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1 fected by soluble components of the platelet releasate.
2 ving fibrin, human fibroblasts, and platelet releasate.
3 onfocal imaging, and measurement of platelet releasates.
4 mography demonstrated free PAI-1 in cellular releasates.
5 e report the presence of proSAAS peptides in releasates.
6 n measured LTGF-beta1 activation in platelet releasates.
7 e indirect interactions mediated by platelet releasates.
8 ost abundant proteins contained in the BMCMC releasates.
9                                         This releasate activates other platelets, promotes wound repa
10 generation and activity, as well as platelet releasate activity may be drastically impacted by the in
11  peptide mixtures, including neuronal tissue releasate and protein tryptic digests.
12 human platelets, thrombin-activated platelet releasate, and synthetic platelet-associated antimicrobi
13                                 Observed SCN releasates are peptide rich and demonstrate the co-relea
14 t tryptase, were identified in the mast cell releasates as the likely culprits that digest these cyto
15  on exposure to activated platelets or their releasates, as judged by immunoblotting for phospho-amin
16 -embedded monolith to condition neuropeptide releasates collected from several Aplysia neurons cultur
17 omatography indicated that staphylocidal PLT releasates contained PMPs and PKs.
18  analyses and immunoassays of human platelet releasates coupled with angiogenesis assays to search fo
19                                           MC releasate elevated ICAM-1 (intercellular adhesion molecu
20  mast cells produced substantially different releasates following IgE-mediated activation.
21  that treating megakaryocytes (MKs) with the releasate from activated platelets increased proplatelet
22                Similar to recombinant CXCL4, releasate from human platelets also reduced CD163 expres
23 lated secretion of VEGF and a pro-angiogenic releasate from platelets.
24                                          The releasate from these platelets contained decreased proan
25 slices demonstrates their ability to collect releasates from a variety of neuronal tissues.
26 dition to prostanoids such as thromboxane A2 Releasates from activated platelets caused cell migratio
27                        Moreover, dilution of releasates from thrombin-stimulated platelets showed tha
28                             Because platelet releasates from TSP-1 null mice contain active TGF-beta1
29 from WT platelets or purified TSP-1, but not releasates from TSP-1-/- platelets, reduced the inhibito
30 trast, incubation of TSP-1-/- platelets with releasates from WT platelets or purified TSP-1, but not
31                                     Platelet releasates generated by activation with ADP promoted mig
32 data indicate that Vn is present in platelet releasates in two molecular weight (M(r) forms.
33                          Platelets and their releasate, including granules, microparticles, microRNAs
34       Conversely, TXA(2)-stimulated platelet releasate inhibited migration and formation of capillary
35             Additionally, the content of SCN releasate is stimulation specific.
36 ion of the retinohypothalamic tract, produce releasate mass spectra that are notably different from t
37     We show that platelets, but not platelet releasate, modulate the migration and intercellular adhe
38  also could be generated by beta-tryptase in releasates of activated skin mast cells.
39                                 Furthermore, releasates of immature WPBs from either BLOC-2 or exocys
40 o define the proteome contained in mast cell releasates on activation to better understand the factor
41 ed platelets showed that the toxicity of the releasates on C. albicans is concentration dependent.
42  purified protein complex or in the platelet releasates or sera of mice engineered to contain an LAP
43 ved either fibrin alone, fibrin and platelet releasate, or fibrin and fibroblasts.
44 merases in the activation of LLC in platelet releasates (PR) and recombinant LLC.
45 n trypsin inhibitor, when added to mast cell releasates, prevented the degradation of exogenously add
46             Increasing viscosity in platelet releasates produced higher shear stress and higher LTGF-
47 und that different agonists evoked different releasate profiles, with aspirin having a general modera
48 the mast cell protease content can shape its releasate proteome.
49 e tissue mast cells, respectively, and their releasate proteomes were analyzed by mass spectrometry.
50 m, DBP-depleted serum, or activated platelet releasate provides a required factor and permits DBP to
51 nished 95% and 70% of the effect of platelet releasate, respectively, suggesting CCL5 derived from pl
52          Fractionation of activated platelet releasate revealed that the additional factor possessed
53  have been characterized, including platelet releasates (the 'secretome'), alpha and dense granules,
54 igated the effect of aspirin on the platelet releasate using mass spectrometry and found that differe
55                     In some wounds, platelet releasate was added to the fibrin clot.
56 ured human fibroblasts, fibrin, and platelet releasate were 14% filled with granulation tissue compar
57 sma and total and size-fractionated platelet releasates were compared (1) immunologically using three
58 ld reproduce the effect of serum or platelet releasate, whereas Abs to TSP-1 could block these effect
59 y sustained accumulation of Abeta(42) in the releasate, which was blocked by the group II mGluR antag
60  by Western blotting of platelet lysates and releasates with anti-FV antibodies.