ライフサイエンスコーパス: antiprotease

1 teases as well as the inhibition of specific antiproteases.

2 cell death regulators and the inhibition of antiproteases.

3 They show immunomodulatory as well as antiprotease activity and may be useful for treatment of

4 Insufficient antiprotease activity because of AAT deficiency in the l

5 ffect of SLPI was largely independent of its antiprotease activity because SLPI muteins, with signifi

6 rease in alpha1-AT concentration, functional antiprotease activity could not be detected.

7 onsidered to be an imbalance of protease and antiprotease activity in the lower respiratory tract lea

8 An imbalance of protease-antiprotease activity is also detected in the airways of

9 ops is based on an imbalance of protease and antiprotease activity leading to the degradation of elas

10 hat of bikunin, which is responsible for the antiprotease activity of IalphaI.

11 es that could potentiate fibrosis, namely an antiprotease activity that inhibits the generation of pl

12 cause SLPI muteins, with significantly lower antiprotease activity, also suppressed the induction of

13 independent of its previously characterized antiprotease activity, appears to reside in disruption o

14 uitment into the lung may be linked to their antiprotease activity, directed, perhaps, at the intrace

15 bacterial infection regulating protease and antiprotease activity.

16 latory properties of A1AT independent of its antiprotease activity.

17 of its specific physiological inhibitor, the antiprotease alpha(2)-antiplasmin.

18 neutrophil influx and degranulation, alpha1-antiprotease (alpha1-AP) concentrations, and unopposed N

19 Prominent protease and antiprotease alterations were also noted in these mice.

20 They also link inflammation, protease/antiprotease alterations, and protease-dependent apoptos

21 in residues, was found to exhibit antiviral, antiprotease, and antiintegrase activity.

22 terleukin 13 receptor components, proteases, antiprotease, and apoptosis regulators via Smad 2/3-inde

23 Antiprotease antibodies did not significantly alter IgA1

24 ing second order rate constants for protease-antiprotease associations (kass) by 3700-, 32-, and 60-f

25 ve importance in maintenance of the protease-antiprotease balance in the microenvironment of inflamma

26 hysema and alterations in pulmonary protease/antiprotease balance when expressed in pulmonary tissues

27 various growth factors/cytokines, proteases/antiproteases, cell adhesion molecules, and extracellula

28 ed alterations in chemokines, proteases, and antiproteases comparable to those seen after C10/CCL6 ne

29 eased over time, whereas neutrophil elastase antiprotease complexes (NEAPCs) and secretory leukoprote

30 he small volume of apical surface fluid, the antiprotease component of this protein was concentrated

31 an imbalance between cysteine proteases and antiproteases could be seen, which negatively affects ep

32 We conclude that antiprotease defenses in lower respiratory tract secreti

33 nuclear factor kappaB (NF-kappaB), impaired antiprotease defenses, DNA damage, cellular senescence,

34 04 L, mean +/- SEM), five of whom had alpha1-antiprotease deficiency, performed two incremental cycli

35 Targeted antiprotease delivery paralleled hpIgR expression in the

36 The activities of some proteases and antiproteases found in inflammatory fluids can be modifi

37 PI-6, also known as cytoplasmic antiprotease, has been characterized as an intracellular

38 Protease-antiprotease imbalance and oxidative stress are consider

39 s, these assessments clarified that protease-antiprotease imbalance and oxidative stress are critical

40 Although inflammation and protease/antiprotease imbalance have been postulated to be critic

41 teinases and because the concept of protease/antiprotease imbalance is an important concept regarding

42 sema has supported the concept that protease/antiprotease imbalance mediates cigarette smoke-induced

43 luenced by FNf and the ratio of protease and antiproteases in the cells' microenvironment.

44 inase activity, and unlike prostasins resist antiproteases, including leupeptin, aprotinin, serpins,

45 1-antitrypsin (alpha1-AT), the primary PR-3 antiprotease, inhibited the anti-PR-3 induced IL-8 relea

46 An imbalance between proteases and antiproteases is thought to play a role in the inflammat

47 The possibility that H. pylori releases antiproteases may explain, in part, why this bacterium i

48 this system is capable of concentrating the antiprotease of the fusion protein, in the thin film of

49 PAI-1 proteins that possessed either intact antiprotease or vitronectin-binding activity to bleomyci

50 Specific antiprotease production in a patients with genetically d

51 ored area of A1AT biology independent of its antiprotease properties.

52 In addition to its primary function as an antiprotease, SLPI may also influence cellular functions

53 th the ability to deliver therapeutics, like antiproteases, specifically to the lumenal surface of th

54 eukocyte protease inhibitor (SLPI), a 12-kDa antiprotease, suppresses the growth of C. albicans in vi

55 al frequency of CD49e(+) monocytes contained antiproteases that partially blocked FNf-induced monocyt

56 A combination of surfactant and antiprotease therapy may improve therapeutic prospects.

57 d by changes in the balance of proteases and antiproteases, tissue damage by oxidative stress, or a c

58 s human tracheal xenografts and delivers the antiprotease to the apical surface to a much greater ext

59 oped a strategy that permits the delivery of antiproteases to the inaccessible CF airways by targetin

60 er adding alpha1-antitrypsin (alpha1-AT), an antiprotease, to surfactant improves its in vivo functio

61 value in CF, preferably in conjunction with antiprotease treatment.

62 The proresolving effect of antiproteases was also observed in a model of monosodium

63 Since secreted Z alpha1AT is a functional antiprotease, we hypothesized that interrupting cataboli

64 Cell-cell adhesion proteins and antiproteases were reduced, and leukocyte recruitment (i