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

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

4 n G4 monoclonal antibody targeting activated factor XII.

5 ves both FXII zymogen and FXIIa but not beta Factor XII.

6 platelets with the activation of coagulation factor XII.

7 olyphosphate nanoparticles potently activate factor XII.

8 mbus formation and activation of coagulation factor XII.

9 ing that polyphosphate drives thrombosis via factor XII.

10 and distinguish them from activation through factor XII.

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

12 leavage and reduced plasma prekallikrein and Factor XII activation in plasma.

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

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

15 cluded the prevalence of reduced coagulation factor XII activity (< 60%) among patients receiving ext

16 ed by 200% per tertile of median coagulation factor XII activity (crude odds ratio, 3.034; 95% CI, 1.

17 endpoint was the association of coagulation factor XII activity and activated partial thromboplastin

18 Fifty patients (98%) had reduced coagulation factor XII activity at any timepoint during extracorpore

19 In heparinase-treated samples, coagulation factor XII activity correlated well with activated parti

20 Median coagulation factor XII activity during extracorporeal membrane oxyge

21 complications had higher median coagulation factor XII activity during extracorporeal membrane oxyge

22 ved a high prevalence of reduced coagulation factor XII activity in adult patients on extracorporeal

23 ilable on contact activation and coagulation factor XII activity in extracorporeal membrane oxygenati

24 rimary outcome was the change in coagulation factor XII activity in response to extracorporeal membra

25 Lower coagulation factor XII activity was associated with less thromboembo

26 e oxygenation and association of coagulation factor XII activity with thromboembolic and bleeding com

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

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

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

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

31 factor and platelets but not on coagulation factor XII and circulating neutrophils.

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

33 Factor XII and factor XI have emerged as targets for new

34 cascade that includes contact activation of factor XII and fibrin production.

35 Abeta protofibrils bind to coagulation factor XII and high molecular weight kininogen and accel

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

37 y degrade the human glycoprotein coagulation factor XII and not its deglycosylated form, but the mech

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

39 lants are needed, provides the rationale for factor XII and XI as targets for such agents, reviews th

40 C1q-NETs also activate the coagulation factors XII and XI, facilitating both intrinsic coagulat

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

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

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

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

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

46 ets for such agents, reviews the data on the factor XII- and factor XI-directed anticoagulants under

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

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

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

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

51 , if incubated in the presence of HK and PK, factor XII became activated.

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

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

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

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

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

57 FXII is converted to FXIIa (activated factor XII) by PKa (plasma kallikrein) or its unique abi

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

59 ght kininogen (HK), plasma prekallikrein and Factor XII cleavage.

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

61 asma-based thrombin generation is reduced at factor XII concentrations reflective of those seen in F1

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

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

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

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

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

67 Factor XII deficiency was not related to VTE risk.

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

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

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

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

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

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

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

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

76 Factor XII did not activate when incubated with HMVECs a

77 ering RNA-mediated depletion of, coagulation factor XII did not alter VT onset, severity, or thrombus

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

79 er, human data to support the development of factor XII-directed therapeutics are lacking.

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

81 in production, through contact activation of factor XII, drives the thrombus formation in medical dev

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

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

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

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

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

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

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

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

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

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

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

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

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

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

96 The plasma proteins factor XII (FXII) and prekallikrein (PK) undergo recipro

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

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

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

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

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

102 deficiency or gain-of-function mutations in factor XII (FXII) cause hereditary angioedema, a life-th

103 Coagulation factor XII (FXII) drives production of the inflammatory

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

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

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

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

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

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

110 RBC-MVs directly activated factor XII (FXII) or prekallikrein, but not FXI or FIX.

111 adykinin and converts the protease precursor factor XII (FXII) to the enzyme FXIIa.

112 Coagulation factor XII (FXII) triggers activation of the contact sys

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

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

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

116 olution may be the inhibition of coagulation factor XII (FXII), because its knock-out or inhibition i

117 The contact system includes factor XII (FXII), FXI, prekallikrein (PK), and high-mol

118 The contact system is composed of factor XII (FXII), prekallikrein (PK), and cofactor high

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

120 the process of surface-induced activation of factor XII (FXII), which initiates blood coagulation and

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

122 Factor XII (FXII)-triggered coagulation promotes thrombo

123 ulting in p.W268R) which encodes coagulation factor XII (FXII).

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

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

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

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

128 ons in the F12 gene encoding for coagulation factor XII (FXII-HAE) causing an overproduction of brady

129 ctivity (nl-C1-INH-HAE), due to mutations in factor XII (FXII-HAE), plasminogen (PLG-HAE), angiopoiet

130 ns that initiates blood clotting when plasma factors XII (FXII) and XI (FXI), prekallikrein (PK), and

131 icient in individual factors of the contact (factor XII [FXII] and prekallikrein) or intrinsic coagul

132 elial heparan sulfate (HS) and inhibition of factor XII (FXIIa) activity, respectively.

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

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

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

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

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

138 monoclonal antibody that inhibits activated factor XII (FXIIa), is being studied for the prevention

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

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

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

142 Activated factor XII generates plasma kallikrein, which proteolyze

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

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

145 Coagulation factor XII has been identified as a potential drug targe

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

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

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

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

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

151 To assess the role of factor XII in venous thromboembolism, we examine genetic

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

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

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

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

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

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

158 Coagulation factor XII is involved in thrombus formation and therefo

159 embolism and that therapeutically inhibiting factor XII is likely to be safe and effective.

160 FXII (coagulation factor XII) is best known for its roles in the contact a

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

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

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

164 quantitative (type I) defect in circulating factor XII levels, though a subset of participants was a

165 hly subcutaneous garadacimab (anti-activated factor XII mAb) in patients with HAE-FXII or HAE-PLG.

166 Factor XII may serve to regulate thrombin binding to the

167 1.03 ng/mL) in patients with HAE-N without a Factor XII mutation (11 samples).

168 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

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

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

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

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

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

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

175 s formation under flow via the polyphosphate/factor XII pathway.

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

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

178 Tissue factor, coagulation factor XII, platelets, and neutrophils are implicated as

179 he involvement of tissue factor, coagulation factor XII, platelets, and neutrophils.

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

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

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

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

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

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

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

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

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

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

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

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

192 h may highlight the potential of coagulation factor XII to serve as a target for anticoagulation in e

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

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

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

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

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

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

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

200 nsic coagulation pathway by interacting with factors XII, XIIa, and XI.

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

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