ライフサイエンスコーパス: ristocetin

1 regation induced by ADP, convulxin, PMA, and ristocetin.

2 complex-binding assay that is independent of ristocetin.

3 mparable with that of WT (36 +/- 12 nm) with ristocetin.

4 -dependent platelet agglutination induced by ristocetin.

5 comes exposed following exposure to shear or ristocetin.

6 hear stress or nonphysiological stimuli, eg, ristocetin.

7 ular weight VWF and reduced agglutination to ristocetin.

8 cant binding to platelets in the presence of ristocetin.

9 ptimal concentrations of both botrocetin and ristocetin.

10 g to platelets in the absence or presence of ristocetin.

11 sults were obtained with multimeric VWF when ristocetin (0.5 mg/ml) was added to blood before perfusi

12 Overall, ristocetin A appears to have the greatest applicability

13 related glycopeptide antibiotics vancomycin, ristocetin A, and teicoplanin can all be used as chiral

14 of the monomer and asymmetric dimer forms of ristocetin A, upon binding of two molecules of ligand, s

15 VWF ristocetin activity and factor VIII binding remained una

16 The first total synthesis of the ristocetin aglycon is described employing a modular and

17 Ristocetin and botrocetin actions on VWF were dissociate

18 WF binding in the presence of the modulators ristocetin and botrocetin and by enhanced adhesion of Ch

19 static VWF binding induced by 2 modulators, ristocetin and botrocetin, and platelet adhesion to VWF

20 d in vitro by two nonphysiologic modulators, ristocetin and botrocetin.

21 ed under static conditions by the modulators ristocetin and botrocetin.

22 ced platelet aggregation in response to both ristocetin and shear stress.

23 mbin, adenosine diphosphate (ADP), collagen, ristocetin, and arachidonic acid) was determined in vitr

24 the response of their platelets to thrombin, ristocetin, and collagen were measured before, immediate

25 reviously characterized for their effects on ristocetin- and botrocetin-dependent vWF-GP Ib-IX-V inte

26 The force required to break the ristocetin- and botrocetin-induced plasma VWF-GP Ib-IX b

27 the first crystal structure of an asymmetric ristocetin antibiotic dimer, as well as the structure of

28 , this crevice is shown to correspond to the ristocetin binding site in the A1 domain and the proteas

29 Because the VWF:RCo assay depends on ristocetin binding to VWF, mutations (and polymorphisms)

30 s in vWF mediate binding to glycoprotein Ib, ristocetin, botrocetin, collagen, sulphatides, and hepar

31 tions and when the interaction is induced by ristocetin but contributes a specific structure to the b

32 slope of platelet aggregation in response to ristocetin, but with a diminished maximal extent.

33 :C activity, vWf-related antigen levels, and ristocetin co-factor activity, respectively, whereas the

34 von Willebrand factor (VWF) antigen and VWF ristocetin cofactor (RC)).

35 onths; starting rVWF dose was 50 +/- 10 VWF: ristocetin cofactor (VWF:RCo) IU/kg twice weekly (prior

36 0 unaffected relatives, as defined by plasma ristocetin cofactor (VWF:RCo) levels.

37 BS >10 and VWF:ristocetin cofactor activity <10 U/dL were associated wi

38 Assessment of ristocetin cofactor activity (VWF:RCo) and von Willebran

39 r (VWF) assays, VWF antigen (VWF:Ag) and VWF ristocetin cofactor activity (VWF:RCo), used for diagnos

40 VWF), including VWF antigen (VWF:Ag) and VWF ristocetin cofactor activity (VWF:RCo).

41 ld vWF deficiency (FvW:antigen 39 IU/dL; FvW:ristocetin cofactor activity 44 IU/dL; factor VIII 99%;

42 ver design (rVWF vs rVWF:rFVIII at 50 IU VWF:ristocetin cofactor activity [RCo]/kg).

43 en-binding activity and the ratio of the VWF ristocetin cofactor activity and VWF antigen was signifi

44 current laboratory testing, particularly the ristocetin cofactor activity assay (VWF:RCo).

45 hich is subject to less variability than the ristocetin cofactor activity assay, and collagen-binding

46 of subjects had VWF antigen (VWF:Ag) or VWF ristocetin cofactor activity below the lower limit of no

47 vestigated the effect of shear stress on the ristocetin cofactor activity of purified von Willebrand

48 Shear stress increased the ristocetin cofactor activity of von Willebrand factor in

49 WF multimer patterns, disproportionately low ristocetin cofactor activity, and significant bleeding s

50 The PK of rVWF ristocetin cofactor activity, VWF antigen, and collagen-

51 Factor VIII, vW antigen, and ristocetin cofactor also decreased with long-term PGI2 i

52 ly stimulated the VWF-GPIbalpha binding in a ristocetin cofactor ELISA and increased platelet adhesio

53 erate von Willebrand disease, defined as VWF ristocetin cofactor less than 0.50 IU/mL, and heavy mens

54 actor VIII, von Willebrand (vW) antigen, and ristocetin cofactor levels were abnormally high in 92%,

55 The ratio of ristocetin cofactor to vW antigen, which may reflect bio

56 nts with vWD type 1 and borderline to normal ristocetin-cofactor (vWF:RCo) activity values, collagen

57 hyperfunctional, agglutinating platelets at ristocetin concentrations that induced minimal agglutina

58 otent than human homologues, and in addition ristocetin could boost platelet aggregation only with th

59 The ristocetin-dependent binding of the mutant cell lines wa

60 lymorphism, D1472H, as was direct binding to ristocetin for a 1472H A1 loop construct.

61 tivated in platelets on stimulation with VWF/ristocetin in a time-dependent manner.

62 bin receptor activating-peptide, U46619, and ristocetin in samples from (1) healthy volunteers (n = 5

63 ne A1-domain could result in the heightened, ristocetin-independent interactions observed with human

64 200 concentrations were necessary to inhibit ristocetin induced aggregation after desmopressin infusi

65 e closure time, and none of the patients had ristocetin induced aggregation in the target range.

66 educed median VWF activity from 178 to < 3%, ristocetin induced platelet aggregation from 40U to < 10

67 vWF/ristocetin-induced agglutination was only slightly reduc

68 rombin activation from those associated with ristocetin-induced agglutination.

69 noid]), an adjuvant antitumor drug, inhibits ristocetin-induced aggregation of human platelets.

70 emically synthesized peptide fully inhibited ristocetin-induced aggregation, with an IC50 of 200-400

71 Q(G -->V) 233VDVK237 peptide fully inhibited ristocetin-induced aggregation, with an IC50 of approxim

72 Ristocetin-induced and botrocetin-induced binding to GPI

73 Whereas ristocetin-induced binding of plasma vWF from affected m

74 and 642-645 do play an important role in the ristocetin-induced binding of vWF to platelets.

75 Ristocetin-induced binding to GPIb was reduced selective

76 This latter aspect is not observed with ristocetin-induced GP Ib-von Willebrand factor agglutina

77 In addition, OS-1 blocked ristocetin-induced platelet agglutination of human plate

78 The mutant blocked 100% ristocetin-induced platelet agglutination, whereas WT fa

79 protein was capable of effectively blocking ristocetin-induced platelet agglutination.

80 atelet adhesion and their ability to inhibit ristocetin-induced platelet agglutination.

81 formation under high shear rates (PFA), and ristocetin-induced platelet aggregation (Multiplate) bef

82 its collagen binding activity (VWF:CBA) and ristocetin-induced platelet aggregation activity.

83 Nd4 and Nd6 inhibit ristocetin-induced platelet aggregation and reduce VWF-m

84 rterial shear rate but in contrast inhibited ristocetin-induced platelet aggregation.

85 ted in mutant recombinant vWF with decreased ristocetin-induced platelet binding, but normal multimer

86 : collagen binding, factor VIII binding, and ristocetin-induced platelet binding.

87 the other hand, were normal with respect to ristocetin-induced vWF binding and adhesion to immobiliz

88 Ristocetin-mediated binding of vWF induced a transient p

89 55A, Clus1, and DC variants caused increased ristocetin-mediated GPIbalpha binding to VWF.

90 attributed to a reduction in vWF binding, as ristocetin-mediated platelet aggregation and agglutinati

91 gion, type 2B VWD mutations, or binding of a ristocetin-mimicking monoclonal antibody, all of which c

92 Ibbeta3 blocked the effect of the mutant and ristocetin on platelet activation/adhesion.

93 heightened response to low concentrations of ristocetin or botrocetin, whereas the loss-of-function m

94 ells spontaneously, requiring the modulators ristocetin or botrocetin.

95 failed to bind vWF in the presence of either ristocetin or botrocetin.

96 presence of optimal concentrations of either ristocetin or botrocetin.

97 87 but did not block platelet aggregation by ristocetin or phorbol myristate acetate (PMA) and only s

98 8K) or failed to bind vWf in the presence of ristocetin or roll on immobilized vWf under fluid shear

99 inding site in GPIb(alpha) markedly enhances ristocetin- (or botrocetin)-induced vWF binding and allo

100 (1), novobiocin), glycopeptides (vancomycin, ristocetin), peptides (bacitracin, cycloserine), and chl

101 en vWF and GP Ibalpha closely correlate with ristocetin- rather than botrocetin-dependent binding und

102 3zeta content is increased following vWF and ristocetin stimulation.

103 ed via diaryl ether formation to provide the ristocetin tetracyclic ring system (15 steps, 8% overall

104 X co-immunoprecipitation, platelet adhesion, ristocetin-, thrombin- or collagen-induced platelet aggr

105 nd its ligand VWF in an assay independent of ristocetin (VWF:IbCo ELISA).

106 ntly prolonged, and response to thrombin and ristocetin was significantly decreased immediately after

107 neous binding of R1450E to GPIbalpha without ristocetin with an apparent K(D) of 85 +/- 34 nm, compar