ライフサイエンスコーパス: factor D

1 with C3b and is cleaved at a single site by factor D.

2 induced reversible conformational changes in factor D.

3 that is cleaved at a single factor B site by factor D.

4 cross a C3b-coated surface in the absence of factor D.

5 nctionally inhibitory antibody against human factor D.

6 ding to the generation of the self-inhibited factor D.

7 f PTHrP 1-86 and vascular endothelial growth factor-D.

8 factors such as vascular endothelial growth factor-D.

9 s are vulnerable to a range of environmental factors [D.

10 n is better ordered in solution than that of factor D; (2) the conformation of the Ba fragment is aff

11 plasmin, a fibrin clot-degrading enzyme, and factor D, a complement-activating enzyme, despite marked

12 al activity of a series of analogs of A54145 factor D (A5D) and A54145 factor A(1) (A5A(1)), two cycl

13 An efficient total synthesis of A54145 factor D (A5D), a member of the A54145 family of cyclic

14 mechanism by which the complement protease, Factor D, achieves its high specificity for the cleavage

15 ssociate with a KD of >/=2.5 microM and that Factor D acts on this complex with a second-order rate c

16 enetic deficiencies in C1q, C4, factor B, or factor D all resulted in increased mortality in mice, su

17 The structures of native factor D and a complex formed with isatoic anhydride inh

18 f classical pathway C4b, alternative pathway factor D and Bb, lectin pathway mannose-binding lectin (

19 y transmitted maternal antibodies against Rh factor D and can cause permanent neurological damage in

20 y to process critical substrates such as pro-factor D and insulin growth factor binding protein-5.

21 blood levels of vascular endothelial growth factor D and stromal cell-derived factor 1alpha (P = .03

22 These results imply that contacts between Factor D and the C3(H2O)B complex, outside the vicinity

23 and homeostasis (vascular endothelial growth factor-D and TM [thrombomodulin]).

24 omplement components (C3, CFB, CFI, CFH, and factor D) and activation fragments (Bb, C3a, C5a, iC3b,

25 Over multiple cycles of flowing factor B, factor D, and C3 over the SPR chip, we amplified C3b fro

26 initiate the alternative pathway (factor B, factor D, and C3) as well as C5 are present for several

27 (in the presence of purified trout C3, trout factor D, and Mg2+ EGTA) into Ba- and Bb-like fragments

28 d using four purified proteins-C3, factor B, factor D, and target protein-and Mg(2+) to allow C3 conv

29 ed growth factor-BB, platelet-derived growth factor-DD, and endothelin-1, critical EC-derived factors

30 The effect is factor D- and, at least in part, C5-dependent, indicatin

31 we demonstrate that chemical modification of Factor D at a single lysine residue that is distant from

32 er acute sTBI, except for elevated levels of factor D, Bb, and MBL.

33 significant elevations of ADE levels of C4b, factor D, Bb, MBL, C3b and C5b-9 terminal C complex, and

34 show opposing functions of two transcription factors, D-binding protein (DBP) and E2F8, in controllin

35 ) dictates the resting-state conformation of factor D by (1) preventing His57 from adopting active ta

36 Of these factors, D(Ca,SR) is the primary determinant of how rele

37 ome of the residues shown to be critical for factor D catalytic activity.

38 explained by decreased levels of complement factor D (CFD) and C7 components of the complement casca

39 noid model and uncover a role for complement factor D (CFD) in mediating microvascular immunothrombos

40 y, including complement factor Ba (CFBa) and factor D (CFD), were increased.

41 d, exposing the scissile bond and permitting factor D cleavage.

42 Factor D cleaved factor B into Bb and Ba in the presence

43 ange of exon 3 through exon 7 (including the factor D cleaving site) with the neor gene.

44 Pretreatment plasma complement factor D concentrations also decreased with time (P<0.00

45 inding to different subpockets of the latent Factor D conformation and was instrumental for understan

46 ll, suggesting that this may be the dominant factor D conformation in solution.

47 The adipokine adipsin/complement factor D controls the alternative complement pathway and

48 EP) before the administration of cobra venom factor; d) CVF-PLV group, animals received partial liqui

49 ve pathway in I/R injury was evaluated using factor D-deficient (-/-) and heterozygote (+/-) mice.

50 Pneumococci also were used to challenge factor D-deficient (FD(-/-)), LFA-1-deficient (LFA-1(-/-

51 gulation of systemic energy balance in vivo, factor D-deficient mice were generated by gene targeting

52 ivation in vitro by CVF demonstrated that in factor D-deficient serum the alpha chain of C3 was cleav

53 neumoniae by C3 fragments was much slower in factor D-deficient serum, suggesting a significant contr

54 ctivated the serum alternative pathway via a factor D-dependent manner.

55 Factor D-depleted and C6-depleted sera neutralized virus

56 crosis factor-a, sE-selectin, von Willebrand factors, d-dimers, matrix metalloproteinases, oxidative

57 brane sequence, and a partial Von Willebrand Factor D domain similar to those known to regulate the f

58 l thrombospondin and platelet-derived growth factor D expression.

59 An anti-factor D Fab fragment (AFD) was generated to inhibit the

60 A general disease factor (d factor) has been recently identified to captur

61 ] = 0.00;0.03) and minimal logical deviation factors (d(factor)=0.03;1.58), confirming Monte Carlo co

62 cytosis, C2, C4, C4b, C3, C3a, Factor B, Bb, Factor D, Factor H, Factor I, C5 and soluble C5b-9.

63 thway complement proteases factor B (FB) and factor D (FD) and the central complement protein C3 in g

64 f noncovalent reversible and selective human factor D (FD) inhibitors with drug-like properties.

65 Complement factor D (FD) is a rate-limiting enzyme of the alternati

66 It had been thought that complement factor D (FD) is activated at the site of synthesis, and

67 Factor D (FD) is an essential element of the alternative

68 The highly specific S1 serine protease factor D (FD) plays a central role in the amplification

69 Complement factor D (FD), a highly specific S1 serine protease, pla

70 Factor D (FD), which is also known as adipsin, is regard

71 AFD potently prevented factor D (FD)-mediated proteolytic activation of its mac

72 leavage of pro-factor D (pro-FD) into mature factor D (FD).

73 Activation by factor D (forming C3bBb) increased the complex half-life

74 ression of the Drosophila AP-1 transcription factor D-Fos in a slightly broader endodermal region tha

75 RNAP backtracking is sensitive to Gre factors, D-galactose, and antisense oligonucleotides.

76 owth factor-beta and platelet-derived growth factor D in driving the recruitment and expansion of can

77 of proteolytically inactive conformations of factor D in the absence of substrate.

78 activities of the complement enzymes Cls and factor D in vitro, also blocked development of RPA-induc

79 CD had selective vascular endothelial growth factor-D in both tumor and host stroma, suggesting a dif

80 t; one limiting diffusion rate (or frequency factor: d(infinity))) suffice to predict complete anisot

81 ion of C5b-9 on cells, but not C3c; however, factor D inhibition prevents both C3c and C5b-9 accumula

82 modified Ham test is blocked by either C5 or factor D inhibition.

83 presence of eculizumab or control complement factor D inhibitor ACH-4471, which blocks the complement

84 ors, was originally designed as a complement factor D inhibitor and exhibited submicromolar FXIa acti

85 kinase inhibitor, corticosteroid, complement factor D inhibitor), highlighting their potential for du

86 stigational, first-in-class, oral complement factor D inhibitor, as add-on therapy to ravulizumab or

87 an anti-C5 monoclonal antibody, but not by a factor D inhibitor, indicating that complement activatio

88 Novel agents, such as factor B and factor D inhibitors, are under study, with very promisin

89 he first known potent noncovalent reversible Factor D inhibitors.

90 tive pathway of complement and is cleaved by factor D into the Ba and Bb fragments in the presence of

91 tive pathway of complement and is cleaved by factor D into the Ba and Bb fragments when complexed wit

92 Factor D is a serine protease essential for the activati

93 Factor D is a trypsin-like serine protease with a narrow

94 in mouse proteolytic cleavage of factor B by factor D is not an absolute requirement for the zymogen

95 results suggest that platelet-derived growth factor-D is a target of itraconazole in infantile hemang

96 The high-resolution structure of the factor D/isatoic anhydride complex reveals the binding m

97 cleavage site were not detectably cleaved by Factor D (kcat/KM </= 0.5 M-1 s-1).

98 of 4 PVAN-specific genes (RPS15, complement factor D, lactotransferrin, and nitric oxide synthase in

99 ignificantly reduced platelet-derived growth factor-D level, resulting in suppression of platelet-der

100 f both factor B and factor D showed that the factor D linewidths were broader than those for factor B

101 We propose that Factor D may exemplify a special case of the induced fit

102 Inhibition of factor D may represent an effective therapeutic approach

103 convertase assembly including C3b-dependent factor D-mediated cleavage and activation of the high af

104 The myogenic factor D-MEF2 is required for the proper differentiation

105 ously removed, the myocyte-specific enhancer-factor d (MEF2D) binds to the promoter and induces the d

106 .6 [6.3] ng/mL; controls, 27.5 [5.0] ng/mL), factor D (MIS-C, 44.0 [17.2] ng/mL; acute COVID-19, 33.8

107 is of Drosophila mitochondrial transcription factor (d-mtTF) B1.

108 The 7-factor D-optimal design training set contained just 55 s

109 is required, since lysis is lost when either factor D or factor B is removed and is restored upon rec

110 The higher specificity towards factor D over trypsin and thrombin is based on hydrophob

111 mixed-effects models, and we computed slope factor, d[PbB]/d[PbA] or the change in PbB per unit chan

112 Platelet-derived growth factor D (PDGF-D), also known as Iris-expressed growth f

113 that binds dimers of platelet-derived growth factor D (PDGF-DD).

114 Platelet-derived growth factor-D (PDGF-D) is a newly discovered member of the PD

115 Platelet-derived growth factor-D (PDGF-D) is a newly recognized growth factor kn

116 Platelet-derived growth factor-D (PDGF-D) mediates glomerulosclerosis and inters

117 Platelet-derived growth factor-D (PDGF-D) signaling plays critical roles in the

118 Platelet-derived growth factor-DD (PDGF-DD) is a recently discovered member of t

119 th the expression of platelet-derived growth factor D (PDGFD).

120 telets and increased platelet-derived growth factor D, Pdgfrb, Itga2, and matrix metalloproteinases 2

121 ed production of vascular endothelial growth factor-D preceded caspase-3 and poly(ADP)ribose polymera

122 Genetic deficiency of complement C3 and factor D prevented both the systemic thrombophilia and r

123 3 (MASP1/3(-/-)) express only the zymogen of factor D (pro-factor D [pro-Df]), a necessary component

124 ice is dependent on MASP-1/3 cleavage of pro-factor D (pro-FD) into mature factor D (FD).

125 )) express only the zymogen of factor D (pro-factor D [pro-Df]), a necessary component of the alterna

126 ith a conserved cleavage site for a putative factor D protease.

127 n the presence of the other significant risk factors: D+/R- CMV serologic status (P < .001) or use of

128 sion of adequacy of prior screening and risk factors (D recommendation).The USPSTF recommends against

129 tro complexes were able to cleave C4 and pro-factor D, respectively.

130 re of its mature serine protease, complement factor D, revealed major conformational changes in the s

131 or Nmnat, antagonizes the axon-destabilizing factors D-Sarm and Axundead (Axed) during axon branch gr

132 ecombinant microplasminogens chimerized with factor D sequences at loops 3, 5, and 7 were cleaved by

133 ectra of the SP domains of both factor B and factor D showed that the factor D linewidths were broade

134 nd large (ss(2)-microglobulin and complement factor D) solutes was significantly greater for hemodiaf

135 rimary specificity (S1) pocket.Comparison of factor D structural variants with other serine protease

136 d their body weights are similar to those of factor D-sufficient littermates.

137 us treatment and vascular endothelial growth factor D testing and recommendations against doxycycline

138 ly conserved RNA polymerase II transcription factor D (TFIID) complex is composed of TATA box-binding

139 regulatory effect on adipsin (or complement factor D), the activity of which modulates the contrasti

140 Addition of human factor D to -/- animals restored GI/R injury and was pre

141 C3 proconvertase (C3bB), which is cleaved by factor D to C3 convertase (C3bBb).

142 into the Ba and Bb fragments by the protease factor D to form the C3 convertase from the complex betw

143 otrypsinogen-like zymogens, is followed by a factor D-unique step, the re-orientation of an external

144 capacity, serum vascular endothelial growth factor D (VEGF-D), and quality of life and functional pe

145 Vascular endothelial growth factor D (VEGF-D), well-characterized as a "lymphangioge

146 c antigen (PSA), vascular endothelial growth factor-D (VEGF-D), ETS-related gene protein (ERG), and i

147 the adult brain, vascular endothelial growth factor D (VEGFD) is required for structural integrity of

148 Vascular endothelial growth factor-D (VEGFD) is a potent pro-lymphangiogenic molecul

149 t inhibitors targeting C3, C5, factor B, and factor D were tested as comparators.

150 oducts Ba and C3d) and an activating enzyme (factor D) were elevated in AMD subjects.

151 produced complement activation factor B and factor D which then enhanced C3 cleavage to activation p

152 ted with the unique functional properties of factor D, which include high specificity toward factor B

153 In contrast, Factor D, which is a member of the trypsin family of ser

154 Xeroderma pigmentosum factor D (XPD) is a 5'-3' superfamily 2 helicase and the