ライフサイエンスコーパス: factor XII

1 = 9.2 +/- 2.1 pmol/L/min in the presence of factor XII).

2 olyphosphate nanoparticles potently activate factor XII.

3 mbus formation and activation of coagulation factor XII.

4 ing that polyphosphate drives thrombosis via factor XII.

5 platelets with the activation of coagulation factor XII.

6 and distinguish them from activation through factor XII.

7 d and dependent on fluid-phase activation of factor XII.

8 of endothelial cells, even in the absence of factor XII.

9 enic growth factor and (ii) demonstrate that factor XII activates a signal transduction pathway, whic

10 On endothelial cells, factor XII activation is secondary to prekallikrein acti

11 dykinin formation can occur without invoking factor XII activation, although the kallikrein formed ca

12 n-HK leads to rapid formation of kallikrein; factor XII alone does not autoactivate.

13 stigated the impact of genetic deficiency of factor XII and acute inhibition of activated factor XII

14 study showed that both genetic deficiency of factor XII and an inhibition of activated factor XII in

15 onged incubation of plasma deficient in both factor XII and C1-INH led to conversion of prekallikrein

16 collagen-coated flow chamber, independent of factor XII and factor VII.

17 n their surface that colocalized with active factor XII and initiated coagulation in a factor XII-dep

18 omboplastin time was associated with reduced factor XII and prekallikrein, whereas levels of factors

19 onents of C1, kallikrein, activated forms of factor XII, and factor XIa in plasma.

20 evels of plasma prekallikrein (PK) activity, factor XII, and high-molecular weight kininogen in the p

21 -a serpin inhibitor of kallikrein, C1r, C1s, factor XII, and plasmin.

22 for the "contact system" factors (factor XI, factor XII, and prekallikrein) could not be identified.

23 esis, the observed synergism between EGF and factor XII, and the differential sensitivity to tyrphost

24 High molecular weight kininogen (HK) and factor XII are known to bind to human umbilical vein end

25 Treatment of aortic SMCs with factor XII, as well as activated factor XII, resulted in

26 adykinin formation is typically initiated by factor XII autoactivation, it is also possible to activa

27 ch provided a negatively charged surface for factor XII autoactivation.

28 rs protein-protein interactions, both HK and factor XII bind to GP Ibalpha.

29 aken together, the data suggest that HK (and factor XII) bind to HUVECs via a 33-kDa cell surface gly

30 rotease-activated receptor-1 failed to block factor XII binding to platelets.

31 bited HK binding to platelets, did not block factor XII binding.

32 HK and low molecular mass kininogen, but not factor XII, blocked biotin-HK binding to cytokeratin, an

33 (plasma) contacts certain foreign surfaces, factor XII can activate and trigger a series of reaction

34 proteolytic cascade involving kallikrein and Factor XII cleaves chromogranins to active compounds bot

35 Targeting polyphosphate or factor XII conferred resistance to prostate cancer-drive

36 Factor XII deficiency has been postulated to be a risk f

37 is associated with a bleeding diathesis, but factor XII deficiency is not, indicating that, in normal

38 y is associated with a hemorrhagic disorder, factor XII deficiency is not, suggesting that fXI can be

39 Higher levels of procoagulant factors and factor XII deficiency may be risk factors for first veno

40 Factor XII deficiency was not related to VTE risk.

41 PKA did not correct the coagulant defect in factor XII deficient plasma, was purified from HUVEC cul

42 ide additional protection from thrombosis in factor XII-deficient animals.

43 Administration of human factor XII in factor XII-deficient mice fully restored injury-induced

44 C1-INH was removed from factor XII-deficient plasma by means of immunoadsorption

45 plasma, was purified from HUVEC cultured in factor XII-deficient serum, was not detected by antibody

46 bolishes procoagulant platelet activity in a factor XII-dependent manner, reduces fibrin accumulation

47 this strategy confers thromboprotection in a factor XII-dependent manner.

48 ve factor XII and initiated coagulation in a factor XII-dependent manner.

49 cient serum, was not detected by antibody to factor XII, did not activate FXI, and was not inhibited

50 ort here that a plasma protease cascade, the factor XII-driven contact system, critically contributes

51 oactivation, it is also possible to activate factor XII either by kallikrein, thus formed, or by plas

52 In this study, we tested whether factor XII exhibits growth factor activity on several ot

53 downstream of the gene encoding coagulation factor XII (f12) and was inadvertently modified while ge

54 A common variant in the factor XII (F12) gene (-4C>T, rs1801020) results in decr

55 e proteolytic enzymes kallikrein (KLKB1) and Factor XII (F12).

56 were developed using biotinylated activated factor XII (factor XIIa) or biotinylated kallikrein boun

57 gether, these data (i) confirm that clotting factor XII functions as a mitogenic growth factor and (i

58 The factor XII (FXII) -initiated contact system can trigger

59 Inhibition of coagulation factor XII (FXII) activity represents an attractive appr

60 le for subsequent DVT propagation by binding factor XII (FXII) and by supporting its activation throu

61 The plasma zymogens factor XII (fXII) and factor XI (fXI) contribute to thro

62 bus stabilization and growth have identified factor XII (FXII) and FXI as targets for new anticoagula

63 Factor XII (FXII) and high molecular weight kininogen (H

64 ered by the activation of the plasma protein factor XII (FXII) and leads to kallikrein-mediated cleav

65 and biologic substances, the plasma proteins factor XII (FXII) and prekallikrein undergo reciprocal p

66 Several distinct mutations in Factor XII (FXII) are associated with hereditary angioed

67 For example, mice deficient in coagulation factor XII (fXII) are protected from arterial thrombosis

68 Factor XII (FXII) autoactivates by contact with a variet

69 Investigations were performed to define the factor XII (FXII) binding site(s) on cultured endothelia

70 Recently, platelets, neutrophils, and factor XII (FXII) have been implicated as important play

71 Factor XII (FXII) is a plasma protease that has emerged

72 vivo in an attempt to verify the claim that factor XII (FXII) is primarily activated by stimulated p

73 Considering that factor XII (FXII) levels may affect bradykinin productio

74 actors, AEG-1 facilitated the association of factor XII (FXII) messenger RNA with polysomes, resultin

75 Mice lacking factor XII (fXII) or factor XI (fXI) are resistant to ex

76 hatase reduced thrombin generation even when factor XII (FXII) was blocked or absent.

77 Factor XII (FXII), a clotting enzyme that can initiate c

78 f serine proteases, prekallikrein (pKal) and factor XII (FXII), and a cofactor, high-MW kininogen (HK

79 Because activation of the contact proteases factor XII (FXII), prekallikrein, and factor XI (FXI) ca

80 vitro in both murine and human plasma, via a factor XII (FXII)-dependent mechanism.

81 oth high molecular weight kininogen (HK) and factor XII (FXII).

82 ons in the gene encoding the plasma protease factor XII (FXII).

83 omboplastin time measurement for coagulation factor XII (FXII).

84 Coagulation factor XII (FXII, Hageman factor, EC = 3.4.21.38) is the

85 The relations of plasma activated factor XII (FXIIa) concentration and a common polymorphi

86 tiated blood coagulation in vitro, activated factor XII (fXIIa) converts factor XI (fXI) to fXIa.

87 Activated factor XII (FXIIa) has plasminogen activator capacity bu

88 Activated factor XII (FXIIa) is selectively inhibited by corn Hage

89 Elevated fibrinogen, activated factor XII (FXIIa), and factor VII coagulant activity (F

90 ssociated with heterozygous mutations in the factor XII gene (FXII-HAE).

91 tion and a common polymorphism (C46T) of the factor XII gene with hemostatic status and risk of coron

92 ation in the C1 inhibitor or the coagulation Factor XII gene.

93 Activated factor XII generates plasma kallikrein, which proteolyze

94 ssue factor (TF) mice whereas the absence of factor XII had no effect.

95 Clotting factor XII (Hageman factor) contains epidermal growth fa

96 in inhibitor (CTI, an inhibitor of activated factor XII), heparin, enoxaparin, recombinant tick antic

97 y independent of the contact phase proteins, factor XII, HK, and prekallikrein.

98 h the kallikrein formed can rapidly activate factor XII if it is surface bound.

99 Administration of human factor XII in factor XII-deficient mice fully restored i

100 of factor XII and an inhibition of activated factor XII in mice minimize trauma-induced microvascular

101 olyphosphate limits its capacity to activate factor XII in vitro.

102 We sought to further define this factor XII-independent mechanism of kinin formation.

103 e the existence of a previously undescribed, factor XII-independent pathway for contact factor activa

104 The factor XII-induced mitogenic response was achieved at co

105 e kinase antagonist, inhibited both EGF- and factor XII-induced responses.

106 a risk factor for thrombosis suggesting that factor XII is an antithrombotic protein.

107 Coagulation factor XII is involved in thrombus formation and therefo

108 Both kallikrein and plasmin activate factor XII; kallikrein is 20 times more potent on a mola

109 mplexes is entirely independent of exogenous factor XII (Km = 30 nmol/L, Vmax = 12 +/- 3 pmol/L/min i

110 The existence of associations between low factor XII levels or F12 variants and thrombotic outcome

111 Factor XII may serve to regulate thrombin binding to the

112 1.03 ng/mL) in patients with HAE-N without a Factor XII mutation (11 samples).

113 n, 0.54 ng/mL) in patients with HAE-N with a Factor XII mutation (12 samples), and from 0.0 to 3.7 ng

114 nhibitor levels (HAE-N) is associated with a Factor XII mutation in 30% of subjects; however, the rol

115 ) in patients with HAE-N with or without the Factor XII mutation.

116 y angioedema with normal C1 inhibitor with a factor XII mutation.

117 Reconstitutions of factor XII null mice with human factor XII restored susc

118 sic" and "extrinsic" components initiated by factor XII or factor VIIa/tissue factor, respectively, a

119 vity was reduced in plasma in the absence of factor XII or its substrate of the intrinsic coagulation

120 amples immunoblotting revealed activation of factor XII, plasma kallikrein, and kininogen during the

121 Deficiency in or pharmacologic inhibition of factor XII, plasma kallikrein, high-molecular-weight kin

122 along cell surfaces requiring interaction of factor XII, prekallikrein, and high M(r) kininogen (HK).

123 nce supporting the hypothesis that targeting factor XII prevents thrombus formation and has a benefic

124 was reduced by popcorn inhibitor, a specific factor XII protease inhibitor.

125 ified: urokinase-type plasminogen activator, factor XII, protein C, trypsinogen IV, and a protease th

126 , factor VII activity and antigen, activated factor XII, prothrombin fragment 1+2, fibrinopeptide A,

127 hostin suggest that the EGF receptor and the factor XII receptor may be nonidentical.

128 Addition of 0.1% factor XII relative to prekallikrein-HK leads to rapid f

129 titutions of factor XII null mice with human factor XII restored susceptibility for allergen/IgE-medi

130 c SMCs with factor XII, as well as activated factor XII, resulted in a rapid and transient activation

131 Factor XII showed displacement of biotin-labeled HK (30

132 We found that factor XII significantly enhanced [3H]thymidine incorpor

133 In addition, PK can activate coagulation factor XII, the origin of the intrinsic coagulation casc

134 g of biotinylated HK as well as biotinylated factor XII to the isolated 33-kDa HUVEC molecule as well

135 illustrate a critical role for polyphosphate/factor XII-triggered coagulation in prostate cancer-asso

136 A high activated factor XII was associated with increased CHD risk, but l

137 h-molecular weight kininogen, factor XI, and factor XII were decreased in the disease-untreated group

138 Although factor XII will bind to the intact platelet through GP I

139 factor XII and acute inhibition of activated factor XII with a single bolus injection of recombinant

140 Inhibition of factor XII with recombinant 3F7 antibody reduced the inc

141 s demonstrated with factor XIIa but not with factor XII zymogen or factor XIIf, indicating that the c

142 port that factor XIIa (0.37 microm), but not factor XII zymogen, is required for the inhibition of th