ライフサイエンスコーパス: C3b

1 C3b binding and functional experiments further demonstra

2 C3b cleavage results in C3c and C3d (thioester-containin

3 C3b deposition on both strains was greatest for sera obt

4 C3b is generated by the removal of C3a from C3.

5 th IgM (Pearson's coefficient [2D] rp=0.88), C3b/c (rp=0.82), C4b/c (rp=0.63), and C6 (rp=0.81) was a

6 th MASP2 (Manders' coefficient [3D] r=0.93), C3b/c (r=0.84), C4b/c (r=0.86), and C6 (r=0.80).

7 the previously solved crystal structure of a C3b:FH1-4 complex.

8 Proper formation of FH-sialic acid-C3b complexes on surfaces exposed to plasma is essential

9 ing activation, C3 is cleaved to form active C3b, then C3b is inactivated by Factor I and Factor H to

10 er the C3 substrate or convertase-affiliated C3b impaired C3 activation and opsonization.

11 A phage Ab against C3b that inhibited the alternative complement pathway, b

12 cules to simultaneously bind sialic acid and C3b on cells provides a unifying explanation for their a

13 7 and, thereby, evade complement attack and C3b-mediated opsonophagocytosis.

14 ably, anti-EGFR-IgG3 promoted strong C1q and C3b, but relatively low C4b and C5b-9 deposition on anal

15 Ethanol-induced deposition of C1q and C3b/iC3b/C3c was colocalized with apoptotic Kupffer cell

16 onent, C3, into activation fragments C3a and C3b confined to the extracellular space.

17 an active convertase that generates C3a and C3b from C3.

18 ctivation, and its cleavage products C3a and C3b mediate several functions in the context of inflamma

19 a-tryptase can act on C3 to generate C3a and C3b, raising the likelihood that mast cells engage compl

20 t cascade is the conversion of C3 to C3a and C3b, the latter typically binds to one or more acceptor

21 rocessed C3 into biologically active C3a and C3b.

22 ve C3 into its activation fragments, C3a and C3b.

23 In order to assess how TT30 binds to C3d and C3b, we determined the TT30 solution structure by a comb

24 C3 forms soluble oligomers, whereas C3u and C3b precipitate.

25 C3, C3u, and C3b associated strongly in >100 muM zinc, whereas C3c an

26 We conclude that the C3, C3u, and C3b association with zinc depended on the relative posit

27 omplement activation, as measured by C4b and C3b deposition, which was decreased by using ficolin-dep

28 olished the ability of FI to degrade C4b and C3b in the fluid phase and on the surface, irrespective

29 e by blocking the interaction between FB and C3b.

30 Our results show that Ecb, FH, and C3b form a tripartite complex.

31 m similar trimolecular complexes with FI and C3b/C4b, and the accessibility of FIMAC and SP domains i

32 1, and the natural substrates fibrinogen and C3b.

33 enhance their interaction with factor I and C3b, the proteolytically cleaved form of C3.

34 ted significant Leishmania antigen, IgG, and C3b deposition in VL dog glomeruli.

35 factor I (FI), C9, and C3 were measured, and C3b degradation ability was determined.

36 serum levels of corresponding proteins, and C3b degradation ability of CFH and CFI variant carriers.

37 the interaction of complement receptors and C3b.

38 Anti-C3b and anti-factor B (anti-FB) IgG have been reported i

39 liferative GN (Ig-MPGN) for anti-FB and anti-C3b autoantibodies using ELISA.

40 IgG, and five patients with anti-FB and anti-C3b IgG.

41 C3 reactivity assessed with anti-C3 and anti-C3b/iC3b/C3c antibodies, and prevented further spontaneo

42 from SLE patients demonstrated elevated anti-C3b IgG that blocked detection of C3 on apoptotic cells,

43 Patients negative for anti-C3b and anti-FB IgG had much lower rates of infection (1

44 In conclusion, the prevalence of anti-C3b/anti-FB Abs and alternative pathway activation is si

45 erapy, we characterized the activity of anti-C3b/iC3b monoclonal antibody 3E7 in an in vitro model of

46 IgG from patients with anti-C3b Abs stabilized C3bBb and perturbed C3b binding to co

47 s with anti-FB IgG, three patients with anti-C3b IgG, and five patients with anti-FB and anti-C3b IgG

48 n vitro and in vivo, as visualized with anti-C3b staining.

49 ertase activity; IgG from patients with anti-C3b/anti-FB Abs enhanced C3 and C5 cleavage.

50 injury, complement component C3 fragment b (C3b) deposition was reduced, whereas proteinuria was dim

51 Because C3b is also the target of the physiological plasma compl

52 urvival of YadA-expressing Yersiniae because C3b becomes readily inactivated by factor H and factor I

53 tron microscopy, we show that these Abs bind C3b via a site that overlaps the binding site on C3 for

54 Plasminogen and Factor H bind C3b; however, the two proteins bind to different sites a

55 fied 45 small molecules that putatively bind C3b near ligand-guided functional hot spots.

56 gested with the IgG lost its ability to bind C3b and inhibit complement-dependent antibody-mediated r

57 brane expression of P-selectin known to bind C3b and trigger the AP, and the release of the prothromb

58 tive bacteria, one of which is known to bind C3b.

59 lanation for the inability of SCIN-D to bind C3b/C3c.

60 On the contrary, by binding C3b, FHR-1 allowed C3 convertase formation and thereby e

61 alternative pathway C3 convertase by binding C3b.

62 elated with the results of factor B binding, C3b/iC3b deposition, and neutrophil association.

63 CFHR4 binds C3b via its C terminus, but the significance of this int

64 This minimal-size FH (mini-FH) binds C3b and has complement regulatory functions similar to t

65 hly conserved in the Pseudomonadaceae) binds C3b.

66 Previously, we have shown that SCIN binds C3b directly and competitively inhibits binding of human

67 AprA specifically blocked C3b deposition via the classical and lectin pathways, wh

68 ge-related macular degeneration contain both C3b and millimolar levels of zinc.

69 omistic scattering modeling showed that both C3b and C3u adopted a compact structure, similar to the

70 ased on the sustained ability of CFHR4-bound C3b to bind factor B and properdin, leading to an active

71 responding larger amount of covalently bound C3b than iC3b on the parasite surfaces of MbetaCD-treate

72 CD59-2a-CRIg dimer bound C3b-coated surfaces with submicromolar affinity (KD).

73 sialic acid in the context of surface-bound C3b explains their pathogenicity.

74 ing pattern for compstatin and surface-bound C3b, and the presence of Thr(373) in either the C3 subst

75 Chlamydia pneumoniae surface, as measured by C3b and C9 deposition.

76 Deposition of C1q, C3b, and C4b from human serum at the surface of pneumoco

77 The activated fragment of C3 (C3b) and factor B form the C3 proconvertase (C3bB), whic

78 Plasminogen binds to C3, C3b, C3d, and C5 via lysine residues, and the interactio

79 eutron scattering studies were used with C3, C3b, C3u, C3c, and C3d, using the wild-type allotype wit

80 nificantly reduced the complement factors C3/C3b in the RPE.

81 Pic cleaves purified C3/C3b and other proteins from the classic and lectin pathw

82 r H complex by zinc explains the reduced C3u/C3b inactivation rates by zinc.

83 central proteolytic fragment of the cascade, C3b.

84 actor H alone, the solubility of the central C3b-Factor H complex was much reduced at 60 muM zinc and

85 that both FI-FH and hPm sequentially cleave C3b.

86 ternative and classical pathways and cleaved C3b to fragments of 68, 40, 30, and 17 kDa.

87 pneumococcal cell wall and directly cleaved C3b and iC3b to generate degradation products.

88 In this case, FH-FI cleaves C3b into iC3b, with negligible degradation of iC3b by hP

89 Whereas FI-FH proteolytically cleaves C3b into iC3b, PAM-bound hPm catalyzes cleavage of iC3b

90 I-like protease activity capable of cleaving C3b into inactive C3b (iC3b).

91 ovide a structural basis for the competitive C3b-binding properties of SCIN.

92 plasmin, degraded fibrinogen and complement C3b and contributed to serum resistance.

93 the interaction between gC-2 and complement C3b, and passive transfer of gC-2 antibody protected com

94 AEC with 10% human plasma induced complement C3b/c and C5b-9 deposition, cellular activation and coag

95 oxidized low-density lipoprotein, complement C3b, IgG, amyloid beta, and BSA immobilized on microtite

96 Moreover, complement C3b deposition was found within the ocular surface tissu

97 ythrocyte lysis and deposition of complement C3b and C5b-9 on endothelial cells and platelets, we now

98 The solution structure of complement C3b is crucial for the understanding of complement activ

99 for factor I-mediated cleavage of complement C3b, thereby shutting down complement activation.

100 antibodies to deposit sufficient complement C3b on the bacterial surface to elicit bactericidal acti

101 We previously demonstrated that complement C3b binding acceptors exist on the P. aeruginosa surface

102 complement factor H that bind to complement C3b.

103 in H to inhibit opsonization with complement C3b and binding of C4BP.

104 (plasmin-antiplasmin [PAP]), and complement (C3b, C5a, C5b-9) in baboons infused with factor Xa (FXa)

105 spot" on the central opsonin of complement, C3b.

106 omolog (SPICE) bound to complement component C3b.

107 upernatants were the complement-3 components C3b, iC3b, and C3d, which were upregulated in LTBI and m

108 by degrading activated complement components C3b and C4b.

109 As a consequence, C3b deposition and phagocytosis increased in the absence

110 ment regulator factor H and did not decrease C3b deposition on the pneumococcal surface.

111 d C4BP binding to and subsequently decreased C3b deposition on pneumococci was observed.

112 t GAS utilizes diverse mechanisms to degrade C3b and thus to protect bacterial cells from the complem

113 ed in the validation of seven dose-dependent C3b-binding compounds.

114 rix, promoting the deactivation of deposited C3b.

115 creatinine and urea), complement deposition (C3b/c and C9), and infiltration of neutrophils and macro

116 ariations in CCP domains explain the diverse C3b-binding patterns, with limited or no contribution of

117 he early, ethanol-induced increase in either C3b or TNF-alpha.

118 This resulted in elevated C3b deposition on AP53/covR(+)S(+) cells, a high level o

119 erial Ecb in a concerted action to eliminate C3b at the site of infection.

120 us expression of OprF significantly enhanced C3b binding and increased serum-mediated bactericidal ef

121 ell as loss of MSP, a protease that enhances C3b cleavage to iC3b.

122 Binding of complement factors C3b, IgM, C1q, mannose-binding lectin (MBL), and properd

123 tional change of FH doubles its affinity for C3b and increases 5-fold its ability to accelerate decay

124 es not efficiently compete with factor B for C3b binding.

125 tor factor H (FH) competes with factor B for C3b binding; however, the capability of FH to prevent C3

126 Direct competition of SCIN with factor B for C3b slightly decreased the formation of surface-bound co

127 rminal cryptic second binding site in FH for C3b, the activation-specific fragment of the pivotal com

128 surface and recruits C3b or C3(H2O) to form C3b,Bb or a novel cell-bound C3 convertase [C3(H2O),Bb],

129 onformational changes in complement fragment C3b that propagate across several domains and influence

130 lement activation-specific protein fragment, C3b, forming iC3b that no longer participates in the com

131 s as well as complement activation fragments C3b and C3d.

132 ement components showed that SV5 virions had C3b cofactor activity, resulting in specific factor I-me

133 We show that at high C3b densities required for binding and activation of C5,

134 by neutrophils, which correlated with higher C3b deposition on the bacterial surface.

135 lding CD59-2a-CRIg dimer with increased iC3b/C3b binding avidity and MAC inhibitory activity.

136 Colocalization of MBL/MASP2 with IgM, C3b/c, C4b/c, and C6 was investigated by immunofluoresce

137 Although PfRh4 does not impact C3b/C4b binding, it does inhibit this convertase disasso

138 and loss of PspC also reduced differences in C3b/iC3b deposition between strains.

139 of a DAF-blocking antibody, the reduction in C3b deposition was reversed.

140 e moderate IRI model, despite a reduction in C3b/c and C9 deposition and innate cell infiltration.

141 thrombospondin repeat and a small region in C3b.

142 he high conformational variability of TED in C3b in physiological buffer showed that C3b is more reac

143 n synergy with host regulators to inactivate C3b.

144 se FHR3 and FHR1 bind to C3d and inactivated C3b, which are ligands for complement receptor type 2 (C

145 ent pathway toward generation of inactivated C3b (iC3b).

146 opsonin, to an inactive product, inactivated C3b (iC3b), in a step catalyzed by factor I (FI) and its

147 tivity capable of cleaving C3b into inactive C3b (iC3b).

148 complement components on the cell, including C3b and C9, and promote CDC with a very low threshold of

149 eduction in C1-INH recruitment and increased C3b deposition on their surfaces.

150 hat properdin deposition depended on initial C3b deposition followed by properdin in a second step.

151 function as a passive mechanism to intercept C3b from depositing on host cells.

152 bited increased avidity for the FHR1 ligands C3b, iC3b, and C3dg and enhanced competition with comple

153 In addition to its main ligands C3b and C4b, CR1 was reported to interact with C1q and m

154 Likewise, C3b/iC3b is more than the opsonizing fragment that facil

155 ite and produces shorter C3a-like and longer C3b-like fragments.

156 ose-dependently increased deposition of MBL, C3b/c, and C6 on WT PAEC.

157 ts during complement activation by measuring C3b deposition on mGEnCs using flow cytometry.

158 Plasminogen enhanced Factor I-mediated C3b degradation in the presence of the cofactor Factor H

159 e Factor I, suggesting that plasmin-mediated C3b cleavage fragments lack effector function.

160 ed Ligs display cofactor activity, mediating C3b and C4b degradation by factor I.

161 n (C4BP), which concomitantly led to minimal C3b deposition on AP53 cells, further showing that these

162 f functional glomerular DAF able to minimize C3b deposition.

163 with serum or pure FH degraded almost 90% of C3b, suggesting that the GBS-bound FH maintained cofacto

164 ance was associated with the accumulation of C3b/iC3b/C3c in the liver.

165 inactivation (known as cofactor activity) of C3b via FH and MCP.

166 d disease-linked C3F (Gly(102)) allotypes of C3b were experimentally explained for the first time.

167 e observed cell behavior with the amounts of C3b and IgG deposited on the zymosan surface in sera tre

168 the C3 thioester produces C3u, an analog of C3b.

169 affinity to a functionally important area of C3b that lies near the C terminus of its beta-chain.

170 es, they are significantly weaker binders of C3b.

171 Enhanced binding of C3b does not decrease survival of YadA-expressing Yersin

172 nzyme that is essential for the breakdown of C3b.

173 e identification of a promising new class of C3b-binding small-molecule complement inhibitors and, to

174 Smaller VWF multimers enhance cleavage of C3b but large and ultra-large VWF (ULVWF) multimers have

175 resulting in less CR1-dependent cleavage of C3b by factor 1.

176 which promoted factor I-mediated cleavage of C3b into iC3b as well as decay-accelerating factor (DAF)

177 ng in specific factor I-mediated cleavage of C3b into inactive iC3b.

178 a cofactor for factor I-mediated cleavage of C3b into the inactive form iC3b and thus prevents format

179 RDeltafhbA strain and eliminated cleavage of C3b on the cell surface.

180 Y338S) did not enhance factor I cleavage of C3b to iC3b and inhibited the cofactor function of facto

181 factor I and increased factor I cleavage of C3b to iC3b.

182 of CFH in the factor I-mediated cleavage of C3b.

183 Colocalization of C3b/iC3b and CR3 implicated the CR3/iC3b interaction in

184 r H complex during the regulatory control of C3b, the known clinical associations of the major C3S (A

185 f that is liberated during the conversion of C3b to iC3b.

186 binds to bacteria facilitates conversion of C3b to iC3b.

187 l surface by facilitating the degradation of C3b, an opsonin, to an inactive product, inactivated C3b

188 s degradation results in lower deposition of C3b on the bacterial surface.

189 nd that Eap likewise inhibited deposition of C3b on the surface of S. aureus cells.

190 bacteria resulted in decreased deposition of C3b on their surface and in diminished phagocytic killin

191 on A. fumigatus as validated by detection of C3b deposition and formation of the terminal complement

192 cting with both the C345C and vWA domains of C3b and Bb, respectively.

193 and bone morphogenetic protein 1) domains of C3b, which likely impairs C3-convertase inactivation by

194 , Bmp1) and MG2 (macroglobulin-2) domains of C3b.

195 nown to interfere directly with functions of C3b.

196 wild-type FH19-20, at promoting hemolysis of C3b-coated erythrocytes through competition with full-le

197 erving as a cofactor for the inactivation of C3b and C4b and by dissociating the catalytic domain of

198 NiV-dependent inactivation of C3b only occurred with the cofactors factor H and solubl

199 ble of in vitro cleavage and inactivation of C3b, a key component of the complement cascade.

200 ctor I-mediated cleavage and inactivation of C3b.

201 or I and factor H, promoting inactivation of C3b.

202 y, the inhibitor impaired the interaction of C3b with complement factor B and, consequently, formatio

203 derived IgG antibodies on the interaction of C3b with Factor B, Factor H, and complement receptor 1.

204 ted IgG1 and resulted in decreased levels of C3b deposition on the cell surface.

205 nding of the FH domain 19 to the C3d part of C3b next to the binding site of Ecb on C3d.

206 domains 19-20 of FH bind to the C3d part of C3b.

207 Pf92, we observed changes in the pattern of C3b cleavage that are consistent with decreased regulati

208 to these assays, it accelerated the rate of C3b cleavage, and this effect could be modulated by degr

209 in domain 3) could facilitate recognition of C3b via initial anchoring and eventual reorganization of

210 sented in which YadA exploits recruitment of C3b or iC3b to attract large amounts of factor H.

211 used to map the putative binding regions of C3b involved in the interaction with MCP and CR1 and int

212 t out to clarify the functional relevance of C3b binding by CFHR4.

213 ne attack complex (MAC) assembly at sites of C3b/iC3b deposition.

214 readily merged with the crystal structure of C3b to show that the four CR2 domains extend freely into

215 these residues onto the modeled structure of C3b-Kaposica-factor I complex supported the mutagenesis

216 hat SCIN binds a critical functional area on C3b.

217 arge VWF (ULVWF) multimers have no effect on C3b cleavage and permit default complement activation.

218 arrangement at a shared binding platform on C3b.

219 ed for domains binding at the fourth site on C3b, without affecting the overall binding mode.

220 that bind to the central complement opsonin C3b.

221 ent component 3 (C3) into the potent opsonin C3b, which triggers a variety of immune responses and pa

222 rogate extracellular target) and the opsonin C3b/iC3b (serving as the utility molecule).

223 hylatoxins C3a and C5a as well as opsonizing C3b/iC3b.

224 in solution, but do not bind to intact C3 or C3b.

225 t study, we utilized either C3 polyclonal or C3b monoclonal antibodies in a far-Western technique fol

226 ds to interfere with binding of the original C3b ligand that guided their discovery.

227 The conformations of C4b and its paralogue C3b are shown to be remarkably conserved, suggesting tha

228 anti-C3b Abs stabilized C3bBb and perturbed C3b binding to complement receptor 1 but did not perturb

229 on and/or defective clearance of fluid-phase C3b:protein complexes may have pathological consequences

230 modified host proteins and lipids to prevent C3b deposition and, thus, autoimmune cell lysis.

231 anchor fH to self-surfaces where it prevents C3b amplification in a process requiring its N-terminal

232 The importance of AP-produced C3b clusters for C5 activation in the presence of eculiz

233 density of the complement activation product C3b, which autoamplifies via the alternative pathway (AP

234 plement protein C3, the C3 cleavage products C3b and C3d, and C5.

235 umulation of complement activation products (C3b/iC3b/C3c) in liver and adipose tissue.

236 nt activation-specific proteolytic products, C3b and C4b.

237 o PGK cleaved the central complement protein C3b thereby further modifying the complement attack.

238 generated plasmin cleaved complement protein C3b thus assisting in complement control.

239 in direct comparison with its parent protein C3b.

240 e to degrade the central complement proteins C3b and C5 and inhibited the bacteriolytic effects of co

241 atives of C3, explain how SCIN can recognize C3b in the absence of other complement components, and p

242 hen properdin is on the surface and recruits C3b or C3(H2O) to form C3b,Bb or a novel cell-bound C3 c

243 nd show that Y. enterocolitica YadA recruits C3b and iC3b directly, without the need of an active com

244 s, also increased glomerular DAF and reduced C3b deposition after spontaneous complement activation.

245 ctional analysis revealed profoundly reduced C3b binding, cofactor activity, and decay accelerating a

246 3b-binding site showed significantly reduced C3b binding and alternative pathway complement activatio

247 l assays demonstrated the ability of several C3b-binding compounds to interfere with binding of the o

248 nduced complement activation with subsequent C3b opsonization upon incubation with normal human serum

249 e hemolytic assays and increase cell-surface C3b deposition on a mouse kidney proximal tubular cell l

250 of conserved residues within the C-terminal C3b-binding site showed significantly reduced C3b bindin

251 This study demonstrated that C3b:plasma protein complexes form in the fluid-phase dur

252 and C3 glomerulonephritis demonstrated that C3b:protein complexes form spontaneously in the blood of

253 137 mm NaCl, scattering modeling showed that C3b and C3u were both extended in structure, with the TE

254 D in C3b in physiological buffer showed that C3b is more reactive than previously thought.

255 products to cultured neurons suggested that C3b is responsible for the growth inhibitory and neuroto

256 nvertase in complex with C5, suggesting that C3b increases the affinity for the substrate by inducing

257 The C3b fragments generated by plasmin differ in size from t

258 The C3b-like fragment is degraded in the presence of the com

259 oid to the fluid-phase assay accelerated the C3b cleavage, and this effect was lost posttreatment of

260 )-Glu(1032) salt bridge is essential for the C3b-Factor H complex during the regulatory control of C3

261 ollowed by mass spectroscopy to identify the C3b acceptor molecule(s) on the P. aeruginosa surface.

262 e two nonsynonymous SNPs in CR1 are near the C3b/C4b binding site, suggesting a possible mechanism by

263 e CUB domain with respect to the core of the C3b molecule is central for its CFA.

264 The removal of the C3b-Factor H complex by zinc explains the reduced C3u/C3

265 ns target the same functional hotspot on the C3b/C3c surface yet harbor diversity in both the type of

266 ently bound to C3b in a 1:1 molar ratio; the C3b portion was rapidly degraded by factors H and I.

267 Furthermore, the model suggested that the C3b-interacting residues bridge the CUB (complement C1r-

268 adopted a compact structure, similar to the C3b crystal structure in which its TED and macroglobulin

269 o acids, including a bond located within the C3b-binding domain of Efb.

270 of residues and interactions formed at their C3b/C3c interfaces.

271 tion, C3 is cleaved to form active C3b, then C3b is inactivated by Factor I and Factor H to form the

272 and, to a lesser degree, that of factor B to C3b.

273 Ecb and FH enhance mutual binding to C3b and also the function of each other in downregulatin

274 Tyr51 as residues key for SCIN-B binding to C3b and subsequent inhibition of the AP C3 convertase.

275 The decrease of C5 binding to C3b clusters in the presence of C5 inhibitors correlated

276 enhancing effect of Ecb and FH on binding to C3b depends on binding of the FH domain 19 to the C3d pa

277 complex, consistent with mutants binding to C3b with wild-type-like affinity.

278 t the co-crystal structures of SCIN bound to C3b and C3c at 7.5 and 3.5 A limiting resolution, respec

279 sted of a plasma protein covalently bound to C3b in a 1:1 molar ratio; the C3b portion was rapidly de

280 s in many orientations when TT30 is bound to C3b.

281 yme (C3bBb) responsible for converting C3 to C3b in an amplification loop.

282 The key step of C3 cleavage to C3b is regulated by multiple mechanisms that control the

283 In contrast to C3b or Factor H alone, the solubility of the central C3b

284 lesional white matter, in close proximity to C3b/iC3b deposits.

285 resolve functional questions in relation to C3b and C3u, analytical ultracentrifugation and x-ray an

286 inding of properdin and binding secondary to C3b deposition is a critical factor contributing to this

287 eration and cofactor activity, with variable C3b binding through domains at sites ii, iii, and iv, an

288 tors Factor H and complement receptor 1 with C3b.

289 elated with local complement activation with C3b and C5b-9 deposition on the mesangial cell surface i

290 Reduced serum levels were associated with C3b degradation in carriers of CFI but not CFH variants,

291 onvertase assembly, factor B associates with C3b and Mg(2+) forming a pro-convertase C3bB(Mg(2+)) tha

292 ose that when factor B first associates with C3b, it bears two intact Arg(234) salt bridges.

293 host cells and tissues upon association with C3b and surface polyanions such as sialic acids, heparin

294 AprA inhibited opsonization of bacteria with C3b and the formation of the chemotactic agent C5a.

295 y higher deuterium uptake when compared with C3b, revealing more dynamic, solvent-exposed regions.

296 all regulators show extensive contacts with C3b for the domains at the third site.

297 The FH and FI levels correlated with C3b degradation in noncarriers (R2 = 0.35 and R2 = 0.31,

298 d that FH binding negatively correlated with C3b/iC3b deposition and that median FH binding was high

299 d residues critical for its interaction with C3b and factor I.

300 tic studies we found that VWF interacts with C3b through its three type A domains and initiates AP ac

301 complement factor H domains are bound within C3b.