ライフサイエンスコーパス: blood clotting

1 ndent thrombus formation, and agonist-driven blood clotting.

2 sed inflammation, microvascular density, and blood clotting.

3 h those involved in mammalian complement and blood clotting.

4 , interaction which is central to preventing blood clotting.

5 nd pharmacological role in the modulation of blood clotting.

6 posure of anionic phospholipids that support blood clotting.

7 genic effects on bone, lipid metabolism, and blood clotting.

8 and the mice have no overt abnormalities in blood clotting.

9 enzyme gene (ACE) may be related to abnormal blood clotting.

10 ivity of tissue factor that is distinct from blood clotting.

11 erto undiscovered, shape that contributes to blood clotting.

12 mechanical regulation of vWF activity during blood clotting.

13 a activation of FV is pivotal for plasma and blood clotting.

14 ctor IX and prolonged human plasma and whole blood clotting.

15 uclear cell fragments that are essential for blood clotting.

16 by partial loss of pigmentation and impaired blood clotting.

17 platelet stimulation and platelet-activated blood clotting.

18 siologic activator of the contact pathway of blood clotting.

19 identified as a regulatory driving force in blood clotting.

20 shown to be a crucial step in the process of blood clotting.

21 wth by obstructing tumor circulation through blood clotting.

22 ts are anuclear cells that are essential for blood clotting.

23 depleted protein production and inefficient blood clotting.

24 way inhibitor (TFPI) is a major regulator of blood clotting.

25 uid flow in the regulation of propagation of blood clotting.

26 for designing new antithrombotics disrupting blood clotting.

27 ments lacking nuclei that play a key role in blood clotting.

28 sed by blood-sucking insects to inhibit host blood clotting.

29 mone (melanocyte stimulating hormone), and a blood-clotting agent can be anchored to erythrocytes, pr

30 During human blood clotting, alpha2-antiplasmin (alpha2AP) becomes co

31 , serving to activate the contact pathway of blood clotting and accelerate factor V activation.

32 e activation of various proteins involved in blood clotting and bone metabolism.

33 the roles that polyP plays in modulating the blood clotting and complement systems in health and dise

34 It is a potent modulator of the blood clotting and complement systems in hemostasis, thr

35 The importance of factors influencing blood clotting and fibrinolysis in preventing coronary e

36 gulatory actions is its ability to influence blood clotting and fibrinolysis.

37 ns is critical for platelet aggregation upon blood clotting and for leukocyte extravasation to inflam

38 being involved in signalling, vasodilation, blood clotting and immunity and as an intermediate in mi

39 rtant roles in vivo, ranging from regulating blood clotting and inflammation to directly counteractin

40 ear polymers of orthophosphate that modulate blood clotting and inflammation.

41 the rate of mixing, and surface chemistry in blood clotting and its chemical model.

42 ny important biological responses, including blood clotting and pain perception.

43 s may exhibit unique properties analogous to blood clotting and thereby be useful in self-healing app

44 inogen activator inhibitor (PAI-1), controls blood clotting and tissue remodeling events that involve

45 lation reverses the prometastatic effects of blood clotting and tumor cell integrin alphavbeta3.

46 eosinophils, mast cells, mononuclear cells), blood clotting, and microvascular density within the tum

47 f the VKOR gene extends our understanding of blood clotting, and should facilitate development of new

48 ogical processes, including viral infection, blood clotting, and signal transduction, and as such, th

49 extracellular processes such as virus entry, blood clotting, antibody-mediated immune response, infla

50 Substances released by platelets during blood clotting are essential participants in events that

51 generated in a tissue factor-initiated whole blood clotting assay unless exogenous FV was added, cons

52 ons to hemostasis appear to be to accelerate blood clotting but are not required for blood clotting t

53 a potent hemostatic regulator, accelerating blood clotting by activating the contact pathway and pro

54 owed that fibrin(ogen) polymerisation during blood clotting can be affected strongly by LPS.

55 ted allosteric enzyme involved in vertebrate blood clotting, can be converted into a K+-specific enzy

56 integral membrane protein that triggers the blood clotting cascade and for which membrane anchoring

57 Seven proteins in the human blood clotting cascade bind, via their GLA (gamma-carbox

58 , the cell-surface protein that triggers the blood clotting cascade in hemostasis and thrombotic dise

59 The blood clotting cascade is selectively involved in lung m

60 ension, dyslipidemia, and alterations of the blood clotting cascade that accentuate thrombosis.

61 ctor VIII (FVIII), an important co-factor in blood clotting cascade, elicits unwanted anti-FVIII anti

62 our cascades are: the complement system, the blood clotting cascade, the fibrinolytic system, and the

63 hat is exposed upon injury and initiates the blood clotting cascade.

64 iginally well characterized in the mammalian blood clotting cascade.

65 ptidomimetic drugs such as inhibitors of the blood clotting cascade.

66 mbin is a dual action serine protease in the blood clotting cascade.

67 malian serpin antithrombin in localizing the blood-clotting cascade, suggesting that serpin inhibitio

68 n is a dual-action protein that mediates the blood-clotting cascade.

69 ty of 4% to 20% of normal and improved whole blood clotting compared with factor VIII-deficient mice.

70 ecretory pathway (receptors, growth factors, blood-clotting components, and even many viral envelope

71 s of inverse lag times and maximal slopes of blood clotting curves in buffers containing Na+ and Cl-

72 polyphosphate exerts differential effects on blood clotting, depending on polymer length.

73 ase is widely recognized to be a form of the blood clotting disorder hemophilia, its molecular basis

74 Two genes implicated in blood-clotting disorders, von Willebrand factor (vWA) an

75 lasminogen activator widely used in treating blood-clotting disorders.

76 Structures of the blood clotting enzyme thrombin complexed with hirugen an

77 ed by peptides of +3 to +5 net charge and by blood clotting factor V.

78 idues (gamma-carboxyglutamic acid domain) of blood clotting factor VII was carried out to identify si

79 Active site-inhibited blood clotting factor VIIa (fVIIai) binds to tissue fact

80 Blood clotting factor VIIa is involved in the first step

81 VWF also is a carrier protein for blood clotting factor VIII, and this interaction is requ

82 upon expression of a misfolding-prone human blood clotting factor VIII, or after partial hepatectomy

83 s covalently linked to fibrin when activated blood clotting factor XIII (FXIIIa) catalyzes the format

84 he basis of orthologs of genes for mammalian blood clotting factors being present in its genome.

85 ified factor VIIa and to active site-blocked blood clotting factors Xa or IXa was studied.

86 e lectins and to membrane-binding domains of blood-clotting factors V and VIII.

87 At higher settings, a blood clotting formed, leading to complete and permanent

88 here complement the current understanding of blood clotting from the molecular to the physiological l

89 e to release tryptase, and thrombin mediates blood clotting in early wounds.

90 K epoxide reductase, a protein required for blood clotting in humans, as part of a disulfide bond fo

91 ompted by previous observations of defective blood clotting in rabbits deficient in the sixth compone

92 the spatiotemporal dynamics of initiation of blood clotting in the complex network of hemostasis.

93 The extensive blood clotting in the eotaxin-transfected tumors was ass

94 long been considered dispensable for normal blood clotting in vivo because hereditary deficiencies i

95 Blood clotting in vivo is catalyzed by thrombin, which s

96 wound healing is a complex process involving blood clotting, inflammation, migration of keratinocytes

97 Systems as varied as blood clotting, intracellular calcium signaling, and tis

98 Hemostasis and thrombosis (blood clotting) involve fibrinogen binding to integrin a

99 Mammalian blood clotting involves numerous components, most of whi

100 Pathologic blood clotting is a leading cause of morbidity and morta

101 phosphate (S1P) released by platelets during blood clotting is a potent, specific, and selective endo

102 Blood clotting is a process by which a haemostatic plug

103 Thrombosis, or malignant blood clotting, is associated with numerous cardiovascul

104 Tissue factor, the physiologic trigger of blood clotting, is the membrane-anchored protein cofacto

105 expression of the principal initiator of the blood clotting mechanism, tissue factor (TF), and blocki

106 such as dyslipidemia, oxidative stress, and blood clotting mechanisms, we hereby report the synthesi

107 suggest that the previously noted effects of blood clotting on lung metastasis might be mediated in p

108 vity and inhibit activators of the intrinsic blood clotting pathway, such as polyphosphate (polyP) an

109 unexplored problem, despite applications in blood clotting, plasmonics, industrial packaging and tra

110 from inverse lag times and maximal slopes of blood clotting plots, which are also anion and cation de

111 he expression of a cellular receptor for the blood-clotting protease factor Xa, designated effector c

112 serpin, antithrombin, to inhibit its target blood-clotting proteases by generating new protease inte

113 Here, Petersen et al. (2017) show that the blood clotting protein fibrinogen inhibits nerve repair

114 t the worms are capable of cleaving the host blood clotting protein fibronectin and that this activit

115 Proteolysis of the blood-clotting protein von Willebrand factor (VWF) obser

116 n; 5) assess the role of insulin resistance, blood clotting, protein kinase C isoforms, and signal tr

117 in addition to its known role in regulating blood clotting, protein S may also be an important autoc

118 Exosite I of the blood clotting proteinase, thrombin, mediates interactio

119 in activates the primary serpin inhibitor of blood clotting proteinases, antithrombin, both by an all

120 49 of antithrombin, the primary inhibitor of blood clotting proteinases, has previously been implicat

121 antithrombin, the principal inhibitor of the blood-clotting proteinases factor Xa and thrombin, is ac

122 ontaining regions of the vitamin K-dependent blood-clotting proteins.

123 ing of many protein-lipid interactions among blood-clotting proteins.

124 onal assays, such as endotoxin-induced whole blood clotting, prothrombin time, as well as factor X an

125 platelets is very efficient at accelerating blood clotting reactions but is less efficient at initia

126 mechanisms by which polyphosphate modulates blood clotting reactions remain to be elucidated.

127 e platelet aggregation, vasoconstriction and blood clotting; saliva of these organisms also has anti-

128 activation, and phosphatidylserine exposure, blood clotting simulations require prediction of platele

129 ndividuals who participated in the Genes and Blood Clotting Study (GABC) or the Trinity Student Study

130 onse to infection includes activation of the blood clotting system, leading to extravascular fibrin d

131 tion of thrombin, which enhances the overall blood-clotting system, both by accelerating fibrin gener

132 ry agent and a potent modulator of the human blood-clotting system.

133 SNPs initiate the contact pathway of the blood-clotting system; short-chain polyP accelerates the

134 tamin K2 is a critical nutrient required for blood clotting that also plays an important role in bone

135 h nonspecific binding and adverse effects on blood clotting that limit their use.

136 role, including the ectoenzyme that triggers blood clotting, the plasma serine protease, factor VIIa,

137 rin alpha(IIb)beta3 initiates the process of blood clotting through binding fibrinogen.

138 to 2.5 months and normalization of the whole blood clotting time (WBCT) for about a month.

139 njury in HemA mice, and fully corrects whole blood clotting time (WBCT) in HemA dogs immediately afte

140 Coagulation tests (whole blood clotting time [WBCT], activated clotting time [ACT

141 Whole blood clotting time analysis confirmed that hemostasis w

142 st, siRNA-mediated knockdown of KLF2 reduced blood clotting time and flow rates.

143 rombin time, partial correction of the whole blood clotting time and thromboelastography parameters,

144 Despite normalization of blood clotting time and thrombus stability after r-FVIII

145 se-dependent partial correction of the whole blood clotting time and, at higher doses, of the activat

146 nfected cells, KLF2 overexpression increased blood clotting time as well as flow rates under basal an

147 Whole blood clotting time in FIX-deficient mice was corrected

148 unction were normal; however, when the whole blood clotting time was measured at 25 degrees C in plas

149 sed onto a factor VIIInull background, whole blood clotting time was partially corrected, equivalent

150 Whole-blood clotting times and FeCl3 carotid artery injury cor

151 Activated clotting times and whole blood clotting times were normalized, activated partial

152 creased levels of liver function enzymes and blood clotting times, decreased levels of platelets, mul

153 rate blood clotting but are not required for blood clotting to happen.

154 Willebrand factor receptor, functions during blood clotting to promote platelet adhesion and activati

155 that the threshold response of initiation of blood clotting to the size of a patch of stimulus is a r

156 ial phosphatidylserine (PS) in apoptosis and blood clotting using annexin V.

157 ther design, thrombin, an enzyme involved in blood clotting, was captured by thrombin-AR-modified cel

158 Here, inspired by blood clotting, we show that polymer-colloid composite a

159 arteriolar vessels, permitting evaluation of blood clotting within small sample volumes under pathoph