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1 vascular endothelium, both produce C3 and C4 complement protein.
2 nhibited the binding of fH, a downregulatory complement protein.
3 receptor for multiple collectins and the C1q complement protein.
4 l as on the local concentration of available complement proteins.
5 and C5a, potent anaphylatoxins derived from complement proteins.
6 ndependent of complement activation or other complement proteins.
7 are considered as extrahepatic producers of complement proteins.
8 re of receptors that directly bind activated complement proteins.
9 data derived from targeted gene deletions of complement proteins.
10 as animals that were deficient in individual complement proteins.
11 s, phosphatidylcholines, and coagulation and complement proteins.
12 1r and C1s, the serine proteases that cleave complement proteins.
13 myloid (fAbeta) and other components such as complement proteins.
14 with thrombospondin, properdin, and several complement proteins.
15 es to or rare pathogenic genetic variants in complement proteins.
16 mmune systems, and reduces the expression of complement proteins.
17 ling, and surprisingly, increased binding of complement proteins.
18 ro-inflammatory pathways and upregulation of complement proteins.
19 ts structure, function, and interaction with complement proteins.
20 ositive selection maturation are targeted by complement proteins.
21 at coagulation proteases can directly cleave complement proteins.
22 nching fibrils (12-24 nm) composed of Ig and complement proteins.
23 immune cell type capable of synthesizing all complement proteins.
24 ent for binding to the excision repair cross-complementing protein 1 (ERCC1)/xeroderma pigmentosum co
25 se) polymerase 1 (PARP1), X-ray repair cross-complementing protein 1 (XRCC1) and tyrosyl-DNA phosphod
26 forms an important complex with X-ray cross complementing protein 1 (XRCC1) during single strand bre
27 SSBR complex mediated by X-ray repair cross-complementing protein 1 (XRCC1) is assembled sequentiall
28 ging, we demonstrate that X-ray repair cross-complementing protein 1 (XRCC1), a key factor in single-
29 polymerase 1 (PARP1), and X-ray repair cross-complementing protein 1 (XRCC1), all essential component
30 edox factor-1 (Ref-1) and X-ray repair cross-complementing protein 1 (XRCC1), relevant to neurodegene
31 d the scaffolding protein X-ray repair cross-complementing protein 1 (XRCC1), which completes the fou
34 In contrast, cells deficient in x-ray cross-complementing protein 1, DNA polymerase beta, or poly (A
37 hrough cross-linking the B-cell receptor via complement protein 3d and antigen to the complement rece
38 dditional factors, XRCC4 (X-ray repair cross-complementing protein 4), XLF (XRCC4-like factor/Cernuno
41 culizumab, a monoclonal antibody against the complement protein 5, stops the intravascular hemolysis
44 with axons and myelin, it is unknown whether complement proteins affect axon growth or regeneration.
45 nd how polymorphisms in genes encoding human complement proteins affect susceptibility to this import
49 d a novel way to coat themselves with the C3 complement protein and invade macrophages by interaction
50 sation by the cleavage products of the third complement protein and might promote inflammatory reacti
51 Here, we investigated whether a panel of complement proteins and activation products would provid
52 available concerning the interaction between complement proteins and capsule type 5 and 8 Staphylococ
53 ecent papers reporting on the association of complement proteins and complement regulators with high
54 (Fc) region, such as interacting with human complement proteins and Fcgamma-receptors (FcgammaRs) th
56 es were able to activate deposition of human complement proteins and passively protect against challe
57 gnificant proteins and oxidative regulators, complement proteins and protease inhibitors were enriche
60 everal other proteins including the terminal complement proteins and the neural adhesion molecules F-
61 I discuss immune and nonimmune functions of complement proteins and the tumor-promoting effect of co
62 Using purified classical activation pathway complement proteins and the Western blot assay, we showe
63 extensive examples that implicate classical complement proteins and their receptors in CNS dysfuncti
64 gocytes, NK cells, NKT cells, cytokines, and complement proteins) and later by the adaptive immune sy
65 n convalescent serum was shown to inactivate complement proteins, and the contribution of complement
68 formation, structures, and interplay between Complement proteins are complex, and this has limited ou
76 ehydrogenase and TM0449 thymidylate synthase-complementing protein are presented as examples of final
77 onclusion, this study documents functions of complement proteins as prosurvival factors that, through
81 e deposits were immunopositive for Abeta and complement proteins but did not stain for conventional a
82 kness or the interaction of the capsule with complement proteins, but the effects of small chemical m
84 mplement is facilitated by the production of complement proteins by MCs and their activation by the M
86 treatments also increased deposition of the complement protein C1q in beta-endorphin neuronal cells
90 rthermore, pharmacological inhibition of the complement protein C1q prevents dorsal horn inhibitory s
91 time, to our knowledge, a unique function of complement protein C1q, as a molecular bridge between pn
92 croglia also express C1qR(P), a receptor for complement protein C1q, ligation of which in vitro enhan
94 interaction, whereby pneumococci use a host complement protein C1q, primarily involved in the host-d
95 ystem to spread apoptotic factors, including complement protein C1q, to induce the membrane attack co
98 he microglial receptor TREM2 and the soluble complement proteins C1q and C3 are recognized as key pla
101 sue, we subjected mice deficient in selected complement proteins (C1q, C3, C5) to transient focal cer
102 ization of fAbeta microaggregates to that of complement protein, C1q-coated fAbeta microaggregates, a
104 lyses identified a gene signature, including complement protein C1qB and eukaryotic translation initi
106 NT003, a mouse monoclonal antibody targeting complement protein C1s, prevents induction of in vitro h
107 ammalian and insect cell-derived NS1 bind to complement proteins C1s, C4, and C4-binding protein, as
110 rprisingly, the functional deficiency of the complement protein C3 did not rescue the abnormal reprod
111 in complement protein C1q or the downstream complement protein C3 exhibit large sustained defects in
112 tor B (FB) and factor D (FD) and the central complement protein C3 in genotyped human postmortem dono
113 sults suggest a novel and prominent role for complement protein C3 in mediating aged-related and regi
118 nd that the opsonic fragments of the central complement protein C3, C3b and iC3b, were present on the
124 m earlier studies by Prodeus et al. in which complement proteins C3 and C4 were shown to be required
125 is known about other neisserial targets for complement proteins C3 and C4, which covalently attach t
130 rum complement, and this inhibition required complement proteins C3 and factor B, but not C4 or C5, s
132 c iron oxide (SPIO) nanoworms with the third complement protein (C3) was dependent on the biomolecule
133 CD27 ligand and 4-1BB ligand, and the third complement protein (C3), which positions LIGHT within th
135 in two flavors: (i) proteolytic fragments of complement proteins (C3, C4, C5) generated during activa
138 asmin(ogen) bound to PGK cleaved the central complement protein C3b thereby further modifying the com
139 minogen activator, generated plasmin cleaved complement protein C3b thus assisting in complement cont
141 ound plasmin was able to degrade the central complement proteins C3b and C5 and inhibited the bacteri
144 35 or transferred into mice deficient in the complement protein C4 are not anergized by soluble self-
148 complement by blocking the activation of the complement protein C5 and shows remarkable clinical bene
151 e of the innate immune system along with the complement protein C5 on exosomes' rate of clearance.
153 mab, a humanized monoclonal antibody against complement protein C5 that inhibits terminal complement
154 ymph tissue of mice immunized with the human complement protein C5, fused with a limited repertoire o
155 rapeutic monoclonal IgG that neutralises the complement protein C5--in neuromyelitis optica spectrum
157 , immunoglobulin light chains, Factor X, and complement proteins (C5 and C5b-9 complex) were identifi
163 is formed by sequential assembly of soluble complement proteins C5b, C6, C7, C8 and C9, but little i
164 bstrate-binding domain, was found to bind to complement proteins C8 and C9 and to inhibit zinc-induce
170 dopeptidase inhibitors, coagulation factors, complement proteins, carbonic anhydrases, and redox enzy
171 healthy controls had a greater abundance of complement proteins CFHR1, C1q chains A, B, and C, and p
173 t the liver, which produces large amounts of complement proteins, clears activators of complement and
174 mined for immunoreactivity (IR) of classical complement proteins (Clq and C3), markers indicating act
175 Experiments using human serum as a source of complement proteins confirmed Pic proteolytic activity o
176 arious inactive mutant permease proteins can complement proteins containing mutations at position 257
178 A fragment of this protein spanning the two complement protein (CP)-modules (residues 126 to 243) wh
179 external factors including immunoglobulins, complement proteins, cytokines, chemokines, integrins, a
180 es are intravenously injected into the body, complement proteins deposit on the surface of nanopartic
184 X3CL1, were marked by profoundly upregulated complement proteins (e.g., C1q and C3), and were surroun
186 h complete deficiencies of one of the plasma complement proteins enabled the field to move beyond the
189 source of C4 and raise the possibility that complement protein expression by the cells plays a role
195 ulin, shows that SpC3 is the first divergent complement protein, falling at the base of the complemen
198 w variants of the streptococcal inhibitor of complement protein has been implicated in the perpetuati
199 C1q signature domain, also found in many non-complement proteins, has a compact jelly-roll beta-sandw
201 luding the major histocompatibility complex, complement proteins, immunoglobulin receptors, cytokines
206 ceptor C3aR, revealing an unexpected role of complement proteins in early vertebrate development.
207 severe COVID-19, with abundant deposition of complement proteins in inflamed tissue and on the endoth
209 nized liver rats expressed human albumin and complement proteins in serum and showed a normal liver z
213 s, because rodent models indicate a role for complement proteins in synaptic pruning and neurodevelop
217 RI) and cardiomyocytes are a known source of complement proteins including the central component C3,
218 cial stress and observed dysregulation of 11 complement proteins, including three that were altered i
219 l or danger-associated molecular patterns by complement proteins initiates a cascade of events that c
220 the increased activation and localization of complement proteins, innate immune molecules, to these s
222 ectrometry was used to specifically quantify complement proteins interacting with the cartilage expla
224 ntigen presentation and protein degradation, complement proteins, interferon-regulated proteins, and
225 t 1, r) and C1s (complement component 1, s), complement proteins involved in vascular collagen metabo
226 in this superfamily, a unique feature of the complement proteins is a 150-residue-long C-terminal ext
228 munoglobulins for the interaction with human complement proteins is demonstrated and potential protec
229 e to proteins provided in trans, even if the complementing protein is translated from a different cis
230 ent peripheral T cells were bound by IgM and complement proteins, leading to the elimination of these
231 tion of human C3 protein with multiple mouse complement proteins, leading to unregulated C3 activatio
236 ral definition and biological activity, thus complementing protein ligation and recombinant protein e
237 0) is a member of the Ixodes scapularis anti-complement protein-like family of tick salivary proteins
239 he alternative pathway and absence of the LP complement protein mannan-binding lectin abrogates elast
240 an improved understanding of locally derived complement proteins, many of which promote host defense.
244 r on cell surfaces through activation of the Complement protein network mainly by infection or injury
245 With the availability of new structures for Complement proteins, new knowledge of how they function,
246 , we demonstrate that C1q, but neither other complement proteins nor FcRgamma, is required for early
251 ttack against host cells due to mutations in complement proteins or autoantibodies against complement
254 findings indicate that dysregulation of the complement protein pathway in blood is associated with i
255 ion, but increasing evidence also implicates complement proteins produced locally within the graft, i
256 C to PMN-synthesized concentrations of these complement proteins promoted astrogliogenesis and cell m
257 first time, to our knowledge, that the human complement protein properdin binds to early apoptotic T
261 the protein to the plasma membrane, thereby complementing protein-protein interactions, located in f
263 cell response more strongly than circulating complement protein, raising the possibility that there i
264 ts cDNA-derived amino acid sequence contains complement protein-repeating modules (CP) 1-6, 28, 29, a
267 eletion strains expressing either one of the complementing proteins revealed that in addition to a cy
268 omplement factor B (Cfb), in detail, because complement proteins secreted by cells other than cardiom
270 e TED (thioester-containing domain) and CUB (complement protein subcomponents C1r/C1s, urchin embryon
271 ency anemia-causing mutant (Mt2I286F) in the complement protein subcomponents C1r/C1s, urchin embryon
273 he liver constitutes the primary circulating complement protein synthesis site, extrahepatic synthesi
274 (W54011) demonstrated that the activation of complement proteins synthesized by pulp fibroblasts and
275 Recent work suggests that genes encoding complement proteins that are active in the innate immune
277 ophism, but also through modulation of local complement proteins that could protect against complemen
278 ack complex generated from the five terminal complement proteins that directly binds to and penetrate
279 role for function-altering mutations in the complement proteins that form or regulate the alternativ
280 AMD is associated with genetic variation in complement proteins that results in enhanced activation
282 sess the structures of these segments of the complement proteins, their relationships with other doma
283 e Fabs shows how Biacore T100 can be used to complement protein therapeutic discovery programs from b
284 proteins are a group of partly characterized complement proteins thought to promote complement activa
285 the contribution of individual inflammatory complement proteins to spinal cord injury (SCI) patholog
286 nionic lipids in the binding of the terminal complement proteins to the membrane and the efficiency o
287 mined the contribution of activated terminal complement proteins to the pathogenesis of the lupus-lik
288 e complement system is critical for enabling complement proteins to titrate immune defense while also
289 e lack of CRP and the exposure of activating complement proteins to tubular cells, alternative comple
290 to quantify the attachment of HUVEC-released complement proteins to ULVWF strings secreted by, and an
291 as ascertained by measuring levels of plasma complement proteins using an enzyme-linked immunosorbent
296 oassay, and CpG interactions with individual complement proteins were evaluated using magnetic beads
299 interact with Xeroderma pigmentosum group A complementing protein (XPA), a key protein involved in n
300 degradation of xeroderma pigmentosum group B-complementing protein (XPB), a component of human transc