ライフサイエンスコーパス: factor D

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

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

3 nctionally inhibitory antibody against human factor D.

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

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

6 induced reversible conformational changes in factor D.

7 factors such as vascular endothelial growth factor-D.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

59 he first known potent noncovalent reversible Factor D inhibitors.

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

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

62 Factor D is a serine protease essential for the activati

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

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

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

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

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

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

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

70 Inhibition of factor D may represent an effective therapeutic approach

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

86 3 (MASP1/3(-/-)) express only the zymogen of factor D (pro-factor D [pro-Df]), a necessary component

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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