ライフサイエンスコーパス: convertase

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

2 se, C3 products and partially stabilizes the convertase.

3 the inhibition of the alternative pathway C3 convertase.

4 mably preventing the formation of the C4bC2a convertase.

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

6 cell surface by accelerating the decay of C3 convertase.

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

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

9 1 and MASP-2 cleave C4 and C2 to generate C3 convertase.

10 cleavage by the nephritic factor-stabilized convertase.

11 y corresponding to a functional form of this convertase.

12 ing the inactivation of the cell-surface APC convertase.

13 nd is integral to the formation of C3 and C5 convertase.

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

15 hrough the activity of furin-like proprotein convertases.

16 0.7 mum but did not bind to other proprotein convertases.

17 ely, autoantibodies that target the C3 or C5 convertases.

18 ional rearrangements are required to form C3 convertases.

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

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

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

22 ta-cells process proinsulin using prohormone convertase 1/3 (PC1/3) and then prohormone convertase 2

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

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

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

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

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

28 e convertase 1/3 (PC1/3) and then prohormone convertase 2 (PC2), this finding has not been verified i

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

30 We found that PC2 proprotein convertase activity contributes to this pattern of ligan

31 tor B antibodies enhance alternative pathway convertase activity in vitro, confirming their pathogeni

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

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

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

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

36 n important function in classical pathway C5 convertase activity.

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

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

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

40 ptide precursors, subtilisin-like prohormone convertases, amidated products, and receptors) in ciliar

41 on the activator, enabling assembly of a C3 convertase and downstream alternative pathway amplificat

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

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

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

45 uential proteolytic processing by prohormone convertases and carboxypeptidase E.

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

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

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

49 Both the receptor-bound toxin and the convertases are of very low abundance at the cell surfac

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

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

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

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

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

55 t inhibits both classical and alternative C3 convertases by accelerating their spontaneous decay.

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

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

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

59 ated by autoantibodies that stabilize the C3 convertase C3bBb.

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

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

62 ing to and inhibiting the function of the C3 convertase, C3bBb.

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

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

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

66 strategy to prevent the formation of the C3 convertase C4bC2a by the rapid conversion of surface bou

67 e event in PC1 at 3048 aa and the proprotein convertase cleavage (PPC) event in fibrocystin at 3616 a

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

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

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

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

72 ophin, was released by furin-like proprotein convertase cleavage.

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

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

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

76 the bacterial surface but no longer forms a convertase complex.

77 We aimed to study the role of the pro-ANP convertase Corin in the pathogenesis of DN.

78 a membrane-bound receptor of C3b/C4b, C3/C5 convertase decay accelerator, and cofactor for factor I-

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

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

81 Protein convertase enzymatic activity is required for PD-1 expre

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

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

84 Here, we show that the role of C5 convertase enzymes in MAC assembly extends beyond the cl

85 V802 turnover was not mediated by complement convertase enzymes.

86 MACs need to be assembled locally by the C5 convertase enzymes.

87 The proprotein convertase family of enzymes includes seven endoprotease

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

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

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

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

92 bitor and structural characterization of the convertase formed by C4b is lacking.

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

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

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

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

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

98 of SARS-CoV-2 is preactivated by proprotein convertase furin, reducing its dependence on target cell

99 the protoxins, which can use the proprotein convertases Furin and PC7 for activation.

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

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

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

103 ession on T cells, and inhibition of protein convertase improves T-cell targeting of microsatellite i

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

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

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

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

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

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

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

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

112 monstrate that hC3Nb2 inhibits the substrate-convertase interaction by binding to the MG3 and MG4 dom

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

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

115 Furin, a proprotein convertase, is highly expressed in high-grade serous car

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

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

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

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

120 AA (for classical and alternative pathway C3 convertases), named decay cofactor protein, we show that

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

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

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

124 FURIN is a proprotein convertase (PC) responsible for proteolytic activation o

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

126 Proprotein convertases (PC) activate precursor proteins that play c

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

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

129 Proprotein convertases (PCs) are highly specific proteases required

130 The proprotein convertases (PCs) form a family of nine secretory subtil

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

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

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

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

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

136 ggesting diminished activation of the proNGF convertase, plasmin.

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

138 Propeptides of proprotein convertases regulate activation of their protease domain

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

140 elerating factor (DAF/CD55), a complement C3 convertase regulator, crucially controls disease in muri

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

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

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

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

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

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

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

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

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

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

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

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

153 PCSK9i (proprotein convertase subtilisin kexin type 9 inhibitors) reduce lo

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

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

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

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

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

159 lonal antibodies directed against proprotein convertase subtilisin-kexin type 9 (PCSK9) have been sho

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

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

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

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

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

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

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

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

168 The impact of lipid lowering by proprotein convertase subtilisin-kexin type 9 inhibition in such pa

169 Cholesterol reduction with proprotein convertase subtilisin-kexin type 9 inhibitors reduces is

170 ss-of-function variants in PCSK9 (proprotein convertase subtilisin-kexin type 9) are associated with

171 Previous trials of PCSK9 (proprotein convertase subtilisin-kexin type 9) inhibitors demonstra

172 oclonal antibody directed against proprotein convertase subtilisin-kexin type 9, is widely used in ad

173 ran inhibits hepatic synthesis of proprotein convertase subtilisin-kexin type 9.

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

175 Proprotein convertase subtilisin-like/kexin type 9 (PCSK9) is a key

176 WT (wild type) or PCSK9 (proprotein convertase subtilisin-like/kexin type-9) gain-of-functio

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

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

179 Proprotein convertase subtilisin/kexin 9 (PCSK9) is a key regulator

180 Proprotein convertase subtilisin/kexin 9 (PCSK9) is responsible for

181 cholesterol due to inhibition of proprotein convertase subtilisin/kexin 9 (PCSK9) reduces cardiovasc

182 PCSK9 (proprotein convertase subtilisin/kexin 9) inhibitors have been show

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

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

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

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

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

188 regulated upon hypoxia was PCSK6 (proprotein convertase subtilisin/kexin type 6).

189 cholesterol with an inhibitor of proprotein convertase subtilisin/kexin type 9 (PCSK9) after acute c

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

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

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

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

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

195 Proprotein convertase subtilisin/kexin type 9 (PCSK9) deficiency le

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

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

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

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

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

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

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

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

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

205 rescription include ezetimibe and proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, w

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

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

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

209 study has shown that circulating proprotein convertase subtilisin/kexin type 9 (PCSK9) levels correl

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

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

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

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

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

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

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

217 RISPR treatment for repression of proprotein convertase subtilisin/kexin type 9 (PCSK9), a gene that,

218 y was aimed at evaluating whether proprotein convertase subtilisin/kexin type 9 (PCSK9), a key regula

219 index, blood glucose, endothelin, proprotein convertase subtilisin/kexin type 9 (PCSK9), adhesion mol

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

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

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

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

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

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

226 emann-Pick C1-Like 1 (NPC1L1) and proprotein convertase subtilisin/kexin type 9 (PCSK9), respectively

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

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

229 V infection induced expression of proprotein convertase subtilisin/kexin type 9 (PCSK9), which reduce

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

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

232 reduced the circulating levels of proprotein convertase subtilisin/kexin type 9 (PCSK9).

233 nstatin medications (ezetimibe or proprotein convertase subtilisin/kexin type 9 [PCSK9] inhibitors) t

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

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

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

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

238 The Proprotein Convertase Subtilisin/Kexin type 9 genetic score finding

239 Surprisingly the Proprotein Convertase Subtilisin/Kexin type 9 genetic score, known

240 the opposite was observed for the Proprotein Convertase Subtilisin/Kexin type 9 genetic score.

241 -Methylglutaryl-CoA Reductase and Proprotein Convertase Subtilisin/Kexin type 9 genetic scores should

242 in clearance (the effect of these Proprotein Convertase Subtilisin/Kexin type 9 genotypes) may contri

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

244 The proprotein convertase subtilisin/kexin type 9 inhibitor evolocumab

245 Proprotein convertase subtilisin/kexin type 9 inhibitor therapy is

246 Alirocumab, a proprotein convertase subtilisin/kexin type 9 inhibitor, lowers lip

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

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

249 , there is interest in leveraging proprotein convertase subtilisin/kexin type 9 inhibitors as a thera

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

251 PCSK9i (protein convertase subtilisin/kexin type 9 inhibitors) are set t

252 sepsis clinical trials involving proprotein convertase subtilisin/kexin type 9 inhibitors.

253 Proprotein convertase subtilisin/kexin type 9 is a central regulato

254 s in hepatocytes, and knocks down proprotein convertase subtilisin/kexin type 9 level in mouse serum

255 Proprotein convertase subtilisin/kexin type 9 loss-of-function decr

256 Proprotein convertase subtilisin/kexin type 9 loss-of-function is a

257 In contrast to the adult host, proprotein convertase subtilisin/kexin type 9 loss-of-function is d

258 Proprotein convertase subtilisin/kexin type 9 monoclonal antibodies

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

260 Proprotein convertase subtilisin/kexin type 9 single-nucleotide pol

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

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

263 erive greater benefit from PCSK9 (proprotein convertase subtilisin/kexin type 9) inhibition has not b

264 to determine the effect of PCSK9 (proprotein convertase subtilisin/kexin type 9) inhibition on the ri

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

266 se events by alirocumab, a PCSK9 (proprotein convertase subtilisin/kexin type 9) inhibitor.

267 trials have suggested that PCSK9 (proprotein convertase subtilisin/kexin type 9) inhibitors are safe

268 PCSK9 (proprotein convertase subtilisin/kexin type 9) inhibitors reduce li

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

270 sis through regulating the PCSK9 (proprotein convertase subtilisin/kexin type 9) levels.

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

272 b, an antibody that blocks PCSK9 (proprotein convertase subtilisin/kexin type 9), was associated with

273 out), LDLr-KO/APOB100, and PCSK9 (proprotein convertase subtilisin/kexin type 9)-overexpressing mice

274 (adenoviral vector overexpressing proprotein convertase subtilisin/kexin type 9).

275 In contrast, bile acids, proprotein convertase subtilisin/kexin type 9, acetate, and acetoac

276 sopressin and Septic Shock Trial, Proprotein Convertase Subtilisin/Kexin type 9, and 3-Hydroxy-3-Meth

277 e-nucleotide polymorphisms, serum proprotein convertase subtilisin/kexin type 9, and lipid profiles i

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

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

280 and higher levels of circulating proprotein convertase subtilisin/kexin type 9.

281 Proprotein convertase subtilisin/kexin type-9 (PCSK9) is a ligand o

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

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

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

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

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

287 PCSKs (Proprotein convertase subtilisins/kexins) are a protease family wit

288 e not associated with changes in polyprotein convertase subtisilin/kexin type 9 concentrations.

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

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

291 herein surface-deposited C3b participates in convertases that cleave C3, thereby depositing more C3b.

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

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

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

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

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

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

298 B (a component of the alternative pathway C3 convertase) were found in a significantly higher proport

299 for binding to the alternative pathway C3bBb convertase, whereas SCR-1 is dispensable.

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