ライフサイエンスコーパス: classical pathway

1 c UFA synthesis is distinct from that of the classical pathway.

2 natural IgM antibody and propagated via the classical pathway.

3 D, NFKB1, and TACI) selectively activate the classical pathway.

4 uld lead to activation of complement via the classical pathway.

5 s not cause injury through activation of the classical pathway.

6 group leads to failure of signaling via this classical pathway.

7 uired by the alternative pathway but not the classical pathway.

8 ay of complement and is not dependent on the classical pathway.

9 by immune complexes occurs primarily by the classical pathway.

10 -that could mediate its nuclear import via a classical pathway.

11 eration of pathogenic antibodies through the classical pathway.

12 ctivity for the C3 and C5 convertases of the classical pathway.

13 I/R injury is mediated via the lectin and/or classical pathway.

14 cked by Brefeldin A, suggesting export via a classical pathway.

15 ical role for OAT1 in the functioning of the classical pathway.

16 ement is relatively inactive compared to the classical pathway.

17 onservation of the mode of activation of the classical pathway.

18 at H. felis activates complement through the classical pathway.

19 pA may inhibit complement deposition via the classical pathway.

20 the complement cascade is initiated via the classical pathway.

21 aved C4b are catalyzed by antibodies via the classical pathway.

22 e thymocytes required the lectin but not the classical pathway.

23 by delaying the synthesis of C3b through the classical pathway.

24 at binds C1q, the recognition protein of the classical pathway.

25 between components C1q, C1r, and C1s of the classical pathway.

26 ative Pathway compared with that made by the Classical Pathway.

27 lement activation via the alternative or the classical pathway.

28 rs derived from cells that had activated the Classical Pathway.

29 T3 predominantly activated complement by the classical pathway.

30 sequent activation of complement through the classical pathway.

31 y of the complement system is older than the classical pathway.

32 re effective than factor H at inhibiting the classical pathway.

33 rum (NHS) allows C. albicans to initiate the classical pathway.

34 own to interact with other activators of the classical pathway.

35 he more potent inhibition of only C1s of the classical pathway.

36 ific inhibition of either the alternative or classical pathway.

37 d mechanistically distinct inhibitors of the classical pathway.

38 Complement C1q is the activator of the classical pathway.

39 CDC," remained to be dependent on C1 and the classical pathway.

40 ways, whereas pneumolysin inhibited only the classical pathway.

41 tion of endogenous antigens by MHC-I via the classical pathway.

42 early steps of complement activation via the classical pathway.

43 nhances complement C3 deposition through the classical pathway.

44 nanobody prevents C3 deposition through the classical pathway.

45 s deposited on pneumococci primarily via the classical pathway.

46 he lectin/alternative pathways or C4b in the classical pathway.

47 nner analogous to that of C1r and C1s of the classical pathway.

48 inB2, and this depended on components in the classical pathway.

49 in machinery and mediate signalling via 'non-classical' pathways.

50 To explore the mechanism, classical pathway-activating immune complexes were infus

51 anisms appear to be partially independent of classical pathway activation and apoptotic cell clearanc

52 C4BP, secondary to kinetically overwhelming classical pathway activation and possibly increased alte

53 , the molecular mechanisms governing optimal classical pathway activation are unknown.

54 nonenveloped icosahedral virus CP inhibiting classical pathway activation at C1.

55 actors demonstrated that HAstV CP suppresses classical pathway activation at the first component, C1.

56 the specific serum components necessary for classical pathway activation by F. tularensis in nonimmu

57 In contrast, classical pathway activation by high-titer antibody over

58 Ab-dependent classical pathway activation is required for complement-

59 tion was not blocked on MCP(+) cells because classical pathway activation occurred before substantial

60 Classical pathway activation was less robust than TNF-in

61 Classical pathway activation was observed in 90.5% of TM

62 he bacterium is opsonized by C3 cleavage via classical pathway activation within the alveolus, provid

63 ment pathway inhibitor) and also by limiting classical pathway activation.

64 mation of the active C1 complex required for classical pathway activation.

65 ollowing CRP interaction and thereby inhibit classical pathway activation.

66 embled by the initiating complex (C1) of the classical pathway, activation of complement component C5

67 Pooled NHS was rendered free of classical pathway activity by chelation of serum Ca2+ wi

68 by a week, resulted in profound reduction of classical pathway activity lasting for at least 7 weeks.

69 age fluid contains C3 protein and functional classical pathway activity that mediates the binding of

70 , SP-A blocked the ability of C1q to restore classical pathway activity to C1q-depleted serum.

71 dose-dependently reduces free C2 levels and classical pathway activity.

72 ternative pathway activity without affecting classical pathway activity.

73 These data indicate that blockade of the classical pathway alone (C1q) is protective against perm

74 mouse embryo fibroblasts was mediated by the classical pathway and by an alternative or second pathwa

75 may help to explain how deficiencies of the classical pathway and certain pentraxins lead to impaire

76 d C1q activate complement; C1q activates the classical pathway and MBL the lectin pathway.

77 17 was responsible for the activation of the classical pathway and the observed killing of FX517 as o

78 t that was activated via the alternative and classical pathways and cleaved C3b to fragments of 68, 4

79 ent landscape of cell competition, including classical pathways and models, fitness fingerprint mecha

80 i-fHbp MAbs elicited greater C4b deposition (classical pathway) and greater bactericidal activity tha

81 easured complement activation products, C4d (classical pathway) and SC5b-9 (terminal pathway), at the

82 the complement system, predominantly via the classical pathway, and causes increased C4 activation an

83 iated C3 activation but had no effect on the classical pathway, and N-glycans in IgG were required by

84 ms the initial and rate-limiting step in the classical pathway, and sterol 27-hydroxylase (CYP27A1) i

85 ernative pathway as well as C4 and C2 of the classical pathway are required for complement-dependent

86 Here we have identified C1q in the classical pathway as required for activation of compleme

87 As in the classical pathway, BCR-induced ERK activation in the new

88 ree main mechanisms of action; these are the classical pathway, beta-arrestin scaffold signaling, and

89 g isotype, cannot activate complement by the classical pathway, binds more avidly to an inhibitory th

90 Both MAbs were potent activators of the classical pathway but poor facilitators of alternative p

91 tudies have confirmed the importance of many classical pathways but also revealed novel pathways.

92 Activation of the classical pathway by immune complexes leads to the gener

93 lling of gonococcal strains that inhibit the classical pathway by recruiting C4BP.

94 ement cascade appears to be mediated via the classical pathway by the binding of C1q to ligands in AP

95 antibody against the first component of the classical pathway, C1q, were resistant to experimental B

96 n the well-defined activation complex of the classical pathway, C1qC1r(2)C1s(2), and the composition

97 f Crry and DAF in regulating alternative and classical pathway C3 activation.

98 by dissociating the catalytic domain of the classical pathway C3 convertase.

99 Ps exhibited full activity against the human classical pathway C3 convertase.

100 the C1 complex and prevented assembly of the classical pathway C3-convertase.

101 dy we examined the C5 cleaving properties of classical pathway C3/C5 convertase either bound to the s

102 findings differ from those reported for the classical pathway C3/C5 convertase, where only one of fo

103 are probably involved in the assembly of the classical pathway C3/C5 convertases and C4b binding to r

104 nvertases were similar to those reported for classical pathway C3/C5 convertases, studies on the abil

105 CD81 exosome marker-normalized ADE levels of classical pathway C4b, alternative pathway factor D and

106 alternative pathway C3bBb compared with the classical pathway C4b2a were tested in classical pathway

107 ent origin, while a homologous member of the classical pathway (C4bpalpha) appeared later in evolutio

108 h the classical pathway C4b2a were tested in classical pathway C5 convertase (C4b2a3b) assays.

109 l domain of C3b has an important function in classical pathway C5 convertase activity.

110 e propose an overall molecular model for the classical pathway C5 convertase in complex with C5, sugg

111 t the 6-9-fold greater catalytic rate of the classical pathway C5 convertase may compensate for the f

112 Pathway activity, but when measured for the Classical Pathway, C6des-748-914 was only 4-6% as effect

113 ind to and are internalized by ECs via a non-classical pathway, CAM-mediated endocytosis.

114 complement cascade via the antibody-mediated classical pathway can initiate red blood cell (RBC) dest

115 According to the "classical" pathway, CD4 cells secrete cytokines, such as

116 r and vitreous inhibited the activity of the classical pathway (CH(50)).

117 This review emphasizes that both the lack of classical pathway complement activation and excessive ac

118 appears to be at least partly independent of classical pathway complement activation by C1q.

119 n-initiated bystander and antibody-triggered classical pathway complement activation in vitro, result

120 P) that functions to inhibit alternative and classical pathway complement activation.

121 which promote C1q binding, the first step in classical pathway complement activation.

122 The classical pathway complement regulator C4b-binding prote

123 -/-) -Crry(+/+) or wild-type erythrocytes to classical pathway complement-mediated C3 deposition in v

124 pathway protein factor B (Bf(-/-)) or in the classical pathway component C4 (C4(-/-)).

125 Mice deficient in the classical pathway component complement component 4 (C4)

126 of complement activation is critical, while classical pathway components are entirely dispensable.

127 in MyoD-expressing fibroblasts deficient in classical pathway components RelA/p65, inhibitor of kapp

128 In contrast, inherited deficiency of classical pathway components, particularly C1q, is power

129 The classical pathway contributes to IC and apoptotic cell c

130 hough excessive activation of the lectin and classical pathways contributes to multiple autoimmune an

131 l hemolysis after forceful activation of the classical pathway could be reduced by blocking the AP.

132 ial recognition cascades that constitute the classical pathway (CP) and lectin pathway (LP).

133 inhibited the AP with minimal effect on the classical pathway (CP) and no effect on the lectin pathw

134 or decay-accelerating activity (DAA) for the classical pathway (CP) C3 and C5 convertases and, using

135 ese three mutants were also resistant to the classical pathway (CP) C5 convertase, with sensitivities

136 A promising therapeutic approach may be classical pathway (CP) inhibition at the level of early

137 onsiderable attention, little is known about classical pathway (CP) inhibition by meningococci, which

138 Activation of the classical pathway (CP) of complement is often associated

139 The classical pathway (CP) of complement may contribute to t

140 endent cytotoxicity (CDC) of B cells via the classical pathway (CP) of complement.

141 , the complement system is activated via the classical pathway (CP), the lectin pathway (LP), or the

142 ding; enhanced C3b and factor Bb binding was classical pathway dependent.

143 ted by either the alternative pathway or the classical pathway, depending on the concentration of ser

144 athway-mediated C3 cleavage, hC3Nb3 inhibits classical pathway-driven hemolysis, suggesting that the

145 Recently, a role has been suggested for the classical pathway during innate immunity that is activat

146 e also compared the performance of TPIEA and classical pathway enrichment analysis, and TPIEA present

147 MAbs but exhibited reduced support of early classical pathway-facilitated accumulation of C3.

148 pattern is consistent with engagement of the classical pathway followed by amplification through the

149 Exogenous GAD followed the classical pathway for antigen processing, with an absolu

150 ells lacking protein kinase C (PKC)beta, the classical pathway for BCR signaling is blocked, whereas

151 These data demonstrate the vital role of the classical pathway for innate immunity to a bacterial pat

152 However, the functional importance of the classical pathway for innate immunity to S. pneumoniae a

153 thway for pERK operates in parallel with the classical pathway for pERK, whereas PKCdelta phosphoryla

154 ion of STAT1, indicating divergence from the classical pathway for terminating IFN-gamma-signaling.

155 DNA in digitonin-permeabilized cells via the classical pathway for the nuclear transport of karyophil

156 this study, we report that the alternate and classical pathways for BCR signaling are differentially

157 ls, whereas the established mediators of the classical pathways for beta(2) integrin activation (PKC,

158 ve, Lyn-dependent alternate pathway, and the classical pathway, for BCR signaling operate in parallel

159 The classical pathway, found throughout higher eukaryotic or

160 Although the classical pathway had been assumed to be the major pathw

161 ntification of different costimulators, this classical pathway has been shown to significantly impact

162 oradiography of radiolabeled protein; 2) for classical pathway hemolytic activity; 3) for susceptibil

163 s not required for B cell activation via the classical pathway; however, Lyn is indispensable and irr

164 Among the initiators of the classical pathway, IgG deposition contributes most of th

165 The classical pathway implicated in ubiquitination of the ep

166 ontaneously activated complement through the classical pathway in normal and immunoglobulin-deficient

167 tudy demonstrating an important role for the classical pathway in promoting SCI, it is likely that th

168 Btk appears to regulate directly the classical pathway in response to BAFF such that Btk-defi

169 in Candida albicans and comparison with the classical pathway in Saccharomyces cerevisiae have revea

170 ation and suggest a predominant role for the classical pathway in stimulating alloimmunity.

171 mplification via the lectin pathway than the classical pathway in the generation of C3/C5 convertases

172 ssible scenario, which parallels that of the classical pathway, in which MASP-1 and MASP-2 are found

173 luding binding to C4b-binding protein (C4BP; classical pathway inhibitor) and factor H (alternative p

174 There are major 2 types of NHEJ: (1) the classical pathway initiated by the Ku complex, and (2) t

175 pathway plays a critical role in amplifying classical pathway initiated complement activation.

176 ransglutaminase 2 (TG2) is secreted by a non-classical pathway into the extracellular space, where it

177 The classical pathway involved the IkappaB kinase (IKK)beta-

178 e of vesicles into astrocytes follows a more classical pathway involving dynamin, clathrin, sorting e

179 he lower CPE dose was shown to proceed via a classical pathway involving mitochondrial membrane depol

180 on of NF-kappaB is partially mediated by the classical pathway involving the interaction between the

181 ntation through mechanisms distinct from the classical pathways involving H-2DM molecules.

182 Because the classical pathway is an important and specific mediator

183 ay for BCR signaling is blocked, whereas the classical pathway is little affected.

184 The classical pathway is more efficient at inducing CD8 cell

185 complement, and recent data suggest that the classical pathway is required for complement factor C3 d

186 activation through the alternative, but not classical, pathway is required to initiate antibody-indu

187 aracterized import pathway, often termed the classical pathway, is utilized by many basic-type (lysin

188 gG1-Lec 1 was deficient in activation of the classical pathway, it had a superior capacity to activat

189 ve the activation of fetal complement by the classical pathway leading to the formation of membrane a

190 three pathways of complement activation, the classical pathway, lectin pathway, and alternative pathw

191 fold or if Mg(2+)-EGTA was used to block the classical pathway, MCP efficiently inhibited C3b deposit

192 Thus, for the classical pathway, MCP is the cofactor for C4b cleavage

193 hrocyte lysis by both the reactive lysis and classical pathway mechanisms.

194 were operative, group II MAbs induced early classical pathway-mediated binding of C3 but reduced the

195 ingly, although the nanobody does not affect classical pathway-mediated C3 cleavage, hC3Nb3 inhibits

196 pecific for the APC C3/C5 convertase because classical pathway-mediated hemolysis is unaffected by 3E

197 , and both C4 molecules equally restored the classical pathway-mediated hemolytic activity of serum d

198 Furthermore, hC4Nb8 inhibits the classical pathway-mediated immune complex delivery to fo

199 hritis, DAF serves as the primary barrier to classical pathway-mediated injury, while CD59 limits con

200 greater deposition of C1q and thus increased classical-pathway-mediated C3 deposition.

201 While the classical pathway mediating this response is via mTOR in

202 From this, it follows that the classical pathway might be needed in order to kick-start

203 e duplication that gave rise to the earliest classical pathway molecules.

204 B cells, serum IgE, and likely activated the classical pathway of anaphylaxis.

205 se (Cyp7a1), the rate-limiting enzyme in the classical pathway of bile acid synthesis, has been impli

206 ydroxylase, the rate-limiting enzyme for the classical pathway of bile salt synthesis.

207 The classical pathway of complement (CP) can mediate C3 opso

208 rior functional data suggest that C1s in the classical pathway of complement activated by, e.g., anti

209 These studies show that BrkA inhibits the classical pathway of complement activation and prevents

210 a Ca(2+)-dependent manner and augmented the classical pathway of complement activation but protected

211 d prevented erythrocyte lysis by controlling classical pathway of complement activation by cleaving t

212 t recombinant PepO specifically inhibits the classical pathway of complement activation in both hemol

213 dies reveal an important role for C1q in the classical pathway of complement activation in the develo

214 component C1, the complex that initiates the classical pathway of complement activation, is a 790-kDa

215 C1, the first protein of the classical pathway of complement activation, is a calcium

216 C1q is the recognition component of the classical pathway of complement activation.

217 anifest hyperacute rejection mediated by the classical pathway of complement activation.

218 tivation of the innate immune system via the classical pathway of complement activation.

219 r membrane porin (Por) molecules to bind the classical pathway of complement down-regulatory protein

220 man fetal neurons activate spontaneously the classical pathway of complement in an antibody-independe

221 tribution of CRP's ability of activating the classical pathway of complement in the protection of mic

222 odies with limited abilities to activate the classical pathway of complement in vitro have been impli

223 The classical pathway of complement is activated upon bindin

224 The classical pathway of complement is crucial to the immune

225 Results demonstrated that the classical pathway of complement mediated serum neutraliz

226 bs may be capable of directly activating the classical pathway of complement under certain circumstan

227 In situ activation of the classical pathway of complement was evident by depositio

228 Sle1c Crry and their ability to regulate the classical pathway of complement were not significantly d

229 natural IgM and the early components of the classical pathway of complement work in concert to neutr

230 We found that glomerular IgM activates the classical pathway of complement, but it does not cause s

231 ce binding of IgM, a potent activator of the classical pathway of complement, to both Rd and NT127.

232 e protease, C1r, initiates activation of the classical pathway of complement, which is a crucial inna

233 ng that blocking resulted from inhibition of classical pathway of complement.

234 preserving important immune functions of the classical pathway of complement.

235 -induced inflammation can be mediated by the classical pathway of complement.

236 92 was delayed, suggesting regulation of the classical pathway of complement.

237 ndependent of CRP-mediated activation of the classical pathway of complement.

238 esults in antibody-dependent killing via the classical pathway of complement.

239 important role for natural antibody and the classical pathway of complement.

240 mplement C1 that initiates activation of the classical pathway of complement.

241 ally specific natural IgM that activates the classical pathway of complement.

242 resulting from enhanced serum killing by the classical pathway of complement.

243 are sequentially activated and initiate the classical pathway of complement.

244 use natural antibodies and activation of the classical pathway of complement.

245 and antibody-antigen complexes [6,7] in the classical pathway of complement.

246 ween starter molecules of hemostasis and the classical pathway of complement.

247 m the conformational model suggested for the classical pathway of complement.

248 s in increased sensitivity to killing by the classical pathway of complement.

249 s inhibits killing by the antibody-dependent classical pathway of complement; however, susceptibility

250 of quiescent fibroblast does not induce the classical pathway of NF-kappaB activation through Ikappa

251 In addition to the classical pathway of secretion, some transmembrane prote

252 the early components (C1, C4, or C2) of the classical pathway of the complement cascade is one of th

253 C2, yet play a role in both alternative and classical pathways of complement activation.

254 eumoniae, thereby reducing activation of the classical pathway on the bacterial surface.

255 ns at the level of the second enzyme of this classical pathway or of the noninducible system had no s

256 actor 4 (C4-/-), a critical component of the classical pathway, or factor B (fB-/-), an essential pro

257 Furthermore, the classical pathway, partially targeted by the binding of

258 In the classical pathway, pathogen-bound antibody recruits the

259 Together, these data suggest that the classical pathway plays a major role in complement activ

260 hysiological action of the early part of the classical pathway protects against the development of SL

261 ically have autoantibodies to the complement classical pathway protein C1q.

262 er hand, homozygous deficiency of any of the classical pathway proteins is strongly associated with t

263 Furthermore, mice deficient in classical pathway proteins were not protected from injur

264 de sialylation of N. gonorrhoeae resulted in classical pathway regulation as evidenced by decreased C

265 ypass the requirements for engagement of the classical pathway remain to be defined but do not appear

266 ured to examine activation of the lectin and classical pathways, respectively.

267 rowing evidence that proteins fold through a classical pathway sequence of native-like intermediates

268 plement activation occurred primarily by the classical pathway, since a deficiency in the C4 componen

269 reperfusion injury compared with wild-type, classical pathway-specific C1q-deficient mice, or MBL-de

270 ses suggest that SGSs are secreted via a non-classical pathway that involves cleavage into a 300-kDa

271 ting system for novel cell biology even with classical pathways that have been studied extensively in

272 However, unlike the classical pathway, the alternative pathway is also depen

273 In the classical pathway, the ER binds directly to an estrogen

274 Although IgG can activate the classical pathway, there also is evidence that alternati

275 ent surface deposition of complement via the classical pathway, thereby contributing to the ability o

276 scussed in terms of the energy landscape and classical pathway time regimes of folding, for which the

277 ed significantly below basal levels, whereas classical pathway titers were unchanged.

278 The proposed model for ClyA represents a non-classical pathway to attack eukaryotic host cells.

279 Blocking either the classical pathway (treatments with EGTA-Mg2+ or soluble

280 factor-induced AP complement activation, and classical pathway-triggered AP complement amplification

281 ogens or altered self through the lectin and classical pathways, two of the three well-established ac

282 e borders, which are usually assigned in the classical pathway view of molecular events (e.g. signal

283 her antibody-mediated activation through the classical pathway was a major mechanism for complement a

284 n serum in untreated animals showed that the classical pathway was activated during the first 2 hours

285 When the classical pathway was blocked, group II and III MAbs mar

286 ent strain or a complemented mutant when the classical pathway was inactivated by depleting NHS of C1

287 , PspA also inhibited C3 deposition when the classical pathway was initiated by antibodies to capsula

288 The classical pathway was required in vitro, whereas complem

289 In nonimmune mouse serum, the classical pathway was the dominant activation pathway tr

290 alternative complement pathway, but not the classical pathway, was described in 2009.

291 To better understand the evolution of the classical pathway, we have evaluated the degree of funct

292 nt T cell disappearance, both the lectin and classical pathways were genetically ablated.

293 strain rates of quantal neurotransmission if classical pathways were solely responsible for vesicle r

294 C4, the complement components unique to the classical pathway, were not detected in the diabetic ret

295 Binding of LDL to CR1 is mediated via the classical pathway, whereas binding of acLDL is mediated

296 pneumoniae bound by C3 depends mainly on the classical pathway, whereas the intensity of C3 binding d

297 leted serum through both the alternative and classical pathways; whether Bf-1 possess similar activit

298 more familiar but evolutionarily more recent classical pathway, which is triggered by antibody bindin

299 on proceeds approximately 70-75% through the classical pathway while only approximately 25-30% seems

300 ent C1q and activation of complement via the classical pathway without any concomitant engagement of