ライフサイエンスコーパス: complement inhibitor

1 trophil elastase inhibitor), and eculizumab (complement inhibitor).

2 and the characterization of a novel targeted complement inhibitor.

3 n digestion with and without the addition of complement inhibitor.

4 ize of CR1, is a therapeutic candidate for a complement inhibitor.

5 evels and localization of intrinsic membrane complement inhibitors.

6 ications for the design of clinically useful complement inhibitors.

7 for the design of antiviral therapeutics and complement inhibitors.

8 ntaneous activation of which is regulated by complement inhibitors.

9 y the lack of nontoxic and/or nonimmunogenic complement inhibitors.

10 pecies selectivity of endogenously expressed complement inhibitors.

11 ue to increased expression of membrane-bound complement inhibitors.

12 rious disease-associated pathways, including complement inhibitors.

13 the complement system, including binding to complement inhibitors.

14 an additional 15% by blocking CD55 and CD59 complement inhibitors.

15 protein (C4BP) and factor H, which are both complement inhibitors.

16 rats and MCF7 cells expressing different rat complement inhibitors, a model of human breast cancer wa

17 Although the majority of staphylococcal complement inhibitors act on the alternative pathway to

18 e investigated a novel strategy to overwhelm complement inhibitor activity and amplify complement act

19 cipients were conditioned by combinations of complement inhibitors, adsorption of natural antibodies,

20 ay revealed an increase in the expression of complement inhibitors and a decrease in the expression o

21 udies addressing therapeutic options such as complement inhibitors and anti-inflammatory agents.

22 hus, diabetes causes defective regulation of complement inhibitors and complement activation that pre

23 his model may be useful in the evaluation of complement inhibitors and other neuroprotectants intende

24 cooperation between membrane and fluid phase complement inhibitors and the body's ability to adaptive

25 Treatment of xenograft recipients with complement inhibitors and xenoreactive natural antibody

26 sing new class of C3b-binding small-molecule complement inhibitors and, to our knowledge, provides th

27 h as statins, hydroxychloroquine, rituximab, complement inhibitors, and interventions aimed at disrup

28 receptors (TLR1-6-10 cluster), cytokine and complement inhibitors, and the kallikrein system.

29 the clinician by providing several different complement inhibitors/antagonists for controlling comple

30 ctivation of complement (C4d and C5b-9), the complement inhibitor apolipoprotein J (apo J), and marke

31 Various novel complement inhibitors are being developed and several ar

32 er have been hampered by the fact that human complement inhibitors are not effective against rodent c

33 cesses and in xenograft rejection, efficient complement inhibitors are of great interest.

34 ells from inadvertent complement attack, and complement inhibitors are often up-regulated on tumors,

35 Because the membrane-associated complement inhibitors are very effective, recombinant so

36 t positions 4 and 7 of compstatin, a peptide complement inhibitor, are crucial for its interaction wi

37 found that IalphaI is not an essential human complement inhibitor as was reported for mice and that s

38 iscuss various injury site-specific targeted complement inhibitors as potential therapeutic agents fo

39 ational engineering approaches using natural complement inhibitors as potential therapeutics are high

40 rcinomas of the lung, do express one or more complement inhibitors at a level likely to inhibit compl

41 ay suggest templates for the design of novel complement inhibitors based upon the SCIN structure.

42 Microbial complement inhibitor-binding molecules can be promising

43 The targeted complement inhibitors bound to C3-opsonized cells, and a

44 pplement the activity of membrane-associated complement inhibitors by release of soluble forms of DAF

45 eterozygous deficiency of first component of complement-inhibitor (C1INH).

46 el, hitherto unknown interaction between the complement inhibitor C4b-binding protein (C4BP) and plas

47 type, uses exclusively protein H to bind the complement inhibitor C4b-binding protein (C4BP).

48 serum killing by recruiting to its surface a complement inhibitor C4b-binding protein, which is also

49 study, PRELP was found to interact with the complement inhibitor C4b-binding protein, which was sugg

50 The structurally related soluble complement inhibitors C4b-binding protein (C4BP) and fac

51 The complement inhibitors C4b-binding protein and factor H a

52 tion and suggests that GPI-anchored membrane complement inhibitors can regulate T cell immunity to vi

53 t difference in the expression of individual complement inhibitor CD46 (mean channel fluorescence [MC

54 tumor effect of rituximab, the expression of complement inhibitors CD46, CD55, and CD59 was analyzed

55 g neovessel clearance by down-regulating the complement inhibitor Cd55 specifically on neovessels, al

56 neovessels, decreased the expression of the complement inhibitor Cd55.

57 ion-selective channel protein 3 (VDAC3), and complement inhibitor CD55.

58 y in follicular lymphoma cells in vitro, and complement inhibitors CD55 and CD59 may regulate this pr

59 Expression of the complement inhibitors Cd55 and Cd59 was significantly de

60 These proteins include the complement inhibitors CD55 and CD59, and this explains t

61 By contrast, mRNAs for the complement inhibitor CD59 and the cytokine IL-1beta were

62 internalization and rapid degradation of the complement inhibitor CD59, and highlights the potential

63 wn that for effective functioning of soluble complement inhibitor CD59, binding of CD59 to the cell s

64 ked surface proteins, including the terminal complement inhibitor CD59, on hematopoietic stem cells.

65 ions of the heterodimeric apolipoprotein and complement inhibitor, clusterin (CL, 80 kDa), with activ

66 combinant soluble form of the mouse membrane complement inhibitor complement receptor-related gene y

67 o efficiently compete with the physiological complement inhibitor, complement factor H (CFH), for lig

68 We describe a targeted complement inhibitor, comprising complement receptor of

69 14 inhibition alone and combined with the C3 complement inhibitor compstatin (Cp40), on the bacteria-

70 of C3, which contains a binding site for the complement inhibitor compstatin and is considered critic

71 Pretreatment of plasma with the complement inhibitor compstatin reduced opsonization >2-

72 le cystathionine (thioether) analogue of the complement inhibitor compstatin.

73 y-Ig), whether exogenous administration of a complement inhibitor could lessen renal injury.

74 Disruption of the ability of NiV to recruit complement inhibitors could form the basis for the devel

75 Recipient mice were treated with the complement inhibitor CR2-Crry or vehicle control (n=6).

76 ermore, treatment of wild-type mice with the complement inhibitor CR2-Crry provided protection equiva

77 ice were treated with the targeted murine C3 complement inhibitor, CR2-Crry, from 16 to 24 wk of age

78 combinant soluble form of the mouse membrane complement inhibitor Crry (complement receptor-related g

79 erfering RNA-mediated down-regulation of the complement inhibitor Crry on MB49 murine bladder cancer

80 h H(2)O(2) reduced surface expression of the complement inhibitors DAF, CD55, and CD59, and impaired

81 ive and retro-oriented versions of the human complement inhibitor decay-accelerating factor (DAF), as

82 -12 levels in mice deficient in the membrane complement inhibitor decay-accelerating factor (DAF).

83 C terminus of soluble forms of the membrane complement inhibitors decay accelerating factor (DAF) or

84 roteins, we examined the distribution of the complement inhibitors decay-accelerating factor (DAF), C

85 tructural and functional analog of the human complement inhibitors decay-accelerating factor and memb

86 t study, we investigated the consequences of complement inhibitor down-regulation on the effector and

87 components (e.g., Factor B) and infusion of complement inhibitors (e.g., Crry, anti-C5 Ab) protect a

88 lthough early reports of the efficacy of the complement inhibitor eculizumab are promising, the outco

89 In the last year the complement inhibitor eculizumab has been used successful

90 The terminal complement inhibitor eculizumab was recently shown to be

91 These data indicate that complement inhibitors expressed on a tumor cell can supp

92 It has been hypothesized that complement inhibitors expressed on the surface of tumor

93 Complement inhibitors expressed on tumor cells provide a

94 Complement inhibitors expressed on tumor cells provide a

95 pendent of a requirement to target and block complement inhibitor expression or function, which is di

96 of carcinomas and showed no correlation with complement inhibitor expression.

97 Binding of the complement inhibitor factor H (fH) to the surface of Nei

98 e evolutionarily and structurally related to complement inhibitor factor H (FH), the initial assumpti

99 that NspA is a human-specific ligand of the complement inhibitor factor H (FH).

100 enhances binding of the alternative pathway complement inhibitor factor H and renders otherwise seru

101 paper we report that the ability to bind the complement inhibitor factor H is a general characteristi

102 our results suggest that, in contrast to the complement inhibitor factor H, CFHR4 acts as an enhancer

103 activates complement, but it also binds the complement inhibitor factor H.

104 the Lyme disease spirochete, binds the host complement inhibitors factor H (FH) and FH-like protein

105 Furthermore, IAPP also bound complement inhibitors factor H and C4b-binding protein (

106 oproteins on its surface that bind the human complement inhibitors factor H and factor H-like protein

107 gonorrhoeae to bind the alternative pathway complement inhibitor, factor H (fH), and evade killing b

108 specifically interacts with the soluble host complement inhibitor, factor H.

109 ctural homology with the alternative pathway complement inhibitor FH.

110 idal activity (SBA) and block binding of the complement inhibitor fH.

111 t approval of eculizumab as a first-in-class complement inhibitor for the treatment of PNH validates

112 this review, possible applications of these complement inhibitors for treatment of complement-mediat

113 substitutions that occur in the more potent complement inhibitor from Variola (small pox) virus.

114 hese data support a hypothesis that blocking complement inhibitor function on tumor cells will not on

115 ypothesis, the species-selective activity of complement inhibitors has been a hindrance to investigat

116 These data suggest that sLex-decorated complement inhibitors have enhanced antiinflammatory eff

117 Complement inhibitors have entered clinical use and have

118 was engineered to express the human terminal complement inhibitor hCD59.

119 Recombinant soluble complement inhibitors hold promise for the treatment of

120 s This protein is composed of two domains of complement inhibitor human FH (FH complement control pro

121 tigated the therapeutic effect of a targeted complement inhibitor in recipients of BD donor hearts an

122 retinal vessels and the decreased levels of complement inhibitors in diabetic rats, as well as the l

123 Transgenic expression of human complement inhibitors in donor cells and organs has sign

124 to investigate the role of these endogenous complement inhibitors in renal IRI.

125 to investigating the role of membrane-bound complement inhibitors in rodent models of human cancer.

126 utic implications for use of MCP isoforms as complement inhibitors in such areas as xenotransplantati

127 ed to investigate the role of complement and complement inhibitors in tumor progression.

128 lement receptor-related protein y (sCrry), a complement inhibitor, in the brains of hAPP mice.

129 To date several complement inhibitors, including recombinant forms of co

130 viruses SV5 and MuV incorporate cell surface complement inhibitors into progeny virions as a mechanis

131 recombinant fusion proteins consisting of a complement inhibitor linked to a C3 binding region of co

132 the retinal levels of CD55 and CD59, the two complement inhibitors linked to the plasma membrane by g

133 e, we describe the function of an endogenous complement inhibitor, mannan-binding lectin (MBL)-associ

134 The targeting of systemically administered complement inhibitors markedly enhanced their efficacy a

135 of the TMA samples, suggesting that terminal complement inhibitors may have a beneficial effect in th

136 and strongly suggest that in disease flares complement inhibitors might have therapeutic value.

137 Endogenous membrane-associated complement inhibitors normally protect endothelial cells

138 emic inhibition, CR2-mediated targeting of a complement inhibitor of activation improved bioavailabil

139 )S(-) cells displayed potent binding of host complement inhibitors of C3 convertase, viz.

140 compared functional profiles of the poxviral complement inhibitors of smallpox, vaccinia, and monkeyp

141 hibits different relative affinities for the complement inhibitors of various potential animal hosts.

142 eutic effect to that of Ornithodoros moubata complement inhibitor (OmCI), a known inhibitor of C5 act

143 eukotriene B4 inhibitor Ornithodoros moubata complement inhibitor (OmCI; also known as coversin) alon

144 data show directly that the expression of a complement inhibitor on a tumor cell promotes tumor grow

145 These results show that expression of complement inhibitors on a tumor cell has functional con

146 to determine the effect of pexelizumab, a C5 complement inhibitor, on infarct size in patients with S

147 plicating IalphaI as a potentially important complement inhibitor once enriched onto hyaluronan moiet

148 ch a chimaera has therapeutic potential as a complement inhibitor or immune modulator.

149 Supplementing an exogenous complement inhibitor, or up-regulating MSC expression le

150 cophore models have been constructed for the complement inhibitor peptide compstatin, using first pri

151 To determine whether complement inhibitors play a role in regulating the anti

152 t model, neither of two potent soluble-phase complement inhibitors prevented complement activation or

153 study suggested that eculizumab, a terminal complement inhibitor, produced clinically meaningful imp

154 Membrane-bound complement inhibitors protect host cells from inadverten

155 MG to investigate the efficacy of a novel C5 complement inhibitor rEV576, recombinantly produced prot

156 The staphylococcal complement inhibitor (SCIN) protein exhibits a particula

157 One of these, the staphylococcal complement inhibitor (SCIN), acts at the level of the C3

158 Among these are the staphylococcal complement inhibitors (SCIN), which are composed of thre

159 Staphylococcal complement inhibitors (SCINs) are one important class of

160 Thus, rMil2, particularly combined with complement inhibitors, should be well suited for in vivo

161 The complement inhibitor soluble complement receptor type 1

162 Thus, pneumococci bind complement inhibitors such as C4b-binding protein (C4BP)

163 Certain pathogens recruit host complement inhibitors such as factor H (fH) to evade the

164 ing a single chain Ab fragment and show that complement inhibitors targeted to the tubular epithelium

165 fore, mini-FH could potentially be used as a complement inhibitor targeting host surfaces, as well as

166 sotype and, when fused to Crry, results in a complement inhibitor that should not be recognized as fo

167 Compstatin peptides are complement inhibitors that bind and inhibit cleavage of

168 ne system, and the rational design of potent complement inhibitors that might be used as therapeutic

169 t treatment is plasma infusion/exchange, but complement inhibitor therapy provides hope for the futur

170 amined the capability of a novel therapeutic complement inhibitor to prevent pathological complement

171 nd that it fulfills this role by acting as a complement inhibitor to prevent virus-triggered compleme

172 In a strategy to specifically target complement inhibitors to sites of complement activation

173 come these limitations, approaches to target complement inhibitors to specific sites have been invest

174 ent years have not only introduced the first complement inhibitors to the clinic but also filled the

175 Targeting complement inhibitors to the site of complement activati

176 onectin, the human adhesive glycoprotein and complement inhibitor, to facilitate attachment to epithe

177 ribe a strategy for Ag-specific targeting of complement inhibitors using a single chain Ab fragment a

178 In a therapeutic paradigm using targeted complement inhibitors, we investigated the role of compl

179 Subsequently, complement inhibitors were tested on serum from the pati

180 stance is a unique protein, FACIN (F. alocis complement inhibitor), which binds to C3, resulting in s

181 enotypes via CD55, an intrinsic cell surface complement inhibitor, which was identified in a comparat

182 CD46 is a cell surface complement inhibitor widely expressed in human tissues,

183 Whether complement inhibitors will be useful to treat TSEs remai

184 ction and the use of new therapies including complement inhibitors will contribute to increasing succ

185 e use of complement receptor 2 (CR2)-Crry, a complement inhibitor with the ability to target C3 break

186 nearly natural sequences that act as potent complement inhibitors with greatly improved therapeutic

187 Thus, altered expression of a complement inhibitor within the tubular epithelium appea

188 However, expression of complement inhibitors without eliminating xenogeneic nat