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1 P and is integral to the formation of C3 and C5 convertase.
2 , and promoted formation of an overactive C3/C5 convertase.
3 t C5 activation occurs in ECM independent of C5 convertases.
4  formation or accelerate decay of the C3 and C5 convertases.
5 namely, autoantibodies that target the C3 or C5 convertases.
6 ators on murine erythrocytes that inhibit C3/C5 convertases.
7 arranged, are required for efficient DAA for C5 convertases.
8 sical (C4bC3bC2a) and alternative (C3bC3bBb) C5 convertases.
9  that mediate the dissociation of the C3 and C5 convertases.
10 the catalytic sites of the complement C3 and C5 convertases.
11 etween the classical and alternative pathway C5 convertases.
12  as a scaffolding protein in both the C3 and C5 convertases.
13 a properdin levels are a sensitive marker of C5 convertase activity in factor H deficiency.
14                                 Importantly, C5 convertase activity was also fully restored when prop
15 s an important function in classical pathway C5 convertase activity.
16 lial, and epithelial cells, which reduces C3/C5 convertase activity.
17 3, thrombin-mediated complement component 5 (C5) convertase activity leads to the generation of C5a (
18 s AP activation, although assembly of active C5 convertase and formation of the terminal complement p
19 y proteins CD46 and CD55, inactivates the C3/C5 convertases and blocks in vitro generation of C3a, C5
20  in the assembly of the classical pathway C3/C5 convertases and C4b binding to regulators.
21 he classical pathway in the generation of C3/C5 convertases and production of pro-inflammatory produc
22 ator that accelerates the dissociation of C3/C5 convertases and thereby prevents the amplification of
23 ectively, attenuating the activity of the C3/C5 convertases and, consequently, avoiding serious damag
24  (DAA) for the classical pathway (CP) C3 and C5 convertases and, using these results, generate more p
25                                          The C5 convertases appeared to follow Michaelis-Menten kinet
26 complement activation, in which thrombin and C5 convertase are invariant partners, enhancing the term
27 ptible to ECM, indicating that the canonical C5 convertases are not required for ECM development and
28                     The data suggest that C3/C5 convertase assembled with either monomeric C4b or C4b
29    A comparison of the kinetic parameters of C5 convertases assembled on three surfaces (zymosan, rab
30  study kinetic analysis of lectin pathway C3/C5 convertases assembled on two surfaces (zymosan and sh
31      The antibody is specific for the APC C3/C5 convertase because classical pathway-mediated hemolys
32           Decay acceleration by SCR1-4 of C3/C5 convertases bound to nonactivators was strongly depen
33 y (AP) providing stabilization of the C3 and C5 convertases, but its oligomeric nature challenges str
34 a presented demonstrate that the fluid phase C5 convertase, C3b,Bb, can cleave C5 without the aid of
35 thway C4b2a were tested in classical pathway C5 convertase (C4b2a3b) assays.
36 targets C5 itself rather than inhibiting the C5 convertase C4bC3bC2a itself.
37 as been shown to inhibit the formation of C3/C5 convertases, can attenuate myelin-specific T-cell res
38    Residues critical to the interaction with C5-convertase cluster on a mobile, hydrophobic inter-str
39 erdin mediates the assembly of stabilized C3/C5-convertase clusters, which helps to localize compleme
40 operties of the cobra venom factor-dependent C5 convertase (CVF, Bb) made with CVF purified from the
41                             By activating C3/C5 convertase, CVF depletes complement while additionall
42  parameters indicated that although the four C5 convertases (CVFn,Bb, ZymC3b,Bb, CVFh,Bb, and C3b,Bb)
43  as a membrane-bound receptor of C3b/C4b, C3/C5 convertase decay accelerator, and cofactor for factor
44           The results indicate that, for the C5 convertases, decay accelerating activity is mediated
45 were generated only when the low affinity C3/C5 convertases (EAC1,C4b,C2a) were allowed to deposit C3
46  cleaving properties of classical pathway C3/C5 convertase either bound to the surface of sheep eryth
47                                              C5 convertase enzymatic activity was measured as a funct
48               Here, we show that the role of C5 convertase enzymes in MAC assembly extends beyond the
49 um, MACs need to be assembled locally by the C5 convertase enzymes.
50                      These C3b-containing C3/C5 convertases exhibited Km (0.0051 microM) well below t
51   Using several tests for alternative C3 and C5 convertase formation and regulation, we identified tw
52 o preferentially participate in heterodimer (C5 convertase) formation.
53 d Coversin reported here demonstrate that C3/C5 convertases function differently from prevailing conc
54 ll molecular model for the classical pathway C5 convertase in complex with C5, suggesting that C3b in
55 and inactivates classical and alternative C3/C5 convertases in vitro.
56 nt component C5 and prevents its cleavage by C5 convertases, inhibiting release of both the proinflam
57        In the absence of the cell surface C3/C5 convertase inhibitor decay-accelerating factor (DAF),
58                                           C3/C5 convertase is a serine protease that cleaves C3 and C
59                                          The C5 convertase is a serine protease that consists of two
60                            Cleavage of C5 by C5 convertase is the last enzymatic step in the compleme
61 ty previously observed for the surface-bound C5 convertases is not due to higher catalytic efficiency
62 ctivity to increase inhibition of the C3 and C5 convertases is protective against renal IRI, and the
63  unstable protease complexes, denominated C3/C5 convertases, leading to inflammation and lysis.
64                Impaired regulation of C3 and C5 convertases leads to unchecked complement and coagula
65 activation by generating C5a through its own C5 convertase-like enzymatic activity.
66 ater catalytic rate of the classical pathway C5 convertase may compensate for the fewer numbers of C5
67 CE serves to inhibit the formation of the C3/C5 convertases necessary for complement-mediated viral c
68      Inhibition occurred at the point of the C5 convertase of complement, regulating production of C5
69 e have studied the kinetic parameters of the C5 convertase of the alternative pathway of complement,
70 d decay-accelerating activity for the C3 and C5 convertases of the classical pathway.
71 ovides the catalytic activity for the C3 and C5- convertases of the classical and lectin pathways of
72 ions, we studied the effects of thrombin and C5 convertase on C5 in purified and plasma-based systems
73            Regulatory proteins inactivate C3/C5 convertases on host surfaces to avoid collateral tiss
74 actor (CD55) accelerates the decay of C3 and C5 convertases, participating in classical and alternati
75    The new insights into the mechanism of C3/C5 convertases provided here have important implications
76 d activation of C5 by the complement pathway C5 convertase rather than by non-C proteases.
77 OmCI acts by preventing interaction with the C5 convertase, rather than by blocking the C5a cleavage
78 accelerating factor (DAF), a cell surface C3/C5 convertase regulator, exerts control over T cell resp
79 iting C5 cleavage by the alternative pathway C5 convertase, revealing a targetable mechanistic differ
80 thway (called M1 in this study) generates C3/C5 convertases similar to those assembled by the initiat
81                         In contrast, for the C5 convertase, site 1 had only 0.5% of the decay acceler
82 tase may compensate for the fewer numbers of C5 convertase sites generated upon activation of this pa
83 r to those reported for classical pathway C3/C5 convertases, studies on the ability of C4b to bind C2
84 elow the Km determined for the surface-bound C5 convertase suggesting a direct correlation between th
85  that cleaves C3, enabling the assembly of a C5 convertase that cleaves C5.
86 cay-accelerating factor (Daf) dissociates C3/C5 convertases that assemble on host cells and thereby p
87 n pathogen surfaces, properdin stabilizes C3/C5 convertases to efficiently fight infection.
88 ases were generated when the low affinity C3/C5 convertases were allowed to deposit C3b by cleaving n
89                           Very high affinity C5 convertases were generated only when the low affinity
90                           Very-high-affinity C5 convertases were generated when preformed C3 converta
91                           Very high affinity C5 convertases were generated when the low affinity C3/C
92 s, K(m) and k(cat), of the lectin pathway C3/C5 convertases were similar to those reported for classi
93  those reported for the classical pathway C3/C5 convertase, where only one of four C4b molecules depo
94       We show that site 1 dissociates the CP C5 convertase, whereas the role of site 2 is to bind the
95 of C3b converts the enzymes to high affinity C5 convertases, which cleave C5 in blood at catalytic ra
96 also resistant to the classical pathway (CP) C5 convertase, with sensitivities roughly proportional t
97   Combined treatment of C5 with thrombin and C5 convertase yielded C5a and C5b(T), the latter forming
98 compared them to those for two C3b-dependent C5 convertases (ZymC3b,Bb and C3b,Bb).