ライフサイエンスコーパス: complement component

1 ement pathway, and results in consumption of complement components.

2 complement but not by serum lacking terminal complement components.

3 absence of, or prior to, expression of other complement components.

4 Higher BMI is related to increased levels of complement components.

5 6 mice or from mice deficient in informative complement components.

6 s soluble pathogen-recognition receptors and complement components.

7 isease dependent upon activation of terminal complement components.

8 gammaIII, complement receptor 2, and various complement components.

9 y of certain coagulation enzymes to activate complement components.

10 mechanism that is independent of downstream complement components.

11 hemostasis, has been shown to interact with complement components.

12 1207), and explored their recognition by key complement components.

13 ic leukemia cells in sera depleted of single complement components.

14 r, which has a crucial role in inhibition of complement component 1 (C1) and might implicate the clas

15 teases, C1r and C1s, which reside within the complement Component 1 (C1) complex.

16 arious types of tolerogenic DCs, with ANXA1, Complement component 1 (C1Q), CATC, GILZ, F13A, FKBP5, S

17 Complement component 1 Q subcomponent-binding protein (C

18 1 (Tie-1), collagen type IV alpha1 (Col4a1), complement component 1, q subcomponent receptor 1 (C1qr1

19 and VSM from PTH1R-VKO mice identified C1r (complement component 1, r) and C1s (complement component

20 ied C1r (complement component 1, r) and C1s (complement component 1, s), complement proteins involved

21 Mice with a mutation in complement component 1a (C1qa) were protected from glauc

22 ell function, large deposits of antibody and complement component 1q (C1q) accumulated at sites of ax

23 Complement component 1q subcomponent binding protein (C1

24 lta decreases expression of opsonins such as complement component-1qb (C1qb), resulting in impairment

25 ted gene 15 kd], DSP [Desmoplakin], and C1S [complement component 1s subcomplement]) located at three

26 uirement A serine peptidase 1 (ARMS2/HTRA1), complement component 2 (C2), complement factor B (CFB),

27 studies have identified polymorphisms in the complement component 2 (CC2) and factor B (CFB) genes, a

28 tly, polymorphisms in the factor B (CFB) and complement component 2 (CC2) genes were associated with

29 ed a systematic review of the association of complement component 2(C2)/complement factor B (CFB) gen

30 complement factor H) (P =2.3 x 10(-47)), C2 (complement component 2)-CFB (complement factor B) (P =5.

31 emperature requirement A serine peptidase 1, complement component 2, complement component 3, compleme

32 24), complement component 3 (rs2230199), and complement component 2/complement factor B (rs4151667) w

33 rom complement-mediated damage by inhibiting complement component 3 (C3) activation.

34 single nucleotide polymorphisms (nsSNPs) in complement component 3 (C3) alter the risk of age-relate

35 lobulin binding (Sbi) protein interacts with complement component 3 (C3) and its thioester domain (C3

36 Complement component 3 (C3) deficiency and complement in

37 revealed that the Vi capsule interfered with complement component 3 (C3) deposition.

38 nstead of DCs, which was highly dependent on complement component 3 (C3) from HpSCs.

39 Although complement component 3 (C3) inhibition is known to be va

40 surfaces results in proteolytic cleavage of complement component 3 (C3) into the potent opsonin C3b,

41 We have previously shown that complement component 3 (C3) is secreted by malignant epi

42 Complement component 3 (C3) occupies a central position

43 influences activation of the AMD-associated complement component 3 (C3) promoter fragment and CFB in

44 .03) for neovascular AMD; between T280M and complement component 3 (C3) R102G for AMD (P = .03); bet

45 ncident GA among subjects homozygous for the complement component 3 (C3) R102G rs2230199 nonrisk geno

46 modulated effects we measured, expression of complement component 3 (C3) strongly correlated with cys

47 The complement component 3 (C3) tickover hypothesis was put

48 Expression of complement component 3 (C3) was confirmed to be increase

49 Complement component 3 (C3) was upregulated in four lept

50 vestigated the molecular mechanisms by which complement component 3 (C3), a central protein in the co

51 component 2 (C2), complement factor B (CFB), complement component 3 (C3), collagen type VIII alpha 1

52 However, the lack of complement component 3 (C3), the predominant complement

53 d a recombinant adenovirus-expressing murine complement component 3 (C3, AdcmvC3).

54 d maculopathy susceptibility 2 (rs10490924), complement component 3 (rs2230199), and complement compo

55 uman CFH protein inhibited cleavage of mouse complement component 3 and factor B in plasma and in ret

56 s is diagnosed on the basis of either IgG or complement component 3 deposits (or both) at the keratin

57 nvincingly demonstrated to be a receptor for complement component 3 fragments.

58 enhanced uptake was not seen with serum from complement component 3 knockout (C3(-/-)) mice and was a

59 (complement factor B) (P =5.2 x 10(-9)), C3 (complement component 3) (P =2.2 x 10(-3)) and CFI (P =3.

60 serine peptidase 1, complement component 2, complement component 3, complement factor B, collagen ty

61 theless, all three MAbs protected normal and complement component 3-deficient mice from a lethal intr

62 Known sepsis-associated genes included complement component 3; angiopoietin 2; myeloperoxidase;

63 sitive direct antiglobulin tests for IgG and complement component 3; warm autoantibodies were identif

64 n the present study, we examined the role of complement component-3 (C3) using a newly constructed C3

65 mice develop antibodies to this hapten, fix complement component-3 in Bruch's membrane, accumulate d

66 previously reported elevated anaphylatoxins-complement component 3a (C3a) and complement component 5

67 r formation was mediated by EFEMP1(R345W) or complement component 3a (C3a), but not by complement com

68 al lungs, associated with elevated levels of complement component 3a and 5a (C3a and C5a), locally an

69 Targeting the complement component 3a receptor (C3aR) with selective a

70 lidated one of these candidate causal genes, complement component 3a receptor 1 (C3ar1), using a knoc

71 with intravenous immunoglobulin and inactive complement component 3b.

72 rs3818361 single nucleotide polymorphism in complement component (3b/4b) receptor-1 (CR1) is associa

73 1 and ACE were associated with a fragment of complement component 3f.

74 deficient in the classical pathway component complement component 4 (C4) and WT mice pretreated with

75 The complement component 4 (C4) gene is linked to schizophre

76 Here we show that variation of the complement component 4 (C4) genes C4A and C4B, which are

77 rom many structurally diverse alleles of the complement component 4 (C4) genes.

78 human leukocyte antigen (HLA) alleles and 4 complement component 4 (C4) haplotypes in studies from t

79 ity to bind and cleave the effector molecule complement Component 4 (C4).

80 ents positive for the degradation product of complement component 4 (C4d) and acute AMR.

81 ia risk-associated variants within the human complement component 4 locus are associated with increas

82 hose individuals having greater frequency of complement component 4A (C4A) alleles and higher C4A tra

83 Included are new recommendations for complement component 4d tissue staining and interpretati

84 ing leukotriene B(4) (LTB(4)) and inhibiting complement component 5 (C5) activation.

85 the genetic absence of C3, thrombin-mediated complement component 5 (C5) convertase activity leads to

86 We investigated the roles of complement component 5 (C5) in pancreatic fibrogenesis i

87 Using mice genetically deficient in complement component 5 (C5), C6 or the complement regula

88 ceptor-associated factor 1) and C5 (encoding complement component 5).

89 We found a synergistic response to complement component 5a (C5a) in combination with uridin

90 hylatoxins-complement component 3a (C3a) and complement component 5a (C5a)-in IPF, which interact wit

91 generation of the complement anaphylatoxin, complement component 5a (C5a).

92 or complement component 3a (C3a), but not by complement component 5a (C5a).

93 We find that established chemokines, complement component 5a and IL-8 induce chemoattraction

94 Mice deficient for complement component 6 (C6), an essential component for

95 e attack complex (MAC)/perforin-like protein complement component 9 (C9) is the major component of th

96 the successful therapeutic application of a complement component, a recombinant form of properdin (P

97 the capacity of anti-HLA antibodies to bind complement components allows accurate risk stratificatio

98 igen-deficient LVS in serum lacking terminal complement components allows efficient uptake of these l

99 Complement component C3 is the central complement component and a key inflammatory protein acti

100 tics were calculated to assess the effect of complement components and activation fragments in an AMD

101 esponse genes (IFRGs), antigen presentation, complement components and CD163 antigen were strongly up

102 ole for EGFR in regulating the expression of complement components and complement activation in human

103 Urinary cell levels of mRNA for complement components and complement regulatory proteins

104 R4, and TLR9 induces murine DC production of complement components and local production of the anaphy

105 of outer-surface lipoproteins that bind host complement components and manipulate their native activi

106 lization of protein expression for different complement components and regulators were also determine

107 ental factors, including genetic variants in complement components and smoking.

108 with aPL-mediated cell activation, targeting complement components and the innovative concept of bloc

109 y, complement activity and concentrations of complement components and their activation products are

110 ontained small exchangeable apolipoproteins, complement components, and immunoglobulins.

111 IN can recognize C3b in the absence of other complement components, and provide a structural basis fo

112 Mast cells, FcgammaRIII, complement components, and tumor necrosis factor alpha p

113 Polyreactive immunoglobulins (Ig) and complement components are present in tissues and blood o

114 ly of TLRs, C-type lectin receptors, several complement components, as well as FcepsilonR1.

115 C1q, the recognition subunit of the first complement component, binds to apoptotic cells, thereby

116 evidence for direct activation of individual complement components by extrinsic proteinases as part o

117 lation and activation of alternative pathway complement components by recipient APCs.

118 rations of the complement activation product complement component (C)3a, and immunohistochemical anal

119 ifact to direct blockade of IgG detection by complement component C1 as a possible candidate mechanis

120 Complement component C1, the complex that initiates the

121 , enable completely selective binding to the complement component C1q and activation of complement vi

122 urpose of this study was to evaluate whether complement component C1q binding and activation of the c

123 The complement component C1q is known to play a controversia

124 Complement component C1q is required for efficient engul

125 ivity is mediated through the recruitment of complement component C1q or the engagement with Fcgamma

126 Complement component C1q, beta-chain, nonspecific cytoto

127 recognize and engulf apoptotic cells via the complement component C1q.

128 nteraction with cellular Fc receptors or the complement component C1q.

129 week, including inflammatory markers such as complement components C1q and C2.

130 ated the deposition of gamma heavy chain and complement components C1q and C3 on the surfaces of derm

131 s associated with expression of the upstream complement components C1q and C3, in the absence of memb

132 anscripts are immune related and include the complement components C1q, C3, and C4, which we find are

133 ker (Iba1), a T-lymphocyte marker (CD3), and complement components C1q, C3, factor B, factor H, and m

134 The apparent paradox that early complement component (C1q, C2 and C4) deficiencies predi

135 neuroinflammation including up-regulation of complement component C1QA in microglia/monocytes.

136 ollowed by 7 additional T domains and 2 CUB (complement components C1r and C1s, sea urchin protein Ue

137 roximal domains), followed by 7 T and 2 CUB (complement components C1r and C1s, sea urchin protein Ue

138 proconvertase C4b2, followed by cleavage of complement component C2 within C4b2 resulting in the C3

139 of the complex between the d-fragment of the complement component C3 (C3d) and the modular complement

140 We examined the roles of complement component C3 and complement factor B (CFB) in

141 er retina, we examined mice lacking the main complement component C3 and the receptors for complement

142 ) both free and bound to the C3c fragment of complement component C3 at 1.5 and 3.4 A resolution, res

143 O antigen prevented both complement component C3 deposition on the surface and co

144 The nature of complement component C3 deposition, i.e., C3b (opsonizat

145 we found that mice deficient in the central complement component C3 displayed increased neovasculari

146 ibody mediated, complement-dependent injury, complement component C3 fragment b (C3b) deposition was

147 Complement component C3 has established roles in both in

148 Autoantibodies against the central complement component C3 have been reported in systemic l

149 ity to restore physiological serum levels of complement component C3 in Cfh KO mice.

150 ing TMEV infection, whereas mice depleted of complement component C3 in the periphery through treatme

151 In the presence of normal serum, complement component C3 is deposited on pneumococci prim

152 Complement component C3 is the central complement compon

153 py demonstrated no significant deposition of complement component C3 on particles.

154 these exoglycosidases reduced deposition of complement component C3 on the pneumococcal surface, pro

155 Complement component C3 plays a particularly versatile r

156 munohistochemistry, and ELISA to examine the complement component C3 split products, C9, VEGF, TGF-be

157 Complement component C3 was found to be an essential ops

158 , mice depleted of PMNs, or mice depleted of complement component C3 were topically treated with MAb

159 ion but coincided with gliosis and increased complement component C3, but not C1q, at synapses.

160 C57BL/6 mice, deficient in complement component C3, developed significantly fewer b

161 cient mice showed an enhanced rate of death, complement component C3-deficient mice died even more ra

162 The 1.25-A structure of the complement component C3-inhibitory domain of Staphylococ

163 the lung, even in the absence of the central complement component C3.

164 e most upregulated proteins, followed by the complement component C3.

165 ease, which can be rescued by inhibiting the complement component C3.

166 attached, activation-specific, fragments of complement component C3.

167 decay accelerating factor (DAF), and/or the complement component C3.

168 ing to C3d, a cleavage fragment of the major complement component C3.

169 binding of CR2 to the C3d/C3dg fragments of complement component C3.

170 tor, resulting in exhaustion of the maternal complement component C3.

171 dent manner from intracellular stores of the complement component C3.

172 An essential protein in this process is complement component C3.

173 e C-terminal C345c domain of human and mouse complement component C3/C3b/C3c and potently inhibits C3

174 GMVECs were reduced, and gene expression of complement components C3 (C3) and factor B (CFB) was inc

175 The complement components C3 and C1q, but not C5, were requi

176 es for measurement of C1-esterase inhibitor, complement components C3 and C4, and C-reactive protein

177 lysine side chains), whereas those of alphaM complement components C3 and C4B have an increased hydro

178 Among others, we found complement components C3 and C5 in FSAP coimmunoprecipit

179 ubretinal pigmented epithelium deposition of complement components C3 and C5 occurs, suggesting a con

180 Deposition of complement components C3 and C5b-9 (the membrane attack

181 lpha showed that Cpa proteolytically cleaved complement components C3, C3a, and C4b.

182 This included complement components C3, C5, C6, apolipoproteins A-I, A

183 Additionally, the deposition of complement components C3, C6, and C5b-9 was enhanced on

184 plasma are rapidly opsonized with the third complement component (C3) via the alternative pathway.

185 une cell infiltrate in mice deficient in key complement components (C3, C5aR), or treated with C5aRa,

186 ic complement assays (AP50, CP50, and LP50), complement components (C3, CFB, CFI, and CFH), and the a

187 Plasma complement components (C3, CFB, CFI, CFH, and factor D)

188 Here, we studied the role of the central complement component, C3, in synaptic health and aging.

189 leavage and activation of the abundant third complement component, C3, via formation of C3-activating

190 activation-specific fragment of the pivotal complement component, C3.

191 We identify the chemoattractant as the complement component C3a, a factor normally linked with

192 rnative complement pathway and generation of complement component C3a, which acts to augment beta cel

193 ht to evaluate the pathophysiologic roles of complement components C3a and C5a in the human choroid i

194 e evidence that bioactive fragments of these complement components (C3a and C5a) are present in druse

195 C (gC) functions in viral entry and binds to complement component C3b, inhibiting complement-mediated

196 e complement cascade via an interaction with complement component C3b, we speculate that gCsec could

197 nd a smallpox virus homolog (SPICE) bound to complement component C3b.

198 l complement pathways by degrading activated complement components C3b and C4b.

199 Binding experiments with the complement components C3b and C5b-9 showed that the unde

200 Complement component C4 (C4) is a highly variable comple

201 dividual gene copy-number variation (CNV) of complement component C4 and its associated polymorphisms

202 C1s cleaves complement component C4 and then C2 to cause full activa

203 Complete deficiency of complement component C4 confers strong genetic risk for

204 icrobe, Bottermann et al. (2019) reveal that complement component C4 inhibits adenovirus by inactivat

205 Complement component C4 is a central protein in the clas

206 Upon activation of these pathways, complement component C4 is proteolytically cleaved, and

207 C4a is a small protein released from complement component C4 upon activation of the complemen

208 Mice unable to secrete IgM or complement component C4 were not protected by MPL/TDCM t

209 Mice deficient in the downstream complement component C4 were not protected, suggesting t

210 identical steps of proteolytic activation of complement component C4, formation of the C3 proconverta

211 he HLA codes for the immune effector protein complement component C4.

212 Complement components C4 and C1q were necessary but not

213 The synthesis of complement components C4 and C3 is transcriptionally dow

214 The fourth complement component, C4, and the second component, C2,

215 resistance of R2866, we compared binding of complement component C4b to R2866 with a serum-sensitive

216 the proteins that are found in complex with complement component C4d in pooled synovial fluid of rhe

217 B. burgdorferi, and immunohistochemistry for complement components C4d and C9, CD3, CD79a, and decori

218 za B virus, various bacterial pathogens, and complement components C4d and C9, to identify the cellul

219 omplement-specific drug, an antibody against complement component C5 (eculizumab; Soliris), in March

220 Eculizumab binds complement component C5 and prevents its cleavage by C5

221 In addition, we find that the terminal complement component C5 and the C5a receptor (C5aR) are

222 the effect of single and dual inhibition of complement component C5 and TLR coreceptor CD14 on heme-

223 (C1) of the classical pathway, activation of complement component C5 via the lectin pathway has not b

224 ach, knob domain peptides that tightly bound Complement component C5 were obtained, at scale, using c

225 manized monoclonal antibody directed against complement component C5, eculizumab (Soliris; Alexion Ph

226 VA-induced neutrophil recruitment depends on complement component C5.

227 Complement component C5a and ATP are potent effectors of

228 ry protein (MIP)-1alpha, and MIP-1beta], and complement component C5a in bronchoalveolar lavage fluid

229 Inhibiting signaling of the complement component C5a receptor (C5aR) altered the com

230 We explored the role of the innate immune complement component C5a, a potent mediator of inflammat

231 hil chemotaxis by enzymatically cleaving the complement component C5a.

232 tracheal administration of recombinant mouse complement component (C5a) caused alveolar inflammation

233 The human complement component, C5a, binds two different seven-tra

234 ly, the membrane attack complex, composed of complement components C5b-9, has been connected to lytic

235 Human C8 is one of five complement components (C5b, C6, C7, C8, and C9) that ass

236 promoting CDC in sera depleted of individual complement components C6 to C9.

237 C8alpha, C8beta, and complement components C6, C7, and C9 form the MAC family

238 Complement component C8 plays a pivotal role in the form

239 ulates the membrane attack complex (MAC) via complement component C9.

240 ry without the coordinate induction of other complement components, can induce a program of gene expr

241 ctive capture and concentration of activated complement components closer to the cell membrane, poten

242 ion, impairment or inadvertent activation of complement components contribute to the pathogenesis of

243 Despite the early complement component deficiencies, we observed assembly

244 ments using human serum depleted of specific complement components demonstrated that the observed lyt

245 we previously demonstrated that the central complement component deposited on the organism's surface

246 nificant enrichment of fibrinogen, IgG3, and complement components, especially C1q.

247 Whether NK cells affect complement component expression in HCV-infected hepatocy

248 ratinocytes, EGFR inhibition did not enhance complement component expression or cause complement acti

249 Hepatitis C virus (HCV) proteins inhibit complement component expression, which may attenuate imm

250 pha, yielded a significant downregulation of complement component expression.

251 ration, perivascular deposition of activated complement components, extensive demyelination, loss of

252 We have shown that the complement component ficolin-A significantly binds to As

253 microscopy, monospecific antibodies against complement components, fluorescent secondary antibodies,

254 Soluble complement components form the proteolytic cascade, whos

255 se levels, we documented alternative pathway complement component gene expression within the islets o

256 ines and growth factors and their receptors, complement components, genes associated with cell prolif

257 atively regulates beta2 integrin adhesion to complement component iC3b and ICAM-1 in shear-free, but

258 to microbes and parasites and interacts with complement component iC3b, agglutinates erythrocytes, an

259 We quantified gene expression of these complement components in cultured human umbilical vein e

260 ssion and differential regulation of several complement components in glaucomatous samples, which inc

261 tion significantly enhanced the induction of complement components in keratinocytes and epidermis fol

262 Increasing awareness of distinct roles of complement components in normal brain development and fu

263 has been regarded as occurring strictly via complement components in plasma.

264 tory syndrome coronavirus 2 (SARS-CoV-2) and complement components in regions of thrombotic microangi

265 duction in the levels of Abeta and activated complement components in sub-RPE deposits and structural

266 elease signals that induce the expression of complement components in the CNS.

267 rtance of complement (specifically, terminal complement components) in the pathogenesis of CAPS and t

268 isease course is now identified for multiple complement components (including C1q, C4, and C3) in spi

269 Although the presence of complement components increases after SCI in association

270 the regulation of neovascularization by the complement components is scarce.

271 Searching for other complement components localized at the implantation site

272 KLKs in tissues and biological fluids where complement components may also be expressed, we suggest

273 Because complement components may deposit on RBCs, we asked whet

274 rance of immune complexes, autoreactivity to complement components may have considerable pathological

275 ound proteins accelerate the assembly of the complement components of the alternative pathway on the

276 Albicin also inhibited the deposition of complement components on agarose-coated plates, although

277 ed evaluation of the effects of the terminal complement components on graft injury and C4d deposition

278 -activating mAbs efficiently focus activated complement components on the cell, including C3b and C9,

279 es of genetic murine models lacking specific complement components or circulating immunoglobulins, cu

280 D59(-/-) mice with mice deficient in various complement components or receptors including C3, C4, fac

281 ies provide the first direct indication that complement components produced locally by the RPE are in

282 0 gene (one study, 723 participants) and the complement component receptor 1 gene (one study, 544 par

283 o C3, WT BM cells locally produced all other complement components required to activate C3 and to gen

284 Mice lacking complement components show delayed development of prion

285 In vitro cleavage assays with purified complement components showed that SV5 virions had C3b co

286 nexpectedly, because the disruption of other complement components, such as C1Q, is protective in gla

287 urthermore, ES-62 was shown to deplete early complement components, such as the rate-limiting C4, fol

288 lenged this paradigm by demonstrating that a complement component, the anaphylatoxin C5a, promotes th

289 ortalin can potentially target the C8 and C9 complement components through its ATPase domain and inhi

290 In this study, we used mice deficient in complement components to investigate the role of complem

291 yze this reaction assemble from fragments of complement components via multistep reactions.

292 In contrast, the epidermal expression of complement components was downregulated in ex vivo injur

293 However, opsonization of C. gattii with complement components was not sufficient to prolong life

294 found that the epidermal expression of many complement components was only increased to a minor exte

295 Using depleted sera and purified complement components, we demonstrated first that C1q an

296 ed cells reacted with sera depleted of early complement components, we were surprised to discover tha

297 We found that multiple complement components were markedly up-regulated in reti

298 ly in normal or OA ACVs, immunoglobulins and complement components were present only in OA ACVs.

299 ing fibronectin, antimicrobial peptides, and complement components, were associated with S. aureus at

300 rus replication, and increased expression of complement components, which may synergize with vaccine-