ライフサイエンスコーパス: clot retraction

1 on fibrin is involved in the second step of clot retraction.

2 ines markedly reduced beta3-dependent fibrin clot retraction.

3 sponses including adhesion, aggregation, and clot retraction.

4 a3 did not inhibit endothelial cell-mediated clot retraction.

5 telets and mediates platelet aggregation and clot retraction.

6 ith other fibrin(ogen) region(s) can support clot retraction.

7 ites for the integrin receptors that support clot retraction.

8 from the site on fibrin that is required for clot retraction.

9 es the processes of platelet aggregation and clot retraction.

10 telet aggregation, adhesion to collagen, and clot retraction.

11 g on fibrinogen and thrombin-mediated fibrin clot retraction.

12 in the regulation of thrombus formation and clot retraction.

13 haMbeta2 exhibited reduced cell adhesion and clot retraction.

14 atelet adhesion and platelet-mediated fibrin clot retraction.

15 analysis of data from mice with a defect in clot retraction.

16 at results in stable platelet aggregates and clot retraction.

17 that platelet SM-rich rafts are involved in clot retraction.

18 second talin-binding wave is associated with clot retraction.

19 -cyclodextrin impaired myosin activation and clot retraction.

20 ficient mouse platelets, which show impaired clot retraction.

21 n, fibrinogen binding, granule secretion and clot retraction.

22 telet thrombi is required for the control of clot retraction.

23 itating platelet spreading on fibrinogen and clot retraction.

24 aling contributing to platelet-spreading and clot retraction.

25 MAPK activation is important in facilitating clot retraction.

26 he aggregation defect and recovered impaired clot retraction.

27 ole of calpain-1 in platelet aggregation and clot retraction.

28 elated with reduced platelet aggregation and clot retraction.

29 n the regulation of platelet aggregation and clot retraction.

30 on of outside-in signaling, aggregation, and clot retraction.

31 ch as spreading, thrombus consolidation, and clot retraction.

32 n of Bcl-3 in a surrogate cell line enhanced clot retraction.

33 ng, platelet adhesion, and platelet-mediated clot retraction.

34 brinogen lacking these sites still supported clot retraction.

35 inogen and/or other integrins participate in clot retraction.

36 g adhesion, platelet aggregation, and fibrin clot retraction.

37 is generally associated with aggregation and clot retraction.

38 ggregation, cytoskeletal reorganization, and clot retraction.

39 horylation of pp125(FAK), and greater fibrin clot retraction.

40 ading, actin cytoskeleton rearrangement, and clot retraction.

41 n platelet aggregation and platelet-mediated clot retraction.

42 platelet aggregation, and platelet-mediated clot retraction.

43 ysis of fibrin polymers markedly facilitated clot retraction.

44 or both of the RGD sequences are involved in clot retraction.

45 rce to the fibrin clot during the process of clot retraction.

46 ays; (4) prolonged bleeding time; (5) absent clot retraction; (6) decreased glass bead retention; (7)

47 These effects were selective because fibrin clot retraction, a response also dependent on alphaIIbbe

48 sites in the A alpha chains are involved in clot retraction and adhesion, recent data demonstrated t

49 (IIb)beta3 involved in platelet adhesion and clot retraction and define the new recognition specifici

50 380 is replaced by Asn, demonstrated delayed clot retraction and impaired alpha(IIb)beta3 binding.

51 Osaka V (gammaArg375 --> Gly) showed delayed clot retraction and reduced binding to purified alpha(II

52 Chinese hamster ovary cells causes defective clot retraction and RhoA-mediated retraction signaling b

53 The defects in clot retraction and spreading on fibrinogen of Rap1b-def

54 on on collagen I under flow, and accelerated clot retraction and spreading on fibrinogen.

55 a(1) can bind to FN within a clot to promote clot retraction and support cell shape change.

56 ted mechanistically from GPIIb-IIIa-mediated clot retraction and that clot retraction requires additi

57 ariant showed greater alpha-granule release, clot retraction, and adhesion to fibrinogen under shear

58 a with prolonged bleeding times, a defect in clot retraction, and increased extramedullary megakaryoc

59 lpha(E)C, block the alpha(v)beta(3)-mediated clot retraction, and induce the ligand-induced binding s

60 ology under light microscopy, bleeding time, clot retraction, and platelet aggregation and secretion

61 inolytic system as an important regulator of clot retraction, and show that promoting clot retraction

62 y poor spreading on fibrinogen and decreased clot retraction, and they exhibit ineffective Ca2+ signa

63 More importantly, platelet aggregation, clot retraction, and tyrosine dephosphorylation defects

64 Thus, endothelial cell-mediated clot retraction appears to be dependent on fibrinogen ce

65 ion, MAPK-dependent MLC phosphorylation, and clot retraction are inhibited by a Rac1 inhibitor and in

66 408-411 supported endothelial cell-mediated clot retraction as well as intact fibrinogen.

67 Insights into the mechanisms regulating clot retraction at sites of vascular injury have been ha

68 Platelets from LD supported normal clot retraction but failed to bind fibrinogen.

69 re, RhoA was essential for integrin-mediated clot retraction but not for actomyosin rearrangements an

70 ese segments inhibited platelet adhesion and clot retraction but not platelet aggregation, supporting

71 ficant reduction in platelet aggregation and clot retraction but surprisingly the mutant mice display

72 g sites are important for an initial step in clot retraction, but not for a subsequent step.

73 nction, it completely abolishes adhesion and clot retraction by a cell that requires stimulation for

74 We show that recombinant FN monomers support clot retraction by Chinese hamster ovary cells expressin

75 Inhibition of mTOR by rapamycin blocks clot retraction by human platelets.

76 into fibrin matrices significantly improves clot retraction by nucleated cells expressing the integr

77 to activate integrins is required for fibrin clot retraction by platelets.

78 , the formation of large thrombi and delayed clot retraction compared with wild-type littermates.

79 d spreading on Fg and fibronectin and faster clot retraction compared with wild-type.

80 to tissue plasminogen activator and promoted clot retraction during fibrinolysis concomitant with an

81 haIIbbeta3 outside-in signaling that affects clot retraction ex vivo.

82 In vitro clot retraction experiments indicated that subthreshold

83 , that no one of these sites is critical for clot retraction; fibrinogen lacking all three sites stil

84 amma C, designated P3, efficiently inhibited clot retraction in a dose-dependent manner.

85 ons are required for this process, we tested clot retraction in platelets expressing a talin1(L325R)

86 However, the defect in clot retraction in talin1(L325R) platelets, but not tali

87 In addition, D3 also inhibited whole blood clot retraction, in contrast to AP3 and C3, suggesting t

88 , fibrinogen binding, granule secretion, and clot retraction, indicating an important role for connex

89 rding the processes of platelet aggregation, clot retraction, inflammation, and thrombosis.

90 Clot retraction inhibition by D3 was not due to altered

91 of clot retraction, and show that promoting clot retraction is a novel and complementary means by wh

92 These findings indicate that clot retraction is a two-step process, such that one or

93 -in signaling such as platelet spreading and clot retraction is augmented in Jam-A-deficient platelet

94 The stimulatory role of MAPK in clot retraction is mediated by stimulating myosin light

95 ed activation of MAPK and MLC and subsequent clot retraction is Rac1-dependent.

96 is a key component of the clot, its role in clot retraction is unclear.

97 Thus, clot retraction mediated by endothelial cells is not dep

98 The clot retraction of SM-depleted platelets from SM synthas

99 sites described above is required to support clot retraction or that (b) either site alone or in conj

100 ediated effects such as thrombin generation, clot retraction, or smooth muscle cell migration and pro

101 triple mutant fibrinogen, the second step of clot retraction, possibly the development of clot tensio

102 results in reduced platelet aggregation and clot retraction potentially by causing dephosphorylation

103 es including adhesion, spreading, migration, clot retraction, proliferation, and differentiation.

104 s of GT (defects in platelet aggregation and clot retraction, prolonged bleeding times, and cutaneous

105 We evaluated the clot retraction rate (CRR), fibrinolysis rate (FR), clot

106 Clot retraction rate negatively correlated with FENO and

107 Clot retraction refers to the process whereby activated

108 GPIIb-IIIa-mediated clot retraction and that clot retraction requires additional signaling through GP

109 3 signalling, with defective aggregation and clot-retraction responses in vitro, and an in vivo bleed

110 nces spreading on fibrinogen and accelerates clot retraction (see figure).

111 required for alpha v beta 3-mediated fibrin clot retraction, suggesting that fibrinogen may have oth

112 Thus, we propose that clot retraction takes place in SM-rich rafts where a fib

113 Unexpectedly, this variant did support clot retraction that was indistinguishable from retracti

114 d that subthreshold doses of tPA facilitated clot retraction through a plasmin-dependent mechanism.

115 lows myosin to bind to alpha(IIb)beta(3) and clot retraction to occur.

116 Clot retraction was abolished, and platelet spreading on

117 lso, in CypD-deficient platelet-rich plasma, clot retraction was altered.

118 an unaltered basal cAMP level; however, the clot retraction was compromised in the mutant mice.

119 However, with the triple mutant fibrinogen, clot retraction was delayed compared with normal recombi

120 In this study, endothelial cell-mediated clot retraction was supported by fibrin generated from s

121 another alpha IIb beta 3-dependent process, clot retraction, was unaffected by the gamma delta 5 mut

122 a-granule secretion, platelet spreading, and clot retraction were not markedly affected.

123 rotein molecules and yet completely inhibits clot retraction were used.

124 platelet-spreading on fibrinogen as well as clot retraction, whereas OXSI-2 blocked only platelet-sp

125 Furthermore, clot retraction with c-Cbl KO and c-Cbl(YF/YF) platelets