ライフサイエンスコーパス: azurocidin

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1 ricidal/permeability-increasing protein, and azurocidin.

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

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

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

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

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

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

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

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

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

11 To block azurocidin, aprotinin was injected intravenously before

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

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

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

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

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

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

18 Azurocidin/CAP37/HBP is an antimicrobial and chemotactic

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

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

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

22 Azurocidin increases retinal vascular permeability and i

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

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

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

26 Azurocidin is released after activation of polymorphonuc

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

28 Azurocidin may become a new therapeutic target in the tr

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

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

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

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

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

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

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

36 Azurocidin, released by neutrophils during leukocyte-end

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

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

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

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