ライフサイエンスコーパス: fibrinopeptide B

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1 .1 for fibrinopeptide A and -2.5 +/- 0.1 for fibrinopeptide B.

2 suppression is demonstrated for LSIMS of Glu-fibrinopeptide B.

3 tor affecting thrombin-triggered cleavage of fibrinopeptide B.

4 ith desAB-NDSK and (beta15-66)2 both lacking fibrinopeptide B.

5 (both are proteins), and 0.002% (w/v) human fibrinopeptide B (a peptide).

6 [Glu(1)]-Fibrinopeptide B and substance P were used to evaluate t

7 er fragments by thrombin treatment to remove fibrinopeptides B, bound the recombinant VE-cadherin fra

8 e deuterium uptake of Leu-Enkephalin and Glu-Fibrinopeptide B, confirmed that this gas-phase HDX-MS a

9 reported here indicate that IIa-cleavage of fibrinopeptide B enhances exposure of a heparin binding

10 et basic protein, thymosin beta-4 (Tbeta-4), fibrinopeptide B (FP-B), and fibrinopeptide A (FP-A).

11 bin, fibrinopeptide A (FpA) release precedes fibrinopeptide B (FpB) release.

12 receded lysis of the Aalpha chain, such that fibrinopeptide B (FpB) was released prior to F8Y 1-16.

13 d decrease in the rate of thrombin-catalyzed fibrinopeptide B (FpB, Bbeta 1-14) release, whereas the

14 than fibrinopeptide A but more quickly than fibrinopeptide B generation.

15 haC-domains and the central E region through fibrinopeptide B, in agreement with the hypothesis given

16 In rabbit arteries, fibrinopeptide B is reported to have both vasoconstricto

17 o desA-NDSK and (Bbeta1-66)2 containing only fibrinopeptides B; it was poorly reactive with desAB-NDS

18 lease was decreased 27-fold, and the rate of fibrinopeptide B release was decreased 45-fold relative

19 Fibrinopeptide A release was normal, whereas fibrinopeptide B release was delayed approximately 3-fol

20 uced fibrinogen clotting by interfering with fibrinopeptide B release.

21 SdrG could recognize fibrinopeptide B (residues 1-14), but with a substantial

22 ptides P294 and P326, a hydrophilic peptide, fibrinopeptide B, showed much weaker affinity for zwitte

23 Injection of 25 fmol of [Glu1]-fibrinopeptide B using the new device produced a CE-ESI-

24 fibrinopeptide A was similar, the release of fibrinopeptide B was accelerated in STAT5-deficient plas

25 For angiotensin II and [Glu(1)]-fibrinopeptide B we achieved coefficients of determinati

26 clarifies the role played by the release of fibrinopeptide B, which leads to slightly thicker fibers

27 utive Glu residues, and fibrinopeptide A and fibrinopeptide B, with isolated acidic residues, also sh

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