ライフサイエンスコーパス: azurocidin

1 ricidal/permeability-increasing protein, and azurocidin.

2 al proteins, for example, myeloperoxidase or azurocidin.

3 t produce proinflammatory factors, including azurocidin 1, elastase and CXCL16, to disrupt vascular i

4 ductions in cathepsin G and the pseudoenzyme azurocidin-1 (Azu-1) (false discovery rate-adjusted P <

5 Intravitreal injection of azurocidin (20 microg) induced a 6.8-fold increase in va

6 d by NH2-terminal sequence analysis as CAP37/azurocidin, a protein with sequence homology to serine p

7 s identify the antimicrobial proteins, CAP37/azurocidin and defensins HNP-1 and HNP-2, as potent neut

8 se exhibited modest antifungal activity, and azurocidin and proteinase 3 exhibited no significant fun

9 way rats received intravitreal injections of azurocidin and vehicle control.

10 il serine proteases (proteinase 3, elastase, azurocidin, and cathepsin G) on granulopoiesis in vitro.

11 neutrophils including myeloperoxidase (MPO), azurocidin, and neutrophil elastase.

12 ctivity to human granzymes, NE, CG, PR3, and azurocidin, and screened for NSP4 protein expression in

13 ties (ie, neutrophil elastase, proteinase 3, azurocidin, and/or others) can substitute for it in vivo

14 To block azurocidin, aprotinin was injected intravenously before

15 granule proteins, elastase, protease 3, and azurocidin as candidates.

16 e proteinases (cathepsin G, proteinase 3 and azurocidin) at concentrations exceeding 5 mM.

17 nce to the antimicrobial peptides polymyxin, azurocidin (CAP37), bactericidal/permeability-increasing

18 actericidal/permeability-increasing protein, azurocidin (CAP37/heparin-binding protein), and neutroph

19 established that the T cell chemoattractant, azurocidin/CAP37 from human neutrophil granules, at dose

20 hil granule proteins such as cathepsin G and azurocidin/CAP37.

21 Azurocidin/CAP37/HBP is an antimicrobial and chemotactic

22 binding protein (HBP; also known as CAP37 or azurocidin) from azurophilic granules.

23 acent neutrophil elastase, proteinase 3, and azurocidin genes encode serine proteases expressed speci

24 role of polymorphonuclear leukocyte-derived azurocidin in alteration of vascular permeability.

25 Azurocidin increases retinal vascular permeability and i

26 Aprotinin inhibited azurocidin-induced BRB breakdown by more than 95% (P < 0

27 taneous administration of defensins or CAP37/azurocidin into BALB/c mice resulted in a moderate neutr

28 In addition, azurocidin is an inactive serine protease homolog with b

29 Azurocidin is released after activation of polymorphonuc

30 BRB breakdown with aprotinin indicates that azurocidin may be an important mediator of leukocyte-dep

31 Azurocidin may become a new therapeutic target in the tr

32 To investigate whether azurocidin may mediate BRB breakdown in early diabetes,

33 t contribute to the ability of the wild-type azurocidin molecule to bind heparin and to kill E. coli

34 basic region, we produced three recombinant azurocidin mutant proteins that were altered in either o

35 Polymorphonuclear leukocyte-derived azurocidin plays a major role in this polymorphonuclear

36 To investigate whether azurocidin plays a role in vascular endothelial growth f

37 inding protein (HBP), also known as CAP37 or azurocidin, potentiates the LPS-induced release of proin

38 o killing by lysozyme and were not killed by azurocidin, proteinase 3, or lactoferrin.

39 Azurocidin, released by neutrophils during leukocyte-end

40 positively charged amino acids in the 20-44 azurocidin sequence (DMC1: R23Q,H24S,H32S,R34Q), a regio

41 Studies with purified elastase and azurocidin showed that each bound specifically to purifi

42 s are not involved in the binding of BPTI to azurocidin, supporting the notion that the binding site