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1 C3, via formation of C3-activating enzymes (C3 convertases).
2 rolysis of C3, resulting in the formation of C3 convertase.
3 activity against the human classical pathway C3 convertase.
4 activity and also affected formation of the C3 convertase.
5 y affect assembly of the alternative pathway C3 convertase.
6 on of a fully functional alternative pathway C3 convertase.
7 and putative cleavage sites for factor I and C3 convertase.
8 mycobacteria resulting in the formation of a C3 convertase.
9 B comparably to wild-type (WT) C3 to form a C3 convertase.
10 ds to the formation of the classical pathway C3 convertase.
11 st cell surface by accelerating the decay of C3 convertase.
12 itical for the interaction of C3 with the AP C3 convertase.
13 P)-1 and MASP-2 cleave C4 and C2 to generate C3 convertase.
14 g to C3b and subsequent inhibition of the AP C3 convertase.
15 resulted from the formation of a hyperactive C3 convertase.
16 ion and cleavage of C4 and C2 generating the C3 convertase.
17 c site of the complement alternative pathway C3 convertase.
18 B and, consequently, formation of the active C3 convertase.
19 he catalytic domain of the classical pathway C3 convertase.
20 ted by a multi-protein assembly known as the C3 convertase.
21 in the formation of the alternative pathway C3 convertase.
22 ed immune complexes and regulation of C4 and C3 convertase.
23 ly bound to and displaced properdin from the C3 convertase.
24 to block formation and/or activity of the AP C3-convertase.
25 srupting components and regulators of the AP C3-convertase.
26 prevented assembly of the classical pathway C3-convertase.
27 omplement regulator in rodents that inhibits C3 convertases.
28 enhanced decay accelerating activity for the C3 convertases.
29 ion of the classical and alternative pathway C3 convertases.
30 t inhibits classical and alternative pathway C3 convertases.
31 st cell surface by accelerating the decay of C3 convertases.
32 e "conventional" mechanism of stabilizing AP C3 convertases.
33 ock complement by acting at the level of the C3 convertases.
34 gulatory proteins that decay the bimolecular C3 convertases.
35 mbly and function of the alternative pathway C3 convertases.
36 f its anaphylatoxin domain, by either of two C3 convertases.
37 n is critical and that Phe82 may contact the C3 convertases.
38 erdin binds to preformed alternative pathway C3 convertases.
41 or immortalized human hepatocytes inhibited C3 convertase activity and complement-dependent cytolysi
43 hway, IgG deposition contributes most of the C3 convertase activity necessary to start the cascade en
44 onically HCV-infected patient sera inhibited C3 convertase activity, further implicating HCV-specific
46 tients with anti-FB Abs selectively enhanced C3 convertase activity; IgG from patients with anti-C3b/
47 ins are able to form the alternative pathway C3 convertase and are cleaved (in the presence of purifi
48 al reorganization increases stability of the C3 convertase and facilitates recruitment of fluid-phase
49 hat form or regulate the alternative pathway C3 convertase and has opened the door to new therapeutic
50 nts in cluster 3 had prevalent activation of C3 convertase and highly electron-dense intramembranous
51 he recombinant hybrid protein stabilized the C3 convertase and reduced factor H-mediated convertase d
52 itions caused by severe dysregulation of the C3 convertase and, in particular, those that involve nep
55 e alternative pathway and cobra venom factor C3 convertases; and 4) for susceptibility to complement
56 target the alternative pathway of complement C3 convertase are being developed with a goal of inhibit
57 are necessary to mediate its decay of the CP C3 convertase (as opposed to portions of at least three
58 plexes of the pathways, C3 proconvertase and C3 convertase, as well as the unbound zymogen C2 obtaine
61 lement C1 subcomponent, C1q, and assembled a C3 convertase, but without the traditional requirement f
63 -1 did not inhibit regulation of solid-phase C3 convertase by FH and did not inhibit terminal complem
64 l enzymatic complex, the alternative pathway C3 convertase, by targeting a functional "hot spot" on t
65 gher frequency of rare and novel variants in C3 convertase (C3 and CFB) and complement regulator (CFH
66 C3(H2O) to form C3b,Bb or a novel cell-bound C3 convertase [C3(H2O),Bb], which normally is present on
67 acteriolysis but binds the AP proconvertase, C3 convertase, C3 products and partially stabilizes the
70 crystal structure of the alternative pathway C3 convertase C3bBb, which is in accordance with their i
73 o extend the half-life of cell surface-bound C3 convertase C3bBb; it may also initiate AP complement
74 t inhibitor (SCIN), acts at the level of the C3 convertase (C3bBb) and impairs downstream complement
79 ctor B combines with C3b to form the pivotal C3-convertase, C3bBb, of alternative complement pathway.
80 ure of a stabilized form of the active CP/LP C3 convertase C4b2a is strikingly similar to the crystal
87 WFA domain is not sufficient to activate the C3-convertase catalytic apparatus and also provide insig
88 t, C2, are indispensable constituents of the C3 convertase complex, C4bC2a, which is formed by both t
90 found that albicin binds and stabilizes the C3-convertase complex (C3bBb) formed on a properdin surf
92 s formation and promotes dissociation of the C3 convertase enzyme, and, together with factor I, media
94 factor B and increased net formation of the C3 convertase, even after decay induced by decay-acceler
95 nts dysregulation of the alternative pathway C3 convertase, even in the presence of C3 nephritic fact
96 the contrary, by binding C3b, FHR-1 allowed C3 convertase formation and thereby enhanced complement
97 r activity to degrade C4b, and did not block C3 convertase formation or accelerate decay of the C3 an
100 s moreover inhibited already at the level of C3-convertase formation due to an interaction between PR
102 cceleration of factor Bb uncoupling from the C3 convertase generated by the alternative pathway.
103 tions that form a hyperactive or deregulated C3 convertase have been identified in Factor B (FB) liga
105 of the complement cascade in vivo, using the C3 convertase inhibitor complement receptor 1-related ge
106 e, it was investigated, by use of the rodent C3 convertase inhibitor CR1-related gene/protein y-Ig (C
108 r lupus mice was determined using the potent C3 convertase inhibitor, CR1-related y (Crry), administe
111 receptor-related gene y (Crry)-Ig, a potent C3 convertase inhibitor; neutrophils were depleted using
113 nt of properdin accelerated the decay of the C3 convertase, leading to inhibition of the alternative
114 on the T. cruzi surface with the complement C3 convertase, leading to its stabilization and inhibiti
115 factor, an autoantibody directed against the C3 convertase of the AP, but in some patients, mutations
117 lternative pathway, which generated a stable C3 convertase on ECM, but not on endothelial cells.
118 acity of these antibodies to dysregulate the C3 convertase on the surface of endothelial cell was mea
121 ght into the importance of CFHR proteins for C3 convertase regulation and identify a genetic variatio
122 were then tested for their susceptibility to C3 convertase regulation by H and membrane DAF and for t
126 resonance structure of CCP15-16 in the serum C3 convertase regulator factor H proposed a positively c
127 are conservative substitutions in all other C3 convertase regulators that mediate decay acceleration
129 n SCR-2 and SCR-3, while alternative pathway C3 convertase regulatory function resides within SCR-2,
132 fficiently activate complement as far as the C3 convertase stage in comparison with PCh-BSA and PCh-c
133 that continuous complement inhibition at the C3 convertase step is feasible and effective in compleme
134 SPICE inhibited complement activation at the C3 convertase step with equal or greater efficiency than
135 on can be triggered by autoantibodies to the C3 convertase, termed nephritic factors, which cause pat
137 to weakly promote assembly of the classical C3 convertase that is further suppressed in the presence
138 nd provides insight into the function of the C3 convertase, the differential involvement of C3 activi
139 mutation inducing increased formation of the C3 convertase, thus explaining enhanced activation of th
140 e formation of the alternative and classical C3 convertase, thus preventing activation and amplificat
143 in that produces a stable, properdin-free AP C3 convertase, we show that properdin is required for th
144 C5 convertases were generated when preformed C3 convertases were allowed to self amplify by giving th
145 autologous classical and alternative pathway C3 convertases whenever these amplifying enzymes assembl
146 the complement pathway is the assembly of a C3 convertase, which digests the C3 complement component
147 to activated C3 during the formation of the C3 convertase, which it does at its active site cleft; a
148 lement regulator that dissociates autologous C3 convertases, which assemble on self cell surfaces.
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