, which helps to localize complement

80 und that albicin binds and stabilizes the C3-convertase complex (C3bBb) formed on a properdin surface

81 The crystal structure of such a FP-convertase complex suggests that the major contact betwe

82 C2, are indispensable constituents of the C3 convertase complex, C4bC2a, which is formed by both the

83 functional FB blocked the formation of AP C3 convertase complexes (C3bBb) on ULVWF strings.

84 C3 convertase and reduced factor H-mediated convertase decay.

85 However, blockade of proprotein convertases did not impact MERS-S-dependent transduction

86 impact C3b/C4b binding, it does inhibit this convertase disassociating capability.

87 show that TNF-alpha stimulates the TNF-alpha convertase enzyme (TACE/a disintegrin and metalloprotein

88 beta-Site amyloid precursor protein convertase enzyme 1 (BACE1), a type I transmembrane aspa

89 hich cause pathological stabilization of the convertase enzyme and confer resistance to innate contro

90 has a direct impact on the expression of the convertase enzyme carboxypeptidase E (CPE) by inhibition

91 V802 turnover was not mediated by complement convertase enzymes.

92 dysregulation of the alternative pathway C3 convertase, even in the presence of C3 nephritic factors

93 The proprotein convertase family of enzymes includes seven endoprotease

94 eavage sites for proteases of the proprotein convertase family that match the cleavage products.

95 PC7 belongs to the proprotein convertase family, whose members are implicated in the c

96 sing several tests for alternative C3 and C5 convertase formation and regulation, we identified two g

97 e contrary, by binding C3b, FHR-1 allowed C3 convertase formation and thereby enhanced complement act

98 oreover inhibited already at the level of C3-convertase formation due to an interaction between PRELP

99 D, and target protein-and Mg(2+) to allow C3 convertase formation.

100 hereby blocking an interaction essential for convertase formation.

101 ass-3 semaphorins, by furin-like pro-protein convertases (FPPC).

102 be remarkably conserved, suggesting that the convertases from the classical and alternative pathways

103 canonical consensus site for the proprotein convertase Furin (RXXR) between the pro- and the catalyt

104 Here, we show that the proprotein convertase furin is responsible for pro-OCN maturation i

105 rtase-knock-out mice showed that loss of the convertase furin or PC5/6 in hepatocytes results in a ap

106 The proprotein convertase furin requires the pH gradient of the secreto

107 lic tail of PC7 were replaced by that of the convertase furin, lost its ability to cleave the recepto

108 activation by the subtilisin-like proprotein convertase furin.

109 , mouse proprotein C is first cleaved by the convertases furin, PC5/6A, and PACE4.

110 ns that form a hyperactive or deregulated C3 convertase have been identified in Factor B (FB) ligand

111 Unlike other proprotein convertases, however, this retention is permanent, inhib

112 he indispensable role of alternative pathway convertase in amplifying complement cascades, its inhibi

113 omplex with factor B, thereby locking in the convertase in an inactive state.

114 molecular model for the classical pathway C5 convertase in complex with C5, suggesting that C3b incre

115 show that MERS-S is processed by proprotein convertases in MERS-S-transfected and MERS-CoV-infected

116 ides insight into the function of proprotein convertases in nervous system development.

117 n 1) domains of C3b, which likely impairs C3-convertase inactivation by regulatory proteins.

118 This system can be activated in a convertase-independent manner from intracellular stores

119 component C5 and prevents its cleavage by C5 convertases, inhibiting release of both the proinflammat

120 n additional mechanism by which SCIN couples convertase inhibition to direct blocking of phagocytosis

121 light the ability of a particular proprotein convertase inhibitor to effectively reduce the maturatio

122 antly affected by incubation with proprotein convertase inhibitors for up to 8 h, arguing against a m

123 rm a curly vertex that holds together the AP convertase, interacting with both the C345C and vWA doma

124 that the major contact between FP and the AP convertase is mediated by a single FP thrombospondin rep

125 vity to increase inhibition of the C3 and C5 convertases is protective against renal IRI, and the add

126 Indeed, plasma analyses of single-proprotein convertase-knock-out mice showed that loss of the conver

127 model using stable shRNA-induced proprotein convertase knockdown indicate that only furin is the maj

128 stable protease complexes, denominated C3/C5 convertases, leading to inflammation and lysis.

129 t mutations that formed either an overactive convertase (M433I) or a convertase resistant to decay by

130 somerization by cyclophilin B and proprotein convertase-mediated L2 minor capsid protein cleavage tha

131 XXR(179)/S(180)AE subtilisin-like proprotein convertase motif.

132 lthough islet beta cells express AbetaPP and convertases necessary for Abeta production.

133 ty of these antibodies to dysregulate the C3 convertase on the surface of endothelial cell was measur

134 Regulatory proteins inactivate C3/C5 convertases on host surfaces to avoid collateral tissue

135 ove to the cell surface where the proprotein convertase PACE4 selectively supports IRB maturation.

136 The first seven members of the proprotein convertase (PC) family activate protein precursors by cl

137 The secretory proprotein convertase (PC) family comprises nine members: PC1/3, PC

138 ed serpin family inhibitor of the proprotein convertase (PC), furin, that exhibits high specificity b

139 ggesting cleavage by a furin-like proprotein convertase (PC).

140 elix loop helix 2 (NHLH2) and the prohormone convertase PC1 (encoded by PCSK1) were reduced in PWS pa

141 Proprotein convertases (PCs) are crucial in the processing and entr

142 Prohormone convertases (PCs) are endoproteases that process many su

143 Proprotein convertases (PCs) are highly specific proteases required

144 ion depend on PC7 and the related proprotein convertases (PCs) Furin and Pace4 and that these proteas

145 The proprotein convertases (PCs) furin and proprotein convertase 1/3 (P

146 The proprotein convertases (PCs) furin, PC5, PACE4, and PC7 cleave secr

147 The proprotein convertases (PCs) furin, PC5/6, and PACE4 exhibit unique

148 The proprotein convertases (PCs) play an important role in protein prec

149 ies, and mutational analysis that proprotein convertases (PCs) proteolytically process human Pxdn at

150 The propeptides of proprotein convertases (PCs) regulate activation of cognate proteas

151 H and was dependent on furin-like proprotein convertases (PCs).

152 fter intracellular processing by pro-protein convertases (PCs).

153 secreted factors, including the pro-protein convertase PCSK1, which is strongly associated with huma

154 instead lost because of deficiencies in its convertase, proprotein convertase subtilisin/kexin type

155 ctivation of C5 by the complement pathway C5 convertase rather than by non-C proteases.

156 Propeptides of proprotein convertases regulate activation of their protease domain

157 into the importance of CFHR proteins for C3 convertase regulation and identify a genetic variation i

158 Soluble CR1 restored defective C3 convertase regulation; however, neither eculizumab nor t

159 cate that only furin is the major proprotein convertase required for HA5 cleavage.

160 either an overactive convertase (M433I) or a convertase resistant to decay by FH (K298Q).

161 y limited proteolysis mediated by proprotein convertase(s) (PCs) along the secretory pathway.

162 e is also cleaved by a furin-like proprotein convertase(s) (PCs) at KKRSHLKR(199) downward arrow (und

163 ciently activate complement as far as the C3 convertase stage in comparison with PCh-BSA and PCh-cont

164 Since the discovery of proprotein convertase subtilisin kexin 9 (PCSK9) in 2003, this PC h

165 The proprotein convertase subtilisin kexin isozyme 1 (SKI-1)/site 1 pro

166 The proprotein convertase subtilisin kexin isozyme-1 (SKI-1)/site-1 pro

167 acellular endogenous inhibitor of proprotein convertase subtilisin kexin type 9 (PCSK9) activity on c

168 ptor, apolipoprotein B (APOB), or proprotein convertase subtilisin kexin type 9 (PCSK9) genes.

169 Proprotein convertase subtilisin kexin type 9 (PCSK9) inhibitors pr

170 ith beta-blockers, ezetimibe, and proprotein convertase subtilisin kexin type 9 (PCSK9) inhibitors, a

171 Proprotein convertase subtilisin kexin type 9 (PCSK9) levels are fr

172 Proprotein convertase subtilisin kexin type 9 (PCSK9) promotes the

173 Levels of proprotein convertase subtilisin kexin type 9 (PCSK9) vary markedly

174 45, a monoclonal antibody against proprotein convertase subtilisin kexin type 9 (PCSK9), on Lp(a).

175 Monoclonal antibodies against proprotein convertase subtilisin kexin type 9 (PCSK9), such as evol

176 oclonal antibody directed against proprotein convertase subtilisin kexin type 9 (PCSK9), to enable su

177 f cholesterol-lowering drugs, the proprotein convertase subtilisin kexin-9 inhibitors.

178 monoclonal antibody that inhibits proprotein convertase subtilisin-kexin type 9 (PCSK9) and lowers lo

179 monoclonal antibody that inhibits proprotein convertase subtilisin-kexin type 9 (PCSK9) and reduces l

180 Pharmacologic inhibitors of proprotein convertase subtilisin-kexin type 9 (PCSK9) are being eva

181 A new class of drugs that inhibit proprotein convertase subtilisin-kexin type 9 (PCSK9) has been deve

182 Findings from clinical trials of proprotein convertase subtilisin-kexin type 9 (PCSK9) inhibitors ha

183 aging evidence of the efficacy of proprotein convertase subtilisin-kexin type 9 (PCSK9) inhibitors; h

184 , and data on LDL cholesterol and proprotein convertase subtilisin-kexin type 9 (PCSK9) levels were a

185 nt that inhibits the synthesis of proprotein convertase subtilisin-kexin type 9 (PCSK9), a target for

186 monoclonal antibody that inhibits proprotein convertase subtilisin-kexin type 9 (PCSK9), has been sho

187 zed monoclonal antibody targeting proprotein convertase subtilisin-kexin type 9 (PCSK9), reduces leve

188 monoclonal antibody that inhibits proprotein convertase subtilisin-kexin type 9 (PCSK9), significantl

189 locumab, a monoclonal antibody to proprotein convertase subtilisin-kexin type 9 (PCSK9).

190 he renal epithelial expression of proprotein convertase subtilisin-like kexin type 9, a key regulator

191 Proprotein convertase subtilisin/kexin (PCSK) enzymes convert propr

192 ted region in the promoter of the proprotein convertase subtilisin/kexin 9 (PCSK9) gene that was asso

193 onger-term efficacy and safety of proprotein convertase subtilisin/kexin 9 (PCSK9) inhibitors in seco

194 ntly reported that >30% of plasma proprotein convertase subtilisin/kexin 9 (PCSK9) is bound to LDL, t

195 ance antibody-based inhibitors of preprotein convertase subtilisin/kexin 9 (PCSK9) produce reductions

196 Monoclonal antibodies to proprotein convertase subtilisin/kexin 9 (PCSK9) reduce LDL cholest

197 in receptor, apolipoprotein B, or proprotein convertase subtilisin/kexin 9.

198 The proprotein convertase subtilisin/kexin enzymes proteolytically conv

199 cytes was reduced, and intestinal proprotein convertase subtilisin/kexin type 1 (Pcsk1) expression, t

200 r caused by rare mutations in the proprotein convertase subtilisin/kexin type 1 (PCSK1) gene, has bee

201 etamine regulated transcript, and proprotein convertase subtilisin/kexin type 1 inhibitor.

202 ucleotide polymorphisms (SNPs) in proprotein convertase subtilisin/kexin type 1 with modest effects o

203 Proprotein convertase subtilisin/kexin type 2 (PCSK2) is a prohormo

204 f deficiencies in its convertase, proprotein convertase subtilisin/kexin type 5 (PCSK5), causing inac

205 Proprotein convertase subtilisin/kexin type 9 (PCSK9) and inducible

206 reported to individually bind the proprotein convertase subtilisin/kexin type 9 (PCSK9) and regulate

207 onoclonal antibodies that inhibit proprotein convertase subtilisin/kexin type 9 (PCSK9) are an emergi

208 Gain-of-function mutations of the proprotein convertase subtilisin/kexin type 9 (PCSK9) are associate

209 Proprotein convertase subtilisin/kexin type 9 (PCSK9) binds low-den

210 Proprotein convertase subtilisin/kexin type 9 (PCSK9) binds to LDL

211 Proprotein convertase subtilisin/kexin type 9 (PCSK9) binds to the

212 dy was to determine the effect of proprotein convertase subtilisin/kexin type 9 (PCSK9) deficiency on

213 Proprotein convertase subtilisin/kexin type 9 (PCSK9) down-regulate

214 LDLR) degradation mediated by the proprotein convertase subtilisin/kexin type 9 (PCSK9) has been exte

215 Soluble proprotein convertase subtilisin/kexin type 9 (PCSK9) has been show

216 g-term safety and efficacy of the proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor evo

217 The proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor evo

218 ways suggest use of ezetimibe and proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors in

219 Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors su

220 Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors we

221 Monoclonal antibodies targeting proprotein convertase subtilisin/kexin type 9 (PCSK9) is a new lipi

222 The secreted protein proprotein convertase subtilisin/kexin type 9 (PCSK9) is a promisin

223 Proprotein convertase subtilisin/kexin type 9 (PCSK9) is an importa

224 Do elevated proprotein convertase subtilisin/kexin type 9 (PCSK9) levels consti

225 Proprotein convertase subtilisin/kexin type 9 (PCSK9) modulates low

226 Proprotein convertase subtilisin/kexin type 9 (PCSK9) plays a key r

227 Proprotein convertase subtilisin/kexin type 9 (PCSK9) plays an impo

228 to determine the LDL-ApoB-100 and proprotein convertase subtilisin/kexin type 9 (PCSK9) production ra

229 Proprotein convertase subtilisin/kexin type 9 (PCSK9) regulates low

230 Proprotein convertase subtilisin/kexin type 9 (PCSK9) selectively b

231 human monoclonal antibody against proprotein convertase subtilisin/kexin type 9 (PCSK9) serine protea

232 logic-based strategies to inhibit proprotein convertase subtilisin/kexin type 9 (PCSK9) show promise

233 ) binds to its negative regulator proprotein convertase subtilisin/kexin type 9 (PCSK9) through the f

234 Proprotein convertase subtilisin/kexin type 9 (PCSK9) was shown to

235 monoclonal antibodies that block proprotein convertase subtilisin/kexin type 9 (PCSK9), a circulatin

236 ively modulated the expression of proprotein convertase subtilisin/kexin type 9 (PCSK9), a protein th

237 ver, in the presence of exogenous proprotein convertase subtilisin/kexin type 9 (PCSK9), a protein th

238 (LDLR), apolipoprotein B (APOB), proprotein convertase subtilisin/kexin type 9 (PCSK9), and LDL prot

239 Several mutations in the apoB, proprotein convertase subtilisin/kexin type 9 (PCSK9), and MTP gene

240 ully human monoclonal antibody to proprotein convertase subtilisin/kexin type 9 (PCSK9), demonstrated

241 onoclonal antibodies that bind to proprotein convertase subtilisin/kexin type 9 (PCSK9), lowering LDL

242 rocumab, a monoclonal antibody to proprotein convertase subtilisin/kexin type 9 (PCSK9), lowers plasm

243 locumab, a monoclonal antibody to proprotein convertase subtilisin/kexin type 9 (PCSK9), reduced LDL

244 monoclonal antibody that inhibits proprotein convertase subtilisin/kexin type 9 (PCSK9), significantl

245 5), a monoclonal antibody against proprotein convertase subtilisin/kexin type 9 (PCSK9), significantl

246 human monoclonal antibody against proprotein convertase subtilisin/kexin type 9 (PCSK9), significantl

247 y monoclonal antibodies targeting proprotein convertase subtilisin/kexin type 9 (PCSK9).

248 ab, a monoclonal antibody against proprotein convertase subtilisin/kexin type 9 (PCSK9).

249 Importantly, reduced proprotein convertase subtilisin/kexin type 9 activity increases re

250 Plasma proprotein convertase subtilisin/kexin type 9 and total cholesterol

251 Using proprotein convertase subtilisin/kexin type 9 as a representative p

252 t altered vascular pathology in a proprotein convertase subtilisin/kexin type 9 gain-of-function athe

253 ding DNA sequence variants in the proprotein convertase subtilisin/kexin type 9 gene (PCSK9) lower pl

254 ry cost-effectiveness analyses of proprotein convertase subtilisin/kexin type 9 inhibitor (PCSK9i) we

255 The proprotein convertase subtilisin/kexin type 9 inhibitor evolocumab

256 ) vs 0.61 (95% CI, 0.58-0.65) for proprotein convertase subtilisin/kexin type 9 inhibitors (P = .25).

257 Proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9i) a

258 ein B-containing lipoproteins and proprotein convertase subtilisin/kexin type 9 inhibitors hold promi

259 Proprotein convertase subtilisin/kexin type 9 monoclonal antibodies

260 neered to encode gain-of-function proprotein convertase subtilisin/kexin type 9 mutants, and mice wer

261 ol, lathosterol, campesterol, and proprotein convertase subtilisin/kexin type 9 plasma concentrations

262 ly human monoclonal antibodies to proprotein convertase subtilisin/kexin type 9 published in the last

263 Inhibition of proprotein convertase subtilisin/kexin type 9 serine protease (PCSK

264 comprehensive data that targeting proprotein convertase subtilisin/kexin type 9 very effectively redu

265 ic analysis has identified PCSK9 (proprotein convertase subtilisin/kexin type 9) as a crucial gene in

266 t of sdAbs targeting human PCSK9 (proprotein convertase subtilisin/kexin type 9) as an alternative to

267 PCSK9 (proprotein convertase subtilisin/kexin type 9) has emerged as an im

268 The PCSK9 (proprotein convertase subtilisin/kexin type 9) inhibitor evolocumab

269 PCSK9 (proprotein convertase subtilisin/kexin type 9) is a negative regula

270 man monoclonal antibody to PCSK9 (proprotein convertase subtilisin/kexin type 9), markedly reduces lo

271 ich can be achieved by inhibiting proprotein convertase subtilisin/kexin type 9, may decrease the sys

272 Single injections of proprotein convertase subtilisin/kexin type 9-encoding recombinant

273 Proprotein convertase subtilisin/kexin type-9 (PCSK9) is a secreted

274 Proprotein convertase subtilisin/kexin type-9 (PCSK9, a hepatic LDL

275 or trials, pharmacological PCSK9 (proprotein convertase subtilisin/kexin type-9) inhibition was not a

276 The archetype proprotein convertase subtilisin/kexin, FURIN, is a direct target g

277 Here we show that proprotein convertase subtilisin/kexin-6 (PCSK6, also named PACE4;)

278 Recently approved proprotein convertase subtilisin/kexin-type 9 inhibitors and mipome

279 rt that furin is unique among the proprotein convertases subtilisin/kexin in being highly expressed i

280 m by members of the family of the proprotein convertases subtilisin/kexin.

281 Congenital deficiency of the proprotein convertase subtilisine/kexin type 1 gene (PCSK1), which

282 2, regulates the maturation of the TNF-alpha convertase (TACE), which controls shedding of TNF-alpha

283 approach is to target the protease TNF-alpha convertase (TACE), which releases TNF-alpha from cells.

284 can be triggered by autoantibodies to the C3 convertase, termed nephritic factors, which cause pathol

285 Furin is a ubiquitous proprotein convertase that cleaves after basic residues and transfo

286 weakly promote assembly of the classical C3 convertase that is further suppressed in the presence of

287 Inhibition of PACE4, a proprotein convertase that is overexpressed in prostate cancer, has

288 al cell lines indicated that PC7 is the only convertase that sheds this receptor into the medium.

289 and mouse tetramer-forming tryptases are MMP convertases that mediate cartilage damage and the proteo

290 m for assembly of the proteolytically active convertases that mediate downstream complement activatio

291 provides insight into the function of the C3 convertase, the differential involvement of C3 activity

292 nd facilitates recruitment of fluid-phase C3 convertase to the cell surfaces.

293 athogen surfaces, properdin stabilizes C3/C5 convertases to efficiently fight infection.

294 rotein dimers and then cleaved by proprotein convertases to release the C-terminal domain as an activ

295 binding of host complement inhibitors of C3 convertase, viz.

296 In PAM-1/OSX, a cleavage site for furin-like convertases was exposed, generating a shorter form of me

297 its major function in stabilizing the C3bBb convertase, was found to bind both exogenous and endogen

298 We identified that members of the proprotein convertase were rate-limiting enzymes in the truncation

299 wArg cleavage motif of furin-like proprotein convertases, whereas the cleavage motif of FRA (Pro-X-X-

300 s express phc2, a neural specific prohormone convertase, which suggests that they form an early activ