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 is generated by the removal of C3a from C3.

4 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

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

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

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

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

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

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

11 or D, and C3 over the SPR chip, we amplified C3b from ~20 to ~220 molecules.mum(-2) AFM revealed C3b

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 binding to the MG3 and MG4 domains of C3 and C3b.

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 SPR experiments, K(D) values between FH and C3b on a custom-made chip surface were 5-fold tighter th

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

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

33 1, and the natural substrates fibrinogen and C3b.

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

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

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

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

38 the interaction of complement receptors and C3b.

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

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

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

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

43 Blockade of AP activation by anti-C3b or CFB mAbs also extended survival and preserved kid

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

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

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 robe, from its complex with surface-attached C3b.

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

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

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

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

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

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

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

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

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

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

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

62 alternative pathway C3 convertase by binding C3b.

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

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

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

66 hly conserved in the Pseudomonadaceae) binds C3b.

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 CSL040 retained its affinity to both C3b and C4b as well as its cleavage and decay accelerati

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

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

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

74 All rfaH and lpp mutants bound C3b and C5b-9 in large quantities.

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

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

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

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

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

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

81 n of human and mouse complement component C3/C3b/C3c and potently inhibits C3 cleavage by the alterna

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

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

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

85 central proteolytic fragment of the cascade, C3b.

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

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

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

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

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

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

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

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

94 a macrophage receptor for binding complement C3b/iC3b in vitro, recent studies reveal that CRIg funct

95 ns of factor H free to inactivate complement C3b deposited on the trypanosome surface.

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

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

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

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

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

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

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

103 complement factor H that bind to complement C3b.

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

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

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

107 iral entry and binds to complement component C3b, inhibiting complement-mediated immunity.

108 omolog (SPICE) bound to complement component C3b.

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

110 by degrading activated complement components C3b and C4b.

111 g experiments with the complement components C3b and C5b-9 showed that the underlying mechanism of ev

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

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

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

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

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

117 rix, promoting the deactivation of deposited C3b.

118 tive-feedback loop wherein surface-deposited C3b participates in convertases that cleave C3, thereby

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

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

121 ectin (MBL), and shared neurotoxic effectors C3b and C5b-9 terminal C complex were significantly high

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

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

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

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

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

127 nd drusen, and can compete with FH/FHL-1 for C3b binding, preventing FI-mediated C3b cleavage.

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

129 Affinity for C3b, cofactor and decay-accelerating activities, and ser

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

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

132 our-CCP DAF-MCP chimera with robust CFA (for C3b and C4b) and DAA (for classical and alternative path

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

134 that enhance the avidity of the molecule for C3b/C4b.

135 rs that possess additional binding sites for C3b in FHR5.

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

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

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

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

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

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

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

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

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

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

146 thrombospondin repeat and a small region in C3b.

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

148 n synergy with host regulators to inactivate C3b.

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

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

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

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

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

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

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

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

157 ystem proteins at the single-molecule level: C3b, the proteolytically activated form of C3, and facto

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

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

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

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

162 ons of ADE levels of C4b, factor D, Bb, MBL, C3b and C5b-9 terminal C complex, and depressions of CR1

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

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

165 HL-1 for C3b binding, preventing FI-mediated C3b cleavage.

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

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

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

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

170 f functional glomerular DAF able to minimize C3b deposition.

171 ases that cleave C3, thereby depositing more C3b.

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

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

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

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

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

177 es, they are significantly weaker binders of C3b.

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

179 nzyme that is essential for the breakdown of C3b.

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

181 d cofactor for factor I-mediated cleavage of C3b and C4b.

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

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

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

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

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

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

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

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

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

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

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

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

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

195 is, suggesting that the C-terminal domain of C3b has an important function in classical pathway C5 co

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

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

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

199 nown to interfere directly with functions of C3b.

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

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

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

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

204 ctor I-mediated cleavage and inactivation of C3b.

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

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

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

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

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

210 ent pathways as a membrane-bound receptor of C3b/C4b, C3/C5 convertase decay accelerator, and cofacto

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

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

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

214 interfere with the endogenous regulation of C3b deposition mediated by Factors H and I.

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

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

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

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

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

220 arrangement at a shared binding platform on C3b.

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

222 that bind to the central complement opsonin C3b.

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

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

225 istal inhibitors, which do not affect C4b or C3b deposition or noncomplement pathways.

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

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

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

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

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

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

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

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

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

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

245 3b-binding site showed significantly reduced C3b binding and alternative pathway complement activatio

246 m ~20 to ~220 molecules.mum(-2) AFM revealed C3b clusters of up to 20 molecules and solitary C3b mole

247 f C3, and factor H (FH), the surface-sensing C3b-binding complement regulator.

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

249 clusters of up to 20 molecules and solitary C3b molecules deposited up to 200 nm away from the clust

250 Our results show a strong C3b deposition on E faecalis via both the CP and the LP

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

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

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

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

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

256 137 mm NaCl, scattering modeling showed that C3b and C3u were both extended in structure, with the TE

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

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

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

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

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

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

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

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

265 ith FH(D1119G), a variant lacking one of the C3b-binding sites and causing atypical hemolytic uremic

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

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

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

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

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

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

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

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

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

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

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

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

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

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 iants, W1183L, V1197A, R1210C, and G1194D to C3b was increased upon addition of the potentiating Ab a

285 by the enhanced binding of FHR5 oligomers to C3b deposited on host cell surfaces.

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

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

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

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

290 tors Factor H and complement receptor 1 with C3b.

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

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

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

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

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

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

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

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

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

300 complement factor H domains are bound within C3b.