ライフサイエンスコーパス: membrane attack complex

1 ts and promoting efficient generation of the membrane attack complex.

2 C5 cleavage and prevents the assembly of the membrane attack complex.

3 plement protein C5 initiates assembly of the membrane attack complex.

4 nd may facilitate assembly of the complement membrane attack complex.

5 ment molecule effecting cytotoxicity was the membrane attack complex.

6 e pathways as well as the neo-epitope of the membrane attack complex.

7 ting bactericidal activity of the complement membrane attack complex.

8 accine efficacy in the mouse vagina requires membrane attack complex.

9 the first step in the eventual formation of membrane attack complex.

10 and C5, thus preventing the formation of the membrane attack complex.

11 a and C5a, the opsonins C4b and C3b, and the membrane attack complex.

12 posits of IgG, IgM, and the C5b-9 complement membrane attack complex.

13 nant antibody targeting the pro-inflammatory membrane attack complex.

14 ve changed perceptions of the nature of this membrane attack complex.

15 lement injury by inhibiting formation of the membrane attack complex.

16 n of C5b, the initial component of the lytic membrane attack complex.

17 q, C3d, as well as C4BP and factor H but not membrane attack complex.

18 tection was due to the inability to form the membrane attack complex.

19 lement, regulating production of C5a and the membrane attack complex.

20 ently of the downstream generation of C5a or membrane attack complex.

21 ation to diverse osmotic stressors including membrane attack complexes.

22 tly reduced formations of anaphylatoxins and membrane-attack complexes.

23 ent components C1q and C3, in the absence of membrane attack complex activation and neutrophil infilt

24 GC B cell surfaces without the formation of membrane attack complex and activated C3a- and C5a-recep

25 ctor B siRNA resulted in decreased levels of membrane attack complex and angiogenic factors-vascular

26 evaluated the pathogenic roles of complement membrane attack complex and CD59, a key regulator that i

27 ces in understanding of the structure of the membrane attack complex and its by-product the fluid-pha

28 arkedly inhibits formation of the complement membrane attack complex and neutrophil elastase release,

29 9 to preformed C5b-C7 and C5b-C8 to form the membrane attack complex and no effect on the rate of C3a

30 Killing was mediated by complement membrane attack complex and not augmented in the presenc

31 ckout mice exhibited increased levels of the membrane attack complex and of vascular endothelial grow

32 The membrane attack complex and other pore-forming proteins

33 luding complement protein C1q, to induce the membrane attack complex and reactive super-oxygen specie

34 at the complement system involving C1q-C3-C4-membrane attack complex and ROS regulates exosome-mediat

35 echanism, resulting in the deposition of the membrane attack complex and subsequent bacterial lysis.

36 Membrane attack complexes and other osmotic stressors, n

37 of the host cell to lysis by its complement membrane attack complex, apparently by blocking the hCD5

38 of receptors for C3a and C5a, as well as the membrane attack complex, as effector mechanisms in the p

39 red activation of complement and assembly of membrane attack complex, as it was inhibited by soluble

40 t shows that the human CD59 protein inhibits membrane attack complex assembly and reduces tissue dama

41 ence, we suggest a model for an irreversible membrane attack complex assembly in which the C7 FIMs, b

42 teins C3 and C4, which do not participate in membrane attack complex assembly, suggests that this pro

43 onectin, which inhibits the formation of the membrane attack complex at the terminal stage of the com

44 ey RCA member that controls formation of the membrane attack complex at the terminal stage of the com

45 ivated C5b that occur during assembly of the membrane attack complex, but they likely involve some, p

46 2 gC-null virus, or whether formation of the membrane attack complex by C6 to C9 is required for neut

47 1-INH spares the alternative pathway and the membrane attack complex (C5-9) so innate antibacterial d

48 actor-alpha, IL-1beta, IL-10, and complement membrane attack complex C5b-9 concentrations using enzym

49 n of C4 and C3, as well as generation of the membrane attack complex C5b-9.

50 complex, but not lytic pore formation by the membrane attack complex C5b-9.

51 lex, thereby preventing the formation of the membrane attack complex (C5b-9 of complement).

52 s generates anaphylatoxins (C3a and C5a) and membrane attack complex (C5b-9) and opsonizes targeted c

53 Membrane attack complex (C5b-9) formation and Gram's sta

54 A critical role of the complement membrane attack complex (C5b-9) in mediating hyperacute

55 n that inhibits the assembly of the terminal membrane attack complex (C5b-9) of complement.

56 , as they prevented red blood cell lysis via membrane attack complexes (C5b-9) and the formation of c

57 m C3 to C5 cleavage, and generation of lytic membrane attack complexes (C5b-9) on surfaces of pathoge

58 ckers reduced ethanol-induced C3a/b, C4, and membrane attack complex/C5b9 formations; ROS production;

59 The inhibitor of the membrane attack complex, CD46, showed a significant posi

60 Selected biopsy specimens were stained for membrane attack complex, class I major histocompatibilit

61 As part of the membrane attack complex complement protein C9 is respons

62 embrane attack complex; it also binds to the membrane attack complex components C6 and C7 with high a

63 Historically, the membrane attack complex, composed of complement componen

64 anaphylatoxin-mediated inflammation and the membrane attack complex contribute to tissue injury.

65 ordingly, endothelial cell activation by the membrane attack complex depends on both transcriptional

66 enders R. conorii more susceptible to C3 and membrane attack complex deposition and to complement-med

67 plement inhibition, which leads to increased membrane attack complex deposition and VEGF expression.

68 eas HH402/VV62 hRPE cells showed significant membrane attack complex deposition following ingestion o

69 Excitotoxic sensitization did not increase membrane attack complex deposition on cortical neurons a

70 '-treated PIV5 PI cells had extensive C3 and membrane attack complex deposition, as well as productio

71 ent and coagulation activation, resulting in membrane attack complex deposition, severe intestinal ly

72 ions precedes, follows, or is independent of membrane attack complex deposition, what is the mechanis

73 r the third component of complement, C3, and membrane attack complex deposition.

74 vity and a marked reduction in tissue C3 and membrane attack complex deposition.

75 rovascular depletion, and that microvascular membrane attack complex deposits in dermatomyositis resu

76 The condition is of interest because membrane attack complex deposits result in shedding of c

77 ion of C3(-/-) and C4(-/-) mice lacked C3 or membrane attack complex deposits, despite having IgG dep

78 ency of CD59a, the membrane inhibitor of the membrane attack complex, did not induce an increase in n

79 Furthermore, we demonstrated that the membrane attack complex directly induced gene expression

80 The membrane attack complex does not appear to play a major

81 ain, whereas the heavy chain contains the FI membrane attack complex domain (FIMAC), CD5 domain, and

82 CD59, an inhibitor of the terminal cytolytic membrane attack complex, effectively protected the cells

83 ss executed either by the complement-related membrane attack complex, exotoxins, or cytotoxic T cells

84 ain plasma serine protease with one factor I-membrane attack complex (FIMAC) domain, one CD5 domain,

85 (-/-) mice is mediated through inhibition of membrane attack complex formation and not through C5a-in

86 of a subset of these mutated Abs to inhibit membrane attack complex formation as tested in a hemolys

87 ote, at very high C3b densities, we observed membrane attack complex formation in absence of C5-activ

88 -binding protein to bacteria, which enhances membrane attack complex formation on M. catarrhalis and

89 d in a loss of TER, which required transient membrane attack complex formation, activation of the alt

90 Interestingly, sublethal complement membrane attack complex formation, but not the anaphylat

91 unrelated to its function as an inhibitor of membrane attack complex formation.

92 ed to better terminal pathway activation and membrane attack complex formation.

93 nized with activated complement factor 3 and membrane attack complex from serum compared with the oth

94 to the MDR phenotype may result in abnormal membrane attack complex function.

95 to mediate effects; (ii) the multimolecular membrane attack complex generated from the five terminal

96 ting that complement activation to the C5b-9 membrane attack complex had a casual role in renal failu

97 of C6, a component of the terminal cytolytic membrane attack complex, had no effect on outcome after

98 ed proteins, endothelin-1 and the complement membrane attack complex have been recently identified as

99 C6-deficient rats, which cannot form the membrane attack complex, have a normal neuropathic pain

100 n of complement components C3 and C5b-9 (the membrane attack complex), however, was reduced on the su

101 ight on the important pathogenic role of the membrane attack complex in abdominal aortic aneurysm.

102 sembly of the pathogenic terminal complement membrane attack complex in both TM strains.

103 Insertion of the membrane attack complex in cell membranes of vascular en

104 The understanding of the role of the membrane attack complex in some TMAs has led to the intr

105 diate formation of the proinflammatory C5b-9 membrane attack complex, in functionally active form abl

106 with the role of C5, possibly by forming the membrane attack complex, in limiting OLG apoptosis in EA

107 and CD59, a key regulator that inhibits the membrane attack complex, in the development of abdominal

108 red protein that is functionally active as a membrane attack complex inhibitor.

109 r findings show that absent C3aR-, C5aR-, or membrane attack complex-initiated effector mechanisms ea

110 It is not clear whether membrane attack complex is activated by antibody-depende

111 e after ischemic stroke, indicating that the membrane attack complex is not involved in mediating inj

112 lop and ultimately our data confirm that the membrane attack complex is required to develop thromboti

113 ken together, our findings indicate that the membrane-attack complex is a key mediator of streaming.

114 In contrast, when the assembly of the membrane-attack complex is not properly regulated, as in

115 o C5b, the first step in the assembly of the membrane attack complex; it also binds to the membrane a

116 The membrane attack complex (MAC or C5b-9) is an important e

117 in that regulates formation of the cytolytic membrane attack complex (MAC or C5b-9) on host cell memb

118 ent by inhibiting formation of the cytolytic membrane attack complex (MAC or C5b-9).

119 Membrane attack complex (MAC) accumulation correlated wi

120 analysis were used to detect the presence of membrane attack complex (MAC) and C3 activation products

121 nied by endothelial deposition of C3 and the membrane attack complex (MAC) and medullary capillary th

122 D choroids to determine the abundance of the membrane attack complex (MAC) and performed immunofluore

123 loid peptide (A beta) and complement-derived membrane attack complex (MAC) are co-localized in senile

124 5b-9 complement components that comprise the membrane attack complex (MAC) are unclear.

125 lassical pathway leading to the formation of membrane attack complex (MAC) as the effector of cell in

126 In response to complement activation, the membrane attack complex (MAC) assembles from fluid-phase

127 plement regulator CD59a, designed to inhibit membrane attack complex (MAC) assembly at sites of C3b/i

128 CD59 is a key regulator of complement membrane attack complex (MAC) assembly.

129 I)-anchored protein that prevents complement membrane attack complex (MAC) assembly.

130 injury (CCI) reduced the terminal complement membrane attack complex (MAC) at the sciatic nerve injur

131 The C6 deficiency prevents the formation of membrane attack complex (MAC) by C5b-C9.

132 PGK interacted with the membrane attack complex (MAC) components C5, C7, and C9,

133 The absence of membrane attack complex (MAC) components in the gut ensu

134 Membrane attack complex (MAC) deposition in the arthriti

135 Western blot analysis further revealed that membrane attack complex (MAC) expression was up-regulate

136 t C3frag accumulation on activated surfaces, membrane attack complex (MAC) formation and hemolysis of

137 ion of complement activation by Crry, and of membrane attack complex (MAC) formation by CD59 was equa

138 as C5a receptor antagonism and prevention of membrane attack complex (MAC) formation did not have a s

139 Terminal complement membrane attack complex (MAC) formation is induced initi

140 We have shown that membrane attack complex (MAC) formation via the activati

141 to monkeys as demonstrated by inhibition of membrane attack complex (MAC) formation.

142 The complement membrane attack complex (MAC) forms transmembrane pores

143 Moreover, both IgG and complement membrane attack complex (MAC) immunoreactivity was evide

144 pore-forming terminal complement component, membrane attack complex (MAC) in pSC and nerve terminal

145 7BL/6 mice revealed the deposition of C3 and membrane attack complex (MAC) in the neovascular complex

146 olves lysis of cells by the insertion of the membrane attack complex (MAC) in the plasma membrane.

147 Yth53.1 monoclonal antibody neutralized the membrane attack complex (MAC) inhibitor CD59 and allowed

148 The membrane attack complex (MAC) is a hetero-oligomeric pro

149 The complement membrane attack complex (MAC) is classically known as a

150 The complement membrane attack complex (MAC) is formed by the sequentia

151 ement cascade and subsequent assembly of the membrane attack complex (MAC) occur in a number of patho

152 Cell surface assembly of the membrane attack complex (MAC) of complement occurs in a

153 Assembly of the membrane attack complex (MAC) of complement on EC membra

154 that inhibits the formation of the cytolytic membrane attack complex (MAC) of complement on host cell

155 ory protein CD59 increases deposition of the membrane attack complex (MAC) of complement, contributin

156 ed membrane-bound inhibitor of the cytolytic membrane attack complex (MAC) of complement.

157 oprotein CD59 inhibits assembly of the C5b-9 membrane attack complex (MAC) of human complement.

158 he principle cellular inhibitor of the C5b-9 membrane attack complex (MAC) of human complement.

159 The membrane attack complex (MAC) of the complement system i

160 tion of C4b and C3b and the formation of the membrane attack complex (MAC) on bacterial surfaces.

161 mmodation by preventing the formation of the membrane attack complex (MAC) on the accommodated graft.

162 f complement results in the formation of the membrane attack complex (MAC) on the cell surface, resul

163 bits the assembly of the terminal complement membrane attack complex (MAC) pore, whereas Streptococcu

164 minal complement proteins C5b to C9 form the membrane attack complex (MAC) pore.

165 an complement which kills Gram-negatives via membrane attack complex (MAC) pores.

166 e to prevent insertion and polymerization of membrane attack complex (MAC) pores.

167 study, we examined whether HCV regulates the membrane attack complex (MAC) via complement component C

168 plays a pivotal role in the formation of the membrane attack complex (MAC), an important antibacteria

169 ower levels of recipient C7 protein, soluble membrane attack complex (MAC), and IL-1beta expression c

170 ity of C5(-/-) mice to assemble the terminal membrane attack complex (MAC), as determined by compleme

171 igated the interactions among the complement membrane attack complex (MAC), CCL2, and VEGF that occur

172 ived effectors, opsonins, anaphylatoxins and membrane attack complex (MAC), have been implicated as d

173 t with rCD59-APT542 blocked the formation of membrane attack complex (MAC), increased apoptosis and d

174 he activity of the C9 component of the C5b-9 membrane attack complex (MAC), thereby protecting human

175 It plays an essential role in the membrane attack complex (MAC), which forms a lethal pore

176 Both C5a and the membrane attack complex (MAC), which is formed by the te

177 , we show that complement, specifically, the membrane attack complex (MAC)-mediated arm of complement

178 hat culminates in formation of the cytolytic membrane attack complex (MAC).

179 that form during assembly of the complement membrane attack complex (MAC).

180 assemble into a multimolecular complex, the membrane attack complex (MAC).

181 and C9) that interact to form the cytolytic membrane attack complex (MAC).

182 -bound inhibitor of the cytolytic complement membrane attack complex (MAC).

183 ittle attention has been paid to that of the membrane attack complex (MAC).

184 only described for the mammalian complement membrane attack complex (MAC).

185 C9 and thereby prevents the formation of the membrane attack complex (MAC).

186 components C1q, C3, factor B, factor H, and membrane attack complex (MAC).

187 The membrane attack complex (MAC)/perforin-like protein comp

188 lminating in the formation and deposition of membrane attack complex (MAC, C5b-9) in nerve membranes.

189 donor-specific antibody deposits complement membrane attack complexes (MAC) on graft endothelial cel

190 In response to membrane attack complexes (MAC), ZFYVE21 is post-transla

191 In addition, assembly of the membrane-attack complex (MAC) on ECs induced a 3-fold in

192 rial membranes to form the lethal pore-like "membrane attack complex" (MAC) of complement.

193 orm a porelike structure referred to as the "membrane attack complex" (MAC).

194 IR for C4d and C5b-9 (membrane attack complex, MAC) was observed in small numb

195 Internalization of complement membrane attack complexes (MACs) assembles NLRP3 inflamm

196 Electron microscopy of membrane attack complexes (MACs) generated using recombi

197 Complement membrane attack complexes (MACs) promote inflammatory fu

198 tem kills bacteria by the formation of lytic membrane attack complexes (MACs), triggered when complem

199 e terminates in the cell-surface assembly of membrane attack complexes (MACs), which promote inflamma

200 in immunosuppressed C6D rats, suggesting the membrane attack complex may play a minor role in recipie

201 l phenotype in FH(R/R) mice, consistent with membrane attack complex-mediated pathogenesis.

202 Human C8 is one of five components of the membrane attack complex of complement (MAC).

203 h is one of five components of the cytolytic membrane attack complex of complement (MAC).

204 become resistant against cytotoxicity by the membrane attack complex of complement (MAC).

205 poptosis and EC activation and injury by the membrane attack complex of complement are important mech

206 CD59 blocks formation of the membrane attack complex of complement by inhibiting bind

207 Both LTx and the membrane attack complex of complement form membrane pore

208 We investigated the potential role of the membrane attack complex of complement in primary nonfunc

209 Formation of the cytolytic membrane attack complex of complement on host cells is i

210 CD59, an inhibitor of the terminal cytolytic membrane attack complex of complement, had no effect on

211 shown that generation of sublytic C5b-9, the membrane attack complex of complement, induces oligodend

212 hereby preventing formation of the cytolytic membrane attack complex of complement.

213 nd the subsequent formation of the cytolytic membrane attack complex of complement.

214 brane protein that inhibits formation of the membrane attack complex of complement.

215 Human C8 is one of five components of the membrane attack complex of complement.

216 ored protein that regulates formation of the membrane attack complex of complement.

217 D concomitant with elevated formation of the membrane attack complex of complement.

218 nchored molecule, regulates formation of the membrane attack complex of the complement cascade.

219 ms membrane pores in a manner similar to the membrane-attack complex of C.

220 imicrobial peptides, and the assembly of the membrane-attack complexes of the immune system.

221 otoxic effects through the deposition of the membrane attack complex on oligodendrocytes.

222 Immunohistochemical studies showed membrane attack complex on small blood vessels in 6 of 8

223 ting that lysis was caused by formation of a membrane attack complex on the cell surface.

224 independent manner to assemble the cytolytic membrane attack complex on their membranes, whereas astr

225 e used human panel reactive antibody to form membrane attack complexes on allogeneic endothelial cell

226 enuated deposition of C3 fragments and C5b-9 membrane attack complexes on cell surfaces.

227 tide prevented the progressive deposition of membrane attack complexes on red blood cells (RBC) and s

228 erum killing by preventing the deposition of membrane attack complexes on the bacterial cell surface.

229 e roles of the C5a-C5aR1 axis and C5b-9 (the membrane attack complex) on kidney disease.

230 44 ng/ml) and normal (<=244 ng/ml) levels of membrane attack complex or terminal complement complex (

231 and C9) that interact to form the cytolytic membrane attack complex, or MAC.

232 and C-terminal modules and a central 40-kDa membrane attack complex perforin (MACPF) domain that has

233 e-forming member of an ancient branch of the Membrane Attack Complex-Perforin/Cholesterol-Dependent C

234 Perforin contains a membrane attack complex/perforin (MACPF) domain and olig

235 le, described in this manuscript, contains a membrane attack complex/perforin (MACPF) domain present

236 Two groups of PZ-encoded proteins, the membrane attack complex/perforin (MACPF) domain protein

237 ntervening 40-kDa segment referred to as the membrane attack complex/perforin (MACPF) domain.

238 Two recent crystal structures of membrane attack complex/perforin (MACPF) domains found i

239 We identified an insecticidal membrane attack complex/perforin (MACPF) protein, Mpf2Ba

240 diverse group of proteins exemplified by the membrane attack complex/perforin (MACPF), cholesterol-de

241 egment of each protein is referred to as the membrane attack complex/perforin domain (MACPF).

242 The P2 N-glycosylated extracellular membrane attack complex/perforin domain and the P2 domai

243 Hosts use PFTs, including members of the membrane attack complex/perforin protein family, to figh

244 n extended middle segment referred to as the membrane attack complex/perforin region (MACPF), and a p

245 two structurally distinct domains, a MACPF (membrane attack complex/PerForin) and a previously uncha

246 ron microscopy and fitted the C8alpha-MACPF (membrane attack complex/perforin)-C8gamma co-crystal str

247 Membrane attack complex/perforin-like (MACPF) proteins c

248 Membrane attack complex/perforin/cholesterol-dependent c

249 cad1) mutant, carrying a S205F mutation in a membrane-attack-complex/perforin (MACPF)-domain protein,

250 t CD59 (a potent inhibitor of the complement membrane attack complex present on red blood cells) was

251 Knockout of C6, a component of the membrane attack complex, prevented the aforementioned re

252 of many genes, complement, particularly the membrane attack complex, primarily induces release of IL

253 suggest that (i) nonlethal assemblies of the membrane attack complex promote intracellular killing an

254 ng of anaphylatoxin receptors or assembly of membrane attack complex promotes cell dedifferentiation,

255 At a sublytic dose, the C5b-9 membrane attack complex protects oligodendrocytes (OLG)

256 nal aortic aneurysm model, deficiency of the membrane attack complex regulator CD59 in ApoE-null mice

257 urons and produced only a small reduction of membrane attack complex removal, because of a selective

258 and, deficiency of CD59, an inhibitor of the membrane attack complex, resulted in significantly incre

259 ELISAs for SC5b-9, the soluble membrane attack complex, showed that production of SC5b-

260 capture and clear soluble precursors to the membrane attack complex (sMAC).

261 CD59 is a potent inhibitor of membrane attack complex that mediates complement-depende

262 ortant findings related to the deposition of membrane attack complex, the character of the inflammato

263 In addition, in mice unable to form the membrane attack complex, the tumor progression was unalt

264 protein that restricts the formation of the membrane attack complex, thereby inhibiting induction of

265 C5b,6, thereby reducing the capacity of the membrane attack complex to bind to and lyse the target c

266 Quantification of the binding of the C5b-9 membrane attack complex to cells during complement activ

267 ion pathways were involved in generating the membrane attack complex to directly injure MSCs.

268 in coupled with functional impairment of the membrane attack complex underscore HCV-mediated attenuat

269 Rather than inducing cytolysis, membrane attack complexes upregulated inflammatory genes

270 ammatory metabolite C5a and formation of the membrane attack complex via C5b.

271 position of C3, C3 activation fragments, and membrane attack complex was observed in the eyes of Lewi

272 Deposition of the membrane attack complex was observed on endothelial cell

273 r C3aR- or C5aR-mediated inflammation or the membrane attack complex was pathogenic.

274 y or pharmacologically inhibited assembly of membrane attack complex were subjected to hypoxia-ischem

275 2/II62 hRPE cells were more resistant to the membrane attack complex, whereas HH402/VV62 hRPE cells s

276 5a and C5b(T), the latter forming a C5b(T)-9 membrane attack complex with significantly more lytic ac

277 e pathway dysregulation, local generation of membrane attack complex within the kidney is also critic