ライフサイエンスコーパス: coagulation factor VIII

1 require frequent infusion of preparations of coagulation factor VIII.

2 s also a key determinant in the clearance 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 Patients with severe coagulation factor VIII deficiency require frequent infu

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

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

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

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

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

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

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

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

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

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

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

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

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

25 Coagulation factor VIII (FVIII) is a heterodimer consist

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

45 Blood coagulation factor VIII has a domain structure designate

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

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

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

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

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

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

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

53 23/26del) which cannot bind platelets, blood coagulation factor VIII, or collagen, causing VWD throug

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

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