ライフサイエンスコーパス: GPIIIa

1 85%) could be adsorbed to and eluted from a GPIIIa-(49-66) affinity column.

2 udy examined the induction requirements of a GPIIIa LIBS with regard to ligand specificity.

3 VII 10976A, GPIa 807T, GPIbalpha [-5]C, and GPIIIa 1565T variants showed no significant overall asso

4 polymerase chain reaction-amplified cDNA and GPIIIa exon VIII indicated that the patient is homozygou

5 the cytoplasmic sequences of both GPIIb and GPIIIa in mediating this interaction.

6 is (SDS-PAGE) analysis showed only GPIIb and GPIIIa subunits of normal size.

7 IIb (approximately 30% to 35% of normal) and GPIIIa (approximately 10% of normal), and the GPIIb had

8 the cytoplasmic sequences of GPIIb (P2b) and GPIIIa (P3a).

9 localized immunostaining for factor XIII and GPIIIa (P = 0.02).

10 nts contain IgM antiidiotype Ab against anti-GPIIIa, which appears to regulate their serum reactivity

11 5% of normal, whereas the binding of an anti-GPIIIa specific MoAb (7H2) was approximately 12% of norm

12 determined the in vivo effect of human anti-GPIIIa on mouse platelets.

13 a from these patients have little to no anti-GPIIIa activity.

14 specificity for F(ab')(2) fragments of anti-GPIIIa 49-66 of HIV-1-ITP patients and inhibition of rea

15 To study the mechanism of anti-GPIIIa antibody-induced platelet fragmentation, we scree

16 with 25 microgram of affinity-purified anti-GPIIIa 49-66 (mouse GPIIIa has 83% homology with human G

17 Serum anti-GPIIIa-(49-66) concentration correlated inversely with p

18 Preincubation of the anti-GPIIIa Ab with control IgM at molar ratios of IgM/IgG of

19 antibody to platelets could be inhibited by GPIIIa-(49-66) or an equimolar peptide-albumin conjugate

20 ptor variants (GPIa C807T, GPIbalpha T[-5]C, GPIIIa C1565T), involving a total of 66 155 coronary dis

21 PIIIa against a major antigenic determinant, GPIIIa-(49-66), which correlates inversely with platelet

22 properties of an antibody (D3) specific for GPIIIa that induces GPIIb-IIIa binding to adhesive prote

23 ow cells for their expression of CD41 (GPIIb-GPIIIa) and CD4 with specific monoclonal antibody (MoAb)

24 66 amino acids from the HPA-1a form of human GPIIIa and the analogous amino acids from the nonimmunog

25 alogous residues in the HPA-1a form of human GPIIIa, starting and radiating from murine position 33 (

26 HPA-1a epitope(s) in the N-terminus of human GPIIIa, to isolate the murine 5' nucleotide sequence and

27 66 (mouse GPIIIa has 83% homology with human GPIIIa and Fc receptors for human IgG1).

28 t GPIIIa-(49-66) has 83% homology with human GPIIIa and mouse monocytes contain Fc receptors for the

29 Platelet membrane glycoprotein IIIa (GPIIIa) is the most polymorphic integrin subunit in man,

30 c for a single epitope on glycoprotein IIIa (GPIIIa).

31 n the N-terminus of human glycoprotein IIIa (GPIIIa).

32 ies that react with human glycoprotein IIIa (GPIIIa; beta3-integrin subunit) but fail to recognize ra

33 ant epitope of the beta3 (glycoprotein IIIa [GPIIIa]) integrin, GPIIIa49-66.

34 The PMA-induced increase in GPIIIa expression was completely inhibited by GF109203X

35 Ab raised against peptide PHC09 in GPIIIa(-/-) mice induced thrombocytopenia in wild-type m

36 of normal, suggesting that the defect was in GPIIIa (beta 3).

37 Similar results were noted with intact GPIIIa, rGPIIIa 1-66 blocked the binding of anti-PLA1 Ab

38 tinct, but overlapping, structures involving GPIIIa residues 50 to 66.

39 teen of the antibodies reacted with a 29-kDa GPIIIa fragment comprising only the GPIIIa hybrid and pl

40 nd -(1-66) fusion peptide and with an 18-mer GPIIIa-(49-66) peptide but not with seven other GPIIIa p

41 f affinity-purified anti-GPIIIa 49-66 (mouse GPIIIa has 83% homology with human GPIIIa and Fc recepto

42 n be created within the N-terminus of murine GPIIIa and raise the possibility that murine models of H

43 However, studies with mutant GPIIIa and the blocking monoclonal antibody AP3 showed t

44 disulfide bond can alter the conformation of GPIIIa.

45 ubstitution within the RGD binding domain of GPIIIa and anti-Pena human alloantibodies have been show

46 ognized "hybrid" and PSI homology domains of GPIIIa for drug-dependent binding.

47 Since the Pena and Penb allelic forms of GPIIIa are distinguished by a single Arg143Gln amino aci

48 other GPIIIa peptides spanning the length of GPIIIa.

49 showed approximately 35% of normal levels of GPIIIa, approximately 30% of normal levels of GPIIb, and

50 ents in carriers of the PIA2 polymorphism of GPIIIa.

51 The findings suggest this region of GPIIIa may be a favored target for quinine-dependent ant

52 Thus, the region of GPIIIa recognized by D3 may be an important regulatory d

53 istent with the notion that these regions of GPIIIa participate in the conformational change associat

54 her the Cys5Ala or Cys435Ala substitution of GPIIIa on the adhesive properties of the GPIIb-IIIa comp

55 ast to the inhibitory effect of GF109203X on GPIIIa expression, hemin induction of glycophorin A was

56 IIa-(49-66) peptide but not with seven other GPIIIa peptides spanning the length of GPIIIa.

57 ts and inhibition of reactivity with peptide GPIIIa 49-66, not with a control peptide.

58 e, but serum Ig and CIC-IgG against platelet GPIIIa 49-66 was present, although considerably lower th

59 TP patients have high-affinity anti-platelet GPIIIa against a major antigenic determinant, GPIIIa-(49

60 h-affinity (Kd = 1 x 10(-9) M) anti-platelet GPIIIa has been isolated from serum immune complexes of

61 Because mouse platelet GPIIIa-(49-66) has 83% homology with human GPIIIa and mo

62 a 1-66, as well as other site(s) on platelet GPIIIa and insensitive to inhibition.

63 The PLA1 epitope on platelet GPIIIa has a sulfhydryl-dependent conformation and is de

64 reactions of these antibodies with human/rat GPIIIa chimeras and selected GPIIIa mutants, we found th

65 -integrin subunit) but fail to recognize rat GPIIIa, despite close homology between the 2 proteins.

66 ing the platelet glycoprotein IIIa receptor (GPIIIa), shows polymorphism (PIA1/A2).

67 platelet antibody reacted with a recombinant GPIIIa-(1-200) and -(1-66) fusion peptide and with an 18

68 Sequence analysis of the patient's GPIIIa RNA identified a G to A mutation at nucleotide 12

69 with human/rat GPIIIa chimeras and selected GPIIIa mutants, we found that each of 3 quinine-dependen

70 ing sequential overlapping peptides from the GPIIIa cytoplasmic region, an epitope for ITP-1 was loca

71 ed with a synthetic peptide derived from the GPIIIa cytoplasmic tail; however, the PVVWKN was not.

72 t of apparently healthy men, carriage of the GPIIIa PIA2 allele was not associated with any increase

73 revented or reversed by the injection of the GPIIIa-(49-66) albumin conjugate at zero time or 2 hr af

74 a 29-kDa GPIIIa fragment comprising only the GPIIIa hybrid and plextrin-semaphorin-integrin homology

75 Thus, LK-4 binds to GPIIIa at the 1-66 N-terminal region, inhibits binding o

76 , which blocks the binding of these DDAbs to GPIIIa, was found to require a more limited stretch of t

77 zed to the sequence Arg-Ala-Arg-Ala-Lys-Trp (GPIIIa 734-739).

78 the resulting mutants were coexpressed with GPIIIa in COS-1 cells.

79 nic patients gave background reactivity with GPIIIa-(49-66).