ライフサイエンスコーパス: coagulation factor VIII

1 s also a key determinant in the clearance of coagulation factor VIII.

2 require frequent infusion of preparations of coagulation factor VIII.

3 shares homology with the C2 domains of blood coagulation factor VIII and factor V.

4 Using available genomic sequence data on coagulation factor VIII and predictive models of molecul

5 plasma and blood viscosity, platelet count, coagulation factors VIII and IX, von Willebrand factor,

6 Using coagulation factor VIII as a model ligand, we now study

7 arrying complementary DNA for modified human coagulation factor VIII (B domain deleted and replaced w

8 Coagulation factor VIII binds to negatively charged plat

9 The human blood coagulation factor VIII C2 domain (Ser2173-Tyr2332) cont

10 n immunodeficiency virus type 1 antigens and coagulation factor VIII captured on the cantilever in th

11 AAV5)-based gene-therapy vector containing a coagulation factor VIII complementary DNA driven by a li

12 Patients with severe coagulation factor VIII deficiency require frequent infu

13 Coagulation factor VIII deficient (FVIII(-/-)) mice deve

14 function, including synthesis and release of coagulation factor VIII, demonstrated that transplanted

15 We previously demonstrated that coagulation factor VIII (FVIII) accelerates proteolytic

16 and at physiological pH and ionic strength, coagulation factor VIII (FVIII) accelerates, by a factor

17 stasis, by acting as a chaperone protein for coagulation factor VIII (FVIII) and by contributing to t

18 philia A and B are caused by deficiencies in coagulation factor VIII (FVIII) and factor IX, respectiv

19 Coagulation factor VIII (FVIII) and factor V are homolog

20 ophilia A is caused by a deficiency of blood coagulation factor VIII (FVIII) and has been widely disc

21 Coagulation factor VIII (FVIII) and its carrier protein

22 lia A (AHA) is due to autoantibodies against coagulation factor VIII (FVIII) and most often presents

23 Complex formation between coagulation factor VIII (FVIII) and von Willebrand facto

24 The uptake and processing of blood coagulation factor VIII (FVIII) by antigen-presenting ce

25 Deficiency or abnormality of coagulation factor VIII (FVIII) causes a bleeding disord

26 Human and porcine coagulation factor VIII (fVIII) display a biosynthetic e

27 However, declining therapeutic coagulation factor VIII (FVIII) expression has plagued c

28 demonstrated previously that catabolism of a coagulation factor VIII (fVIII) from its complex with vo

29 DLR) was shown to mediate clearance of blood coagulation factor VIII (FVIII) from the circulation.

30 The half-life of coagulation factor VIII (FVIII) in plasma is prolonged b

31 h haemophilia A of all ages with and without coagulation factor VIII (FVIII) inhibitors.

32 Coagulation factor VIII (FVIII) is a heterodimer consist

33 Blood coagulation factor VIII (fVIII) is activated by thrombin

34 Coagulation factor VIII (FVIII) is essential for hemosta

35 e present study, we found that catabolism of coagulation factor VIII (fVIII) is mediated by the low d

36 neutralizing antibodies (inhibitors) against coagulation factor VIII (FVIII) is the most problematic

37 Regulation of the coagulation factor VIII (fVIII) level in circulation inv

38 High coagulation factor VIII (FVIII) levels comprise a common

39 nt of pathogenic antibody inhibitors against coagulation factor VIII (FVIII) occurs in ~30% of patien

40 Despite recent studies, the organization of coagulation factor VIII (FVIII) on a phospholipid (PL) m

41 er caused by mutations in the genes encoding coagulation Factor VIII (FVIII) or FIX.

42 Development of neutralizing Abs to blood coagulation factor VIII (FVIII) provides a major complic

43 The cellular source of coagulation factor VIII (FVIII) remains controversial.

44 Deficiency of coagulation factor VIII (FVIII) results in hemophilia A,

45 bleeding disorder caused by a deficiency in coagulation factor VIII (fVIII) that affects 1 in 5,000

46 ted by plasma von Willebrand factor (VWF) or coagulation factor VIII (FVIII), as VWF is glycosylated

47 Hemophilia A, a deficiency of functional coagulation factor VIII (FVIII), is treated via protein

48 m and also serves as the carrier protein for coagulation factor VIII (FVIII), protecting it from prot

49 We have analyzed expression of coagulation factor VIII (FVIII), the protein deficient i

50 nts in the missing secreted protein product, coagulation factor VIII (FVIII), would result in substan

51 ed bleeding disorder caused by deficiency of coagulation factor VIII (FVIII).

52 development of inhibitor antibodies against coagulation factor VIII (fVIII).

53 ievement of sustained, therapeutic levels of coagulation factor VIII (fVIII).

54 caused by the lack or abnormality of plasma coagulation factor VIII (FVIII).

55 ) that neutralize intravenously administered coagulation factor VIII (FVIII).

56 order caused by inhibiting autoantibodies to coagulation factor VIII (FVIII).

57 a A (HA) requires repetitive IV injection of coagulation factor VIII (FVIII).

58 that circulates noncovalently bound to blood coagulation factor VIII (fVIII).

59 Analogous events were observed following coagulation factor VIII gene transfer in hemophilia A mi

60 isation of expressed sequences distal to the coagulation factor VIII gene.

61 Blood coagulation factor VIII has a domain structure designate

62 Deficiency of coagulation factor VIII in hemophilia A disrupts clottin

63 halomyelitis, and antibody responses against coagulation factor VIII in hemophilia A mice, even in an

64 Deficiency of blood coagulation Factors VIII, IX, or XI is associated with h

65 PTT reagents and for sensitive monitoring of coagulation factors VIII, IX, XI.

66 Deficiency in coagulation factor VIII leads to the bleeding disorder h

67 ciated with plasma von Willebrand factor and coagulation factor VIII levels in GWAS, suggesting that

68 ients of nonleukoreduced red blood cells and coagulation factor VIII manufactured from blood of Unite

69 etic disease caused by a deficiency of blood coagulation factor VIII or IX.

70 order that is due to the deficiency of blood coagulation factor VIII or IX.

71 pression of a gene encoding functional blood coagulation factor VIII or IX.

72 23/26del) which cannot bind platelets, blood coagulation factor VIII, or collagen, causing VWD throug

73 Here we first compare engineered coagulation factor VIII transgenes and show that codon-u

74 rs of the 18 tested (interleukin-6, d-dimer, coagulation factor VIII, von Willebrand factor, and homo

75 ated plasma levels of coagulation factor XI, coagulation factor VIII, von Willebrand factor, histo-bl

76 Given the strong association between VWF, coagulation factor VIII (which is stabilised and transpo

77 cular injury, we hypothesize that storage of coagulation Factor VIII within platelets may provide a l