ライフサイエンスコーパス: factor XIIIa

1 xudate macrophages were OX-62(+), B7(+), and factor XIIIa(+).

2 of N-ethylmaleimide, a specific inhibitor of factor XIIIa.

3 n clot, FN must be cross-linked to fibrin by factor XIIIa.

4 rization and was efficiently cross-linked by factor XIIIa.

5 (FP) B release or impaired cross-linking by factor XIIIa.

6 rmation and stabilization of fibrin clots by factor XIIIa.

7 a C fragments could serve as a substrate for factor XIIIa.

8 protein 1,4-hydroxy-prolyl-hydroxylase, and factor XIIIa.

9 gomers by covalently cross-linking them with factor XIIIa.

10 mers to produce the active transglutaminase, factor XIIIa.

11 ed through ligation with a transglutaminase, factor XIIIa.

12 rFnbA can act as a substrate for coagulation factor XIIIa.

13 stabilized by the transglutaminase action of factor XIIIa.

14 hin the known three-dimensional structure of factor XIIIa.

15 XIII is the zymogen of the transglutaminase factor XIIIa.

16 his molecule, and confirmed that it is avian factor XIIIA.

17 A" subunit of human plasma transglutaminase (factor XIIIA), a member of a family of enzymes that cros

18 treatment of this mixture with thrombin and factor XIIIa, a gamma.gamma dimer, similar to that obtai

19 esults of the present study demonstrate that factor XIIIa, a transglutaminase that catalyzes the form

20 f emboli was determined: (1) control, normal factor XIIIa activity (14.1+/-4.8% lysis); (2) inhibited

21 activity (14.1+/-4.8% lysis); (2) inhibited factor XIIIa activity (42.7+/-7.4%); (3) normal factor X

22 Inhibition of factor XIIIa activity increased endogenous lysis markedl

23 tor XIIIa activity (42.7+/-7.4%); (3) normal factor XIIIa activity+TPA (32.3+/-7.7%); (4) inhibited f

24 Ia activity+TPA (32.3+/-7.7%); (4) inhibited factor XIIIa activity+TPA (76.0+/-11.9%); and (5) inhibi

25 nce fibrin clot turbidity was independent of factor XIIIa activity.

26 Complete inhibition of factor XIIIa also amplified lysis (group 3 versus 4; P<0

27 Soluble factor XIIIa also bound to endothelial cells in solution

28 Factor XIIIa also catalyzes the incorporation in FnbA of

29 In this report, we demonstrate that factor XIIIa also mediates adhesion of endothelial cells

30 in lysine residues that potentially serve as Factor XIIIa amine donor substrates during alpha polymer

31 agment were identified by cross-linking with factor XIIIa and by photoaffinity labeling.

32 which polymerize and serve as a template for factor XIIIa and plasmin formation.

33 ing hemostasis by serving as a substrate for factor XIIIa and plasmin.

34 Two transglutaminases (TGases), Factor XIIIa and tissue TGase (tTGase), are expressed in

35 Both factor XIIIa and tissue transglutaminase catalyzed the p

36 Thus, Factor XIIIa and tTGase activities were increased in agi

37 Increased Factor XIIIa and tTGase activities, achieved via direct

38 ctor-beta and interleukin (IL)-1beta induced Factor XIIIa and tTGase expression in cartilage and meni

39 t FnbA serves as a substrate for coagulation factor XIIIa and undergoes covalent cross-linking to its

40 These cells express Factor XIIIa and VCAM-1 by immunohistochemistry and by W

41 Immunohistochemistry was performed for Factor XIIIa(+) and cluster of differentiation (CD)1a(+)

42 he sequential action of 3 enzymes: thrombin, factor XIIIa, and plasmin.

43 In line with the reported half-life of factor XIIIa, application of alpha2AP-PFCs>60 minutes af

44 d molecule FcRgamma and the transglutaminase factor XIIIA are required for the formation of coated pl

45 gamma'C30 were both readily cross-linked by factor XIIIa, but only rFbggammaC30 was capable of inhib

46 nase and presumably plasma transglutaminase, factor XIIIa, can covalently incorporate into fibrin(oge

47 procally cross-linked peptide resulting from factor XIIIa-catalyzed dimerization of fibrin gamma chai

48 tic phase of blood coagulation, which is the factor XIIIa-catalyzed end-to-end ligation of the gamma

49 Factor XIIIa-catalyzed epsilon-(gamma-glutamyl)-lysyl bo

50 Factor XIIIa catalyzes the formation of covalent bonds b

51 Factor XIIIa catalyzes the incorporation of amine donor

52 analysis, we investigated the expression of Factor XIIIa(+), CD1a(+), CD83(+), and CD207(+) DCs; CD4

53 ls in all layers and increased expression of Factor XIIIa(+) cells, CD4(+) and CD8(+) T cells, CD20(+

54 al assays were conducted to demonstrate that factor XIIIa cross-links Lp(a) with fibrinogen in a time

55 ossibilities, the gamma dimer composition of factor XIIIa-cross-linked fibrin/fibrinogen complexes th

56 th multiple fibrinogen activities, including factor XIIIa crosslinking, platelet adhesion, and platel

57 hrombin and Ca2+-activated human coagulation Factor XIIIa, cytosolic transglutaminases from human red

58 Large numbers of CD68+/factor XIIIa+ dendritic cells and increased expression o

59 ose proximity to several sites important for factor XIIIa-dependent cross-linking, which raises the p

60 cross-linking site occurs in the presence of factor XIIIa due to self-association at a constitutive D

61 n x-ray structure of the related coagulation factor XIIIa enzyme.

62 A previously characterized Factor XIIIa fibrin lysine labeling system was employed

63 may utilize the transglutaminase activity of factor XIIIa for attachment to soluble proteins, cell su

64 of the final step in blood coagulation, the factor XIIIa (FXIIIa) catalyzed cross-linking of fibrin

65 Factor XIIIa (FXIIIa) introduces covalent gamma-glutamyl

66 Coagulation factor XIIIa (FXIIIa) is a transglutaminase that covalen

67 served that the transglutaminase coagulation factor XIIIA (FXIIIA) was one of the most abundant prote

68 in II, red blood cells (RBCs), fibrin(ogen), factor XIIIa (FXIIIa), and thrombin on the kinetics and

69 cated throughout the dermis was positive for factor XIIIA (FXIIIA), but lacked CD11c and BDCA-1.

70 inking of the fibrinogen alphaC domains with factor XIIIa generates ordered alphaC oligomers mimickin

71 Factor XIIIa had similar effects on clots formed from bo

72 of reactive Gln and Lys residues targeted by factor XIIIa in rFnbA.

73 we demonstrated up-regulation of tTGase and Factor XIIIa in superficial and deep zones of knee OA ar

74 cting end-to-end, the findings show that the factor XIIIa-induced cross-linking of gamma chains in th

75 avior associated with network morphology and factor XIIIa-induced cross-linking were studied in fibri

76 In addition, factor XIIIa inhibited endothelial cell capillary tube f

77 Blood coagulation factor XIIIa is a calcium-dependent enzyme that covalent

78 Coagulation factor XIIIa is a transglutaminase that catalyzes covale

79 We conclude that FcRgamma, but not factor XIIIA, is essential for formation of highly proco

80 The finding of upregulation of HLA-DR and factor XIIIa led to the novel identification of activate

81 The presence of the factor XIIIA Leu34 allele was associated with a reduced

82 In particular, factor XIIIa may cross-link pro-CpU to fibrin during the

83 This suggests that factor XIIIa may play a critical role in regulating fibr

84 ions of fibrin, and is further reinforced by factor XIIIa-mediated covalent cross-linking of fibronec

85 Two factor XIIIa-mediated cross-linking conditions were empl

86 It is proposed that factor XIIIa-mediated cross-linking of Lp(a) to fibrin e

87 d in calcium binding, fibrin polymerization, factor XIIIa-mediated cross-linking, and binding to the

88 Factor XIIIa-mediated fibrin-fibrin and alpha2-antiplasm

89 brinolytic effects of specific inhibitors of factor XIIIa-mediated fibrin-fibrin cross-linking and al

90 Factor XIIIa mediates crosslinking of the C-terminal reg

91 The expression of Factor XIIIa(+) monocyte-derived DCs, CD4(+) and CD8(+)

92 Coagulation factor XIIIa, plasma transglutaminase (endo-gamma-glutam

93 d characterized as to their cross-linking by factor XIIIa, polymerization pocket, and calcium-binding

94 Factor XIIIa-positive dendrocytes are abundant within th

95 derived from superficial murine dermis where factor XIIIa-positive dendrocytes are abundant.

96 cells 1) share lineage characteristics with factor XIIIa-positive dermal dendrocytes, 2) produce mRN

97 l interstitium are demonstrated to represent factor XIIIa-positive dermal dendrocytes.

98 Purified cultures of factor XIIIa-positive normal dermal dendrocytes have not

99 The addition of 10 to 100 microg/mL factor XIIIa produced a dose-dependent reduction in capi

100 assembly, as well as the acceleration of the factor XIIIa reaction, could be prevented by Gly-Pro-Arg

101 he present study we investigated the role of factor XIIIa reactive Gln and Lys sites of staphylococca

102 cross-linking suggesting that it also may be factor XIIIa reactive.

103 have been employed for the identification of factor XIIIa-reactive Gln and Lys residues.

104 in the presence of either of its ligands and factor XIIIa results in the introduction of intermolecul

105 transglutaminase with those from homologous factor XIIIA showed that the major fibronectin-binding s

106 However, if the aggregates were treated with factor XIIIa so that all gamma chains became ligated by

107 gree to which the alpha C domain's role as a factor XIIIa substrate in intact fibrinogen is preserved

108 Inherited deficiency of factor XIIIA subunit (FXIIIA) is an autosomal recessive

109 These results show that factor XIIIa supports endothelial cell adhesion in an in

110 Upon treatment with factor XIIIa, the alpha C45K fragment but not the alpha

111 ith a cDNA construct encoding the zymogen of factor XIIIA, the cells convert the translated protein t

112 right) macrophages were OX-62(-), B7(-), and factor XIIIa(-); they were the dominant mediators of pha

113 nt of the blood clot, which is stabilized by factor XIIIa through an amide or isopeptide bond that li

114 -dependent conformational changes that cause factor XIIIa to switch from a protease-sensitive to a pr

115 s the contribution of activated factor XIII (factor XIIIa) to fibrinolytic resistance in experimental

116 ently cross-linked by activated factor XIII (factor XIIIa) to form pFN-fibrin multimers.

117 crosslinking of angiotensin AT1 receptors by factor XIIIA transglutaminase, resulting in stable recep

118 The adhesive activity of factor XIIIa was not dependent on the transglutaminase a

119 Cross-linking of the 70-kDa fragment with factor XIIIa was to molecules that migrated in discontin

120 , CD34, smooth muscle actin (SMA), CD68, and factor XIIIa were performed.

121 35 of Png1p are conserved in the sequence of factor XIIIa, where these amino acids constitute a catal