ライフサイエンスコーパス: high-molecular-weight kininogen

1 bility due to the release of bradykinin from high molecular weight kininogen.

2 radykinin release resulting from cleavage of high-molecular-weight kininogen.

3 ofactor activity was ascribed to domain 5 of high-molecular-weight kininogen.

4 ain plasma protein evolutionarily related to high-molecular-weight kininogen.

5 th dextran sulfate in the presence of either high molecular weight kininogen (45 nm) and ZnCl(2) (25

6 at prothrombin (1 microm) is able to replace high molecular weight kininogen (45 nm) as a cofactor fo

7 the HK31-mer (8 microm) are able to replace high molecular weight kininogen (45 nm) or prothrombin (

8 In the presence of high molecular weight kininogen (45 nm), Zn(2+) and Ca(2

9 sed on the Apple 3 domain in the presence of high molecular weight kininogen and Zn2+ or prothrombin

10 C1 inhibitor deficiency reduced cleavage of high-molecular-weight kininogen and attacks of angioedem

11 ane rafts required prothrombin (and Ca2+) or high molecular weight kininogen (and Zn2+), which are re

12 d by measurement of plasma levels of cleaved high-molecular-weight kininogen, and efficacy was assess

13 omain of factor XI at or near the site where high molecular weight kininogen binds.

14 In microtiter plates, biotinylated high molecular weight kininogen (biotin-HK) or biotin-FX

15 Inherited deficiency in factor XI or XII or high-molecular-weight kininogen, but not plasma kallikre

16 ne monoclonal antibody to the light chain of high molecular weight kininogen, C11C1, to inhibit tumor

17 bradykinin and that a monoclonal antibody to high-molecular weight kininogen, C11C1, blocked its bind

18 High-molecular-weight kininogen can be hydrolysed by pla

19 When the prekallikrein-high molecular weight kininogen complex is bound to endo

20 With higher high molecular weight kininogen concentrations (360 nm),

21 Prekallikrein, high-molecular weight kininogen, factor XI, and factor X

22 flammatory bradykinin peptide and additional high molecular weight kininogen fragments containing the

23 In contrast, only FOG induced cleavage of high molecular weight kininogen, generating the proinfla

24 A titration with high molecular weight kininogen had no effect on FXIa bi

25 The cleaved form of high-molecular-weight kininogen has recently been demons

26 idoma producing a monoclonal antibody to the high molecular weight kininogen heavy chain or to an unr

27 and reversibly to HUVECs in the presence of high molecular weight kininogen (HK) (apparent Kd of 23

28 High molecular weight kininogen (HK) also stimulates the

29 finity (KD </= 0.8 nM) binding site for both high molecular weight kininogen (HK) and factor XII (FXI

30 High molecular weight kininogen (HK) and factor XII are

31 High molecular weight kininogen (HK) and its cleaved for

32 Previously we defined binding sites for high molecular weight kininogen (HK) and thrombin in the

33 (1.3 x 10(10) sites/well, K(D) = 12 nm) when high molecular weight kininogen (HK) and zinc are presen

34 High molecular weight kininogen (HK) and Zn2+ ions exert

35 We have demonstrated that high molecular weight kininogen (HK) binds specifically

36 m 8 to 16 amino acids and derived from human high molecular weight kininogen (HK) domain 5 were inser

37 S565-K595) in domain 6 of the light chain of high molecular weight kininogen (HK) has previously been

38 Previously we defined a binding site for high molecular weight kininogen (HK) in the A1 domain of

39 We have previously reported high molecular weight kininogen (HK) inhibition of throm

40 The nonenzymatic cofactor high molecular weight kininogen (HK) is a precursor of b

41 High molecular weight kininogen (HK) is an endogenous pr

42 Factor XII (FXII) and high molecular weight kininogen (HK) mutually block each

43 endent and not shared by either single-chain high molecular weight kininogen (HK) or low molecular we

44 nin system; thus we explored whether MPO and high molecular weight kininogen (HK) reside on CK1 toget

45 Previous studies on the interaction of high molecular weight kininogen (HK) with endothelial ce

46 prekallikrein activation is the cleavage of high molecular weight kininogen (HK) with liberation of

47 Proteolysis of plasma high molecular weight kininogen (HK) yielding bradykinin

48 a kallikrein, in the presence and absence of high molecular weight kininogen (HK), an important cofac

49 irculates as a complex with the glycoprotein high molecular weight kininogen (HK).

50 essed on their membranes and is able to bind high molecular weight kininogen (HK).

51 plasma prekallikrein (PK) within domain 6 of high molecular weight kininogen (HK).

52 ater than dextran sulfate in the presence of high molecular weight kininogen (HK, 45 nM), ZnCl2 (25 m

53 and leads to kallikrein-mediated cleavage of high molecular-weight kininogen (HK) and release of proi

54 expresses an active site when it is bound to high-molecular-weight kininogen (HK) and can digest HK t

55 serine protease known to induce cleavage of high-molecular-weight kininogen (HK) at sites of inflamm

56 lar artery thrombosis was recognized to have high-molecular-weight kininogen (HK) deficiency.

57 High-molecular-weight kininogen (HK) is an abundant plas

58 High-molecular-weight kininogen (HK) plays an important

59 Cleavage of high-molecular-weight kininogen (HK), a marker for activ

60 diverse proteins, including the known ligand high-molecular-weight kininogen (HK), as well as the ext

61 electively knock down factor (f)XII, fXI, or high-molecular-weight kininogen (HK), key components of

62 inogen activator receptor (uPAR), and gC1qR, high-molecular-weight kininogen (HK)-binding proteins on

63 nant PRCP (rPRCP) activates PK when bound to high-molecular-weight kininogen (HK).

64 A region of 31 amino acids derived from high molecular weight kininogen (HK31-mer) can also bind

65 Cleaved high molecular weight kininogen (HKa) has been shown to

66 ously reported that the binding of two-chain high molecular weight kininogen (HKa) to endothelial cel

67 One example of such a protein is cleaved high molecular weight kininogen (HKa).

68 vious studies have demonstrated that cleaved high-molecular-weight kininogen (HKa) induces endothelia

69 plasma kallikrein to bradykinin and cleaved high-molecular-weight kininogen (HKa).

70 tide bradykinin (BK), leaving behind cleaved high-molecular-weight kininogen (HKa).

71 was also seen against aerosol challenge with high-molecular-weight kininogen (HMWK), a substrate of T

72 prekallikrein (PK) activity, factor XII, and high-molecular weight kininogen in the plasma of 636 typ

73 dose of 300 mg or 400 mg reduced cleavage of high-molecular-weight kininogen in plasma from patients

74 of the precursor proteins prekalli-krein and high-molecular-weight kininogen indicated activation of

75 Cleaved high molecular weight kininogen is antiangiogenic.

76 We have shown that human high molecular weight kininogen is proangiogenic due to

77 High molecular weight kininogen is the precursor for two

78 We reported that high-molecular weight kininogen is proangiogenic by rele

79 HKa (cleaved high molecular weight kininogen) is an endogenous inhibi

80 High-molecular-weight kininogen (KNG) is a central const

81 at measures PK activation only when bound to high molecular weight kininogen linked to microtiter pla

82 molecular weight kininogen, suggesting that high molecular weight kininogen may play a role in regul

83 When prekallikrein (PK) assembles on high molecular weight kininogen on HUVEC, PK is activate

84 Recent studies indicate that assembly of high molecular weight kininogen on its multiprotein rece

85 inhibition of factor XII, plasma kallikrein, high-molecular-weight kininogen, or the bradykinin B2 re

86 ted the consumption of the contact proteins, high molecular weight kininogen (P<0.03), and factor XI

87 Furthermore, peptide RPPGF or high-molecular-weight kininogen prevented alpha-thrombin

88 (t(1/2) approximately 12.5 days) and blocked high molecular weight kininogen proteolysis in activated

89 protease nexin-2 was partially abrogated by high molecular weight kininogen, suggesting that high mo

90 antibody C11C1 efficiently blocks binding of high molecular weight kininogen to endothelial cells in

91 ma kallikrein (pKal) proteolytically cleaves high molecular weight kininogen to generate the potent v

92 nd tissue kallikreins, proteases that cleave high molecular weight kininogen to produce bradykinin.

93 Plasma kallikrein (PK) cleaves high-molecular-weight kininogen to release bradykinin (B

94 whereas levels of factors VIII, IX, XI, and high molecular weight kininogen were elevated.