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1 uired by the alternative pathway but not the classical pathway.
2 ay of complement and is not dependent on the classical pathway.
3  by immune complexes occurs primarily by the classical pathway.
4 ific inhibition of either the alternative or classical pathway.
5 -that could mediate its nuclear import via a classical pathway.
6 eration of pathogenic antibodies through the classical pathway.
7 ctivity for the C3 and C5 convertases of the classical pathway.
8 d mechanistically distinct inhibitors of the classical pathway.
9 I/R injury is mediated via the lectin and/or classical pathway.
10       Complement C1q is the activator of the classical pathway.
11 cked by Brefeldin A, suggesting export via a classical pathway.
12 ical role for OAT1 in the functioning of the classical pathway.
13 ement is relatively inactive compared to the classical pathway.
14 onservation of the mode of activation of the classical pathway.
15 at H. felis activates complement through the classical pathway.
16 pA may inhibit complement deposition via the classical pathway.
17  the complement cascade is initiated via the classical pathway.
18 CDC," remained to be dependent on C1 and the classical pathway.
19 by delaying the synthesis of C3b through the classical pathway.
20 at binds C1q, the recognition protein of the classical pathway.
21  between components C1q, C1r, and C1s of the classical pathway.
22 ative Pathway compared with that made by the Classical Pathway.
23 lement activation via the alternative or the classical pathway.
24 rs derived from cells that had activated the Classical Pathway.
25 T3 predominantly activated complement by the classical pathway.
26 sequent activation of complement through the classical pathway.
27 y of the complement system is older than the classical pathway.
28 re effective than factor H at inhibiting the classical pathway.
29 rum (NHS) allows C. albicans to initiate the classical pathway.
30 ways, whereas pneumolysin inhibited only the classical pathway.
31 osol, where the protein is processed via the classical pathway.
32 at antibody in nonimmune serum initiates the classical pathway.
33  N-glycan conformation primarily affects the classical pathway.
34 gs can lead to complement activation via the classical pathway.
35 own to interact with other activators of the classical pathway.
36 tion of endogenous antigens by MHC-I via the classical pathway.
37 early steps of complement activation via the classical pathway.
38 nhances complement C3 deposition through the classical pathway.
39 s deposited on pneumococci primarily via the classical pathway.
40 he lectin/alternative pathways or C4b in the classical pathway.
41 nner analogous to that of C1r and C1s of the classical pathway.
42 inB2, and this depended on components in the classical pathway.
43 c UFA synthesis is distinct from that of the classical pathway.
44  natural IgM antibody and propagated via the classical pathway.
45 he more potent inhibition of only C1s of the classical pathway.
46 D, NFKB1, and TACI) selectively activate the classical pathway.
47 uld lead to activation of complement via the classical pathway.
48 s not cause injury through activation of the classical pathway.
49 in machinery and mediate signalling via 'non-classical' pathways.
50                    To explore the mechanism, classical pathway-activating immune complexes were infus
51 anisms appear to be partially independent of classical pathway activation and apoptotic cell clearanc
52  C4BP, secondary to kinetically overwhelming classical pathway activation and possibly increased alte
53 nonenveloped icosahedral virus CP inhibiting classical pathway activation at C1.
54 actors demonstrated that HAstV CP suppresses classical pathway activation at the first component, C1.
55  the specific serum components necessary for classical pathway activation by F. tularensis in nonimmu
56                                 In contrast, classical pathway activation by high-titer antibody over
57                                 Ab-dependent classical pathway activation is required for complement-
58 tion was not blocked on MCP(+) cells because classical pathway activation occurred before substantial
59                                              Classical pathway activation was less robust than TNF-in
60                                              Classical pathway activation was observed in 90.5% of TM
61 he bacterium is opsonized by C3 cleavage via classical pathway activation within the alveolus, provid
62 ollowing CRP interaction and thereby inhibit classical pathway activation.
63 mation of the active C1 complex required for classical pathway activation.
64 t not SCR-4, function to selectively inhibit classical pathway activation.
65 embled by the initiating complex (C1) of the classical pathway, activation of complement component C5
66              Pooled NHS was rendered free of classical pathway activity by chelation of serum Ca2+ wi
67 age fluid contains C3 protein and functional classical pathway activity that mediates the binding of
68 , SP-A blocked the ability of C1q to restore classical pathway activity to C1q-depleted serum.
69 vation and binding of C3, characteristics of classical pathway activity, were abolished in yeast- or
70 ternative pathway activity without affecting classical pathway activity.
71     These data indicate that blockade of the classical pathway alone (C1q) is protective against perm
72 ponents that required activation of both the classical pathway and alternative pathway amplification
73 mouse embryo fibroblasts was mediated by the classical pathway and by an alternative or second pathwa
74  may help to explain how deficiencies of the classical pathway and certain pentraxins lead to impaire
75 d C1q activate complement; C1q activates the classical pathway and MBL the lectin pathway.
76 17 was responsible for the activation of the classical pathway and the observed killing of FX517 as o
77 t that was activated via the alternative and classical pathways and cleaved C3b to fragments of 68, 4
78 ent landscape of cell competition, including classical pathways and models, fitness fingerprint mecha
79 i-fHbp MAbs elicited greater C4b deposition (classical pathway) and greater bactericidal activity tha
80 easured complement activation products, C4d (classical pathway) and SC5b-9 (terminal pathway), at the
81 the complement system, predominantly via the classical pathway, and causes increased C4 activation an
82 iated C3 activation but had no effect on the classical pathway, and N-glycans in IgG were required by
83 ernative pathway as well as C4 and C2 of the classical pathway are required for complement-dependent
84           Here we have identified C1q in the classical pathway as required for activation of compleme
85                                    As in the classical pathway, BCR-induced ERK activation in the new
86 ree main mechanisms of action; these are the classical pathway, beta-arrestin scaffold signaling, and
87 g isotype, cannot activate complement by the classical pathway, binds more avidly to an inhibitory th
88      Both MAbs were potent activators of the classical pathway but poor facilitators of alternative p
89 tudies have confirmed the importance of many classical pathways but also revealed novel pathways.
90                            A blockade of the classical pathway by absorption of putative classical pa
91                            Activation of the classical pathway by immune complexes leads to the gener
92 lling of gonococcal strains that inhibit the classical pathway by recruiting C4BP.
93 ement cascade appears to be mediated via the classical pathway by the binding of C1q to ligands in AP
94  antibody against the first component of the classical pathway, C1q, were resistant to experimental B
95 n the well-defined activation complex of the classical pathway, C1qC1r(2)C1s(2), and the composition
96 f Crry and DAF in regulating alternative and classical pathway C3 activation.
97 Ps exhibited full activity against the human classical pathway C3 convertase.
98 2 to C4b which leads to the formation of the classical pathway C3 convertase.
99  by dissociating the catalytic domain of the classical pathway C3 convertase.
100  identify antimannan IgG as the initiator of classical pathway C3 deposition on C. albicans.
101 the C1 complex and prevented assembly of the classical pathway C3-convertase.
102 dy we examined the C5 cleaving properties of classical pathway C3/C5 convertase either bound to the s
103  findings differ from those reported for the classical pathway C3/C5 convertase, where only one of fo
104 are probably involved in the assembly of the classical pathway C3/C5 convertases and C4b binding to r
105 nvertases were similar to those reported for classical pathway C3/C5 convertases, studies on the abil
106  alternative pathway C3bBb compared with the classical pathway C4b2a were tested in classical pathway
107 ent origin, while a homologous member of the classical pathway (C4bpalpha) appeared later in evolutio
108 h the classical pathway C4b2a were tested in classical pathway C5 convertase (C4b2a3b) assays.
109 e propose an overall molecular model for the classical pathway C5 convertase in complex with C5, sugg
110 t the 6-9-fold greater catalytic rate of the classical pathway C5 convertase may compensate for the f
111  Pathway activity, but when measured for the Classical Pathway, C6des-748-914 was only 4-6% as effect
112 ind to and are internalized by ECs via a non-classical pathway, CAM-mediated endocytosis.
113 complement cascade via the antibody-mediated classical pathway can initiate red blood cell (RBC) dest
114                            According to the "classical" pathway, CD4 cells secrete cytokines, such as
115 r and vitreous inhibited the activity of the classical pathway (CH(50)).
116 This review emphasizes that both the lack of classical pathway complement activation and excessive ac
117 appears to be at least partly independent of classical pathway complement activation by C1q.
118 n-initiated bystander and antibody-triggered classical pathway complement activation in vitro, result
119 P) that functions to inhibit alternative and classical pathway complement activation.
120 which promote C1q binding, the first step in classical pathway complement activation.
121                                          The classical pathway complement regulator C4b-binding prote
122 -/-) -Crry(+/+) or wild-type erythrocytes to classical pathway complement-mediated C3 deposition in v
123 pathway protein factor B (Bf(-/-)) or in the classical pathway component C4 (C4(-/-)).
124                        Mice deficient in the classical pathway component complement component 4 (C4)
125  of complement activation is critical, while classical pathway components are entirely dispensable.
126  in MyoD-expressing fibroblasts deficient in classical pathway components RelA/p65, inhibitor of kapp
127         In contrast, inherited deficiency of classical pathway components, particularly C1q, is power
128                                          The classical pathway contributes to IC and apoptotic cell c
129 l hemolysis after forceful activation of the classical pathway could be reduced by blocking the AP.
130 ial recognition cascades that constitute the classical pathway (CP) and lectin pathway (LP).
131  inhibited the AP with minimal effect on the classical pathway (CP) and no effect on the lectin pathw
132 or decay-accelerating activity (DAA) for the classical pathway (CP) C3 and C5 convertases and, using
133 ese three mutants were also resistant to the classical pathway (CP) C5 convertase, with sensitivities
134      A promising therapeutic approach may be classical pathway (CP) inhibition at the level of early
135 onsiderable attention, little is known about classical pathway (CP) inhibition by meningococci, which
136                            Activation of the classical pathway (CP) of complement is often associated
137                                          The classical pathway (CP) of complement may contribute to t
138 endent cytotoxicity (CDC) of B cells via the classical pathway (CP) of complement.
139 ding; enhanced C3b and factor Bb binding was classical pathway dependent.
140                                              Classical pathway-dependent total hemolytic activity was
141 ted by either the alternative pathway or the classical pathway, depending on the concentration of ser
142  Recently, a role has been suggested for the classical pathway during innate immunity that is activat
143 e also compared the performance of TPIEA and classical pathway enrichment analysis, and TPIEA present
144  MAbs but exhibited reduced support of early classical pathway-facilitated accumulation of C3.
145 pattern is consistent with engagement of the classical pathway followed by amplification through the
146                   Exogenous GAD followed the classical pathway for antigen processing, with an absolu
147 ells lacking protein kinase C (PKC)beta, the classical pathway for BCR signaling is blocked, whereas
148 These data demonstrate the vital role of the classical pathway for innate immunity to a bacterial pat
149    However, the functional importance of the classical pathway for innate immunity to S. pneumoniae a
150 ion of STAT1, indicating divergence from the classical pathway for terminating IFN-gamma-signaling.
151 DNA in digitonin-permeabilized cells via the classical pathway for the nuclear transport of karyophil
152 this study, we report that the alternate and classical pathways for BCR signaling are differentially
153 ve, Lyn-dependent alternate pathway, and the classical pathway, for BCR signaling operate in parallel
154                                          The classical pathway, found throughout higher eukaryotic or
155                                 Although the classical pathway had been assumed to be the major pathw
156 ntification of different costimulators, this classical pathway has been shown to significantly impact
157 oradiography of radiolabeled protein; 2) for classical pathway hemolytic activity; 3) for susceptibil
158                  Among the initiators of the classical pathway, IgG deposition contributes most of th
159                                          The classical pathway implicated in ubiquitination of the ep
160                            Activation of the classical pathway in Alzheimer's disease derives from th
161     We believe there is another role for the classical pathway in maintaining immune tolerance.
162 ontaneously activated complement through the classical pathway in normal and immunoglobulin-deficient
163 tudy demonstrating an important role for the classical pathway in promoting SCI, it is likely that th
164         Btk appears to regulate directly the classical pathway in response to BAFF such that Btk-defi
165  in Candida albicans and comparison with the classical pathway in Saccharomyces cerevisiae have revea
166 ation and suggest a predominant role for the classical pathway in stimulating alloimmunity.
167 mplification via the lectin pathway than the classical pathway in the generation of C3/C5 convertases
168 ssible scenario, which parallels that of the classical pathway, in which MASP-1 and MASP-2 are found
169 luding binding to C4b-binding protein (C4BP; classical pathway inhibitor) and factor H (alternative p
170     There are major 2 types of NHEJ: (1) the classical pathway initiated by the Ku complex, and (2) t
171  pathway plays a critical role in amplifying classical pathway initiated complement activation.
172 f the sites for early C3 binding showed that classical pathway initiation led to immediate, synchrono
173 osition of C3 that was characteristic of the classical pathway initiation was reciprocally cross-abso
174                            In the absence of classical pathway initiation, the early cellular sites f
175 G (IgG) in normal human serum (NHS) mediates classical pathway initiation.
176 urring anti-C. albicans immunoglobulin C. in classical pathway initiation.
177  classical pathway by absorption of putative classical pathway initiators or by chelation of calcium
178 ransglutaminase 2 (TG2) is secreted by a non-classical pathway into the extracellular space, where it
179                                          The classical pathway involved the IkappaB kinase (IKK)beta-
180 he lower CPE dose was shown to proceed via a classical pathway involving mitochondrial membrane depol
181 on of NF-kappaB is partially mediated by the classical pathway involving the interaction between the
182 ntation through mechanisms distinct from the classical pathways involving H-2DM molecules.
183                                  Because the classical pathway is an important and specific mediator
184 ay for BCR signaling is blocked, whereas the classical pathway is little affected.
185                                          The classical pathway is more efficient at inducing CD8 cell
186 complement, and recent data suggest that the classical pathway is required for complement factor C3 d
187  activation through the alternative, but not classical, pathway is required to initiate antibody-indu
188 aracterized import pathway, often termed the classical pathway, is utilized by many basic-type (lysin
189 gG1-Lec 1 was deficient in activation of the classical pathway, it had a superior capacity to activat
190 ve the activation of fetal complement by the classical pathway leading to the formation of membrane a
191 three pathways of complement activation, the classical pathway, lectin pathway, and alternative pathw
192 fold or if Mg(2+)-EGTA was used to block the classical pathway, MCP efficiently inhibited C3b deposit
193                                Thus, for the classical pathway, MCP is the cofactor for C4b cleavage
194 hrocyte lysis by both the reactive lysis and classical pathway mechanisms.
195  were operative, group II MAbs induced early classical pathway-mediated binding of C3 but reduced the
196 pecific for the APC C3/C5 convertase because classical pathway-mediated hemolysis is unaffected by 3E
197 , and both C4 molecules equally restored the classical pathway-mediated hemolytic activity of serum d
198 hritis, DAF serves as the primary barrier to classical pathway-mediated injury, while CD59 limits con
199 forms also provided enhanced protection in a classical pathway-mediated system and cleaved cell-bound
200 greater deposition of C1q and thus increased classical-pathway-mediated C3 deposition.
201                                    While the classical pathway mediating this response is via mTOR in
202               From this, it follows that the classical pathway might be needed in order to kick-start
203 e duplication that gave rise to the earliest classical pathway molecules.
204 M and IgG that activate the C system via the classical pathway, normal membrane regulators of C (e.g.
205 se (Cyp7a1), the rate-limiting enzyme in the classical pathway of bile acid synthesis, has been impli
206 rior functional data suggest that C1s in the classical pathway of complement activated by, e.g., anti
207    These studies show that BrkA inhibits the classical pathway of complement activation and prevents
208  a Ca(2+)-dependent manner and augmented the classical pathway of complement activation but protected
209 d prevented erythrocyte lysis by controlling classical pathway of complement activation by cleaving t
210 t recombinant PepO specifically inhibits the classical pathway of complement activation in both hemol
211 dies reveal an important role for C1q in the classical pathway of complement activation in the develo
212 component C1, the complex that initiates the classical pathway of complement activation, is a 790-kDa
213                 C1, the first protein of the classical pathway of complement activation, is a calcium
214      C1q is the recognition component of the classical pathway of complement activation.
215 anifest hyperacute rejection mediated by the classical pathway of complement activation.
216 tivation of the innate immune system via the classical pathway of complement activation.
217 r membrane porin (Por) molecules to bind the classical pathway of complement down-regulatory protein
218 man fetal neurons activate spontaneously the classical pathway of complement in an antibody-independe
219 tribution of CRP's ability of activating the classical pathway of complement in the protection of mic
220 odies with limited abilities to activate the classical pathway of complement in vitro have been impli
221                                          The classical pathway of complement is activated upon bindin
222                                          The classical pathway of complement is crucial to the immune
223                Results demonstrated that the classical pathway of complement mediated serum neutraliz
224 bs may be capable of directly activating the classical pathway of complement under certain circumstan
225                    In situ activation of the classical pathway of complement was evident by depositio
226 Sle1c Crry and their ability to regulate the classical pathway of complement were not significantly d
227  natural IgM and the early components of the classical pathway of complement work in concert to neutr
228   We found that glomerular IgM activates the classical pathway of complement, but it does not cause s
229 ce binding of IgM, a potent activator of the classical pathway of complement, to both Rd and NT127.
230 e protease, C1r, initiates activation of the classical pathway of complement, which is a crucial inna
231 -induced inflammation can be mediated by the classical pathway of complement.
232 92 was delayed, suggesting regulation of the classical pathway of complement.
233 ndependent of CRP-mediated activation of the classical pathway of complement.
234  important role for natural antibody and the classical pathway of complement.
235 ween starter molecules of hemostasis and the classical pathway of complement.
236 mplement C1 that initiates activation of the classical pathway of complement.
237 ally specific natural IgM that activates the classical pathway of complement.
238 resulting from enhanced serum killing by the classical pathway of complement.
239  are sequentially activated and initiate the classical pathway of complement.
240 use natural antibodies and activation of the classical pathway of complement.
241  and antibody-antigen complexes [6,7] in the classical pathway of complement.
242  isoforms preferentially protect against the classical pathway of complement.
243 m the conformational model suggested for the classical pathway of complement.
244 s in increased sensitivity to killing by the classical pathway of complement.
245 ng that blocking resulted from inhibition of classical pathway of complement.
246 preserving important immune functions of the classical pathway of complement.
247 s inhibits killing by the antibody-dependent classical pathway of complement; however, susceptibility
248 asm and is presented to CD8+ T cells via the classical pathway of MHC class I presentation.
249  of quiescent fibroblast does not induce the classical pathway of NF-kappaB activation through Ikappa
250  the early components (C1, C4, or C2) of the classical pathway of the complement cascade is one of th
251  C2, yet play a role in both alternative and classical pathways of complement activation.
252 eumoniae, thereby reducing activation of the classical pathway on the bacterial surface.
253 ns at the level of the second enzyme of this classical pathway or of the noninducible system had no s
254 actor 4 (C4-/-), a critical component of the classical pathway, or factor B (fB-/-), an essential pro
255                             Furthermore, the classical pathway, partially targeted by the binding of
256        Together, these data suggest that the classical pathway plays a major role in complement activ
257 hysiological action of the early part of the classical pathway protects against the development of SL
258 ically have autoantibodies to the complement classical pathway protein C1q.
259 er hand, homozygous deficiency of any of the classical pathway proteins is strongly associated with t
260               Furthermore, mice deficient in classical pathway proteins were not protected from injur
261 de sialylation of N. gonorrhoeae resulted in classical pathway regulation as evidenced by decreased C
262 ypass the requirements for engagement of the classical pathway remain to be defined but do not appear
263 ured to examine activation of the lectin and classical pathways, respectively.
264 rowing evidence that proteins fold through a classical pathway sequence of native-like intermediates
265 plement activation occurred primarily by the classical pathway, since a deficiency in the C4 componen
266  reperfusion injury compared with wild-type, classical pathway-specific C1q-deficient mice, or MBL-de
267  beta-Glucan absorption of NHS abolished the classical pathway, suggesting that cell wall beta-glucan
268 d to the capacity of the Abs to activate the classical pathway, suggesting that the orientation of th
269 ses suggest that SGSs are secreted via a non-classical pathway that involves cleavage into a 300-kDa
270 ting system for novel cell biology even with classical pathways that have been studied extensively in
271                          However, unlike the classical pathway, the alternative pathway is also depen
272                                       In the classical pathway, the ER binds directly to an estrogen
273                Although IgG can activate the classical pathway, there also is evidence that alternati
274 ent surface deposition of complement via the classical pathway, thereby contributing to the ability o
275 scussed in terms of the energy landscape and classical pathway time regimes of folding, for which the
276 ed significantly below basal levels, whereas classical pathway titers were unchanged.
277 The proposed model for ClyA represents a non-classical pathway to attack eukaryotic host cells.
278                          Blocking either the classical pathway (treatments with EGTA-Mg2+ or soluble
279 factor-induced AP complement activation, and classical pathway-triggered AP complement amplification
280 ogens or altered self through the lectin and classical pathways, two of the three well-established ac
281 e borders, which are usually assigned in the classical pathway view of molecular events (e.g. signal
282 her antibody-mediated activation through the classical pathway was a major mechanism for complement a
283 n serum in untreated animals showed that the classical pathway was activated during the first 2 hours
284                                     When the classical pathway was blocked, group II and III MAbs mar
285 ent strain or a complemented mutant when the classical pathway was inactivated by depleting NHS of C1
286 , PspA also inhibited C3 deposition when the classical pathway was initiated by antibodies to capsula
287                                          The classical pathway was required in vitro, whereas complem
288                In nonimmune mouse serum, the classical pathway was the dominant activation pathway tr
289  alternative complement pathway, but not the classical pathway, was described in 2009.
290    To better understand the evolution of the classical pathway, we have evaluated the degree of funct
291 strain rates of quantal neurotransmission if classical pathways were solely responsible for vesicle r
292  C4, the complement components unique to the classical pathway, were not detected in the diabetic ret
293    Binding of LDL to CR1 is mediated via the classical pathway, whereas binding of acLDL is mediated
294 pneumoniae bound by C3 depends mainly on the classical pathway, whereas the intensity of C3 binding d
295 leted serum through both the alternative and classical pathways; whether Bf-1 possess similar activit
296 e possibility of its being secreted by a non-classical pathway, which is not clearly understood.
297 more familiar but evolutionarily more recent classical pathway, which is triggered by antibody bindin
298 on proceeds approximately 70-75% through the classical pathway while only approximately 25-30% seems
299 ent C1q and activation of complement via the classical pathway without any concomitant engagement of
300                        In the absence of the classical pathway, yeast cells bound 80% of the maximum

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