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1 s in the endothelial monolayer (paracellular diapedesis).
2 signaling as well as the adhesion events of diapedesis.
3 poxin A(4) receptor (ALXR/FPRL1) to halt PMN diapedesis.
4 receptors (ChR) for vascular wall arrest and diapedesis.
5 ability, and motility, functions critical to diapedesis.
6 tail of the migrating monocyte and complete diapedesis.
7 or vascular barrier regulation and leukocyte diapedesis.
8 ad, deletion of EVL and VASP impaired T-cell diapedesis.
9 and an adhesion molecule mediating leukocyte diapedesis.
10 ein-coupled chemokine receptors required for diapedesis.
11 early T cell activation and interferes with diapedesis.
12 ced beta2-integrin activation and neutrophil diapedesis.
13 integrin-dependent adhesion, chemotaxis, and diapedesis.
14 n by suppressing CD200R myeloid cells during diapedesis.
15 l motility, are not obligatory for leukocyte diapedesis.
16 helial migration by accelerating the rate of diapedesis.
17 gesting that these molecules are involved in diapedesis.
18 actions may play a role in aiding neutrophil diapedesis.
19 action of serine proteases promote leukocyte diapedesis.
20 ork governing endothelial-cell regulation of diapedesis.
21 n the active role of the endothelial cell in diapedesis.
22 ptosis, vascular permeability, and leukocyte diapedesis.
23 ic activity of MMPs is not just required for diapedesis.
24 ulate a critical step required for leukocyte diapedesis.
25 f mechanical events involved in paracellular diapedesis.
26 lectively blocked the transcellular route of diapedesis.
27 ching for areas permissive for transcellular diapedesis.
28 oing transendothelial migration, also called diapedesis.
29 cale of neutrophil activation, adhesion, and diapedesis.
30 to tissues: tethering, rolling, adhesion and diapedesis.
31 rm adhesion to the nearest junction to begin diapedesis.
32 ling, activation, tight adhesion, arrest and diapedesis.
33 of endothelial barrier function and reduces diapedesis.
34 tracks oriented parallel to the direction of diapedesis.
36 transendothelial migration of leukocytes, or diapedesis, a critical step in the inflammatory response
39 ation of IL-1/inhibition of RXR, granulocyte diapedesis/adhesion, Fc macrophage activation, prothromb
40 the CNS is relatively resistant to leukocyte diapedesis after chemokine injection, leaving their func
42 (Cx-43), known to be involved in tumor cell diapedesis and attachment to endothelial cells, is signi
43 AGEP, converged on neutrophil chemotaxis and diapedesis and cytokines known to drive neutrophil-rich
46 othelial cells is a central event leading to diapedesis and involves the binding of the I-domain of b
47 leukocyte adherence to endothelium, impaired diapedesis and less tissue necrosis in the hearts perfus
48 -lymphocyte polarization and interfered with diapedesis and migration in the narrow subendothelial sp
49 t that in addition to influencing eosinophil diapedesis and survival, anti-CCL11 has an action on T c
51 elial microtubules and kinesins in promoting diapedesis, and a mechanism to explain targeted recyclin
52 diverges into pathways regulating lymphocyte diapedesis, and other pathways modulating gene expressio
53 ammatory functions, including cell adhesion, diapedesis, and phagocytosis, are dependent on the mobil
56 roles in immunity by facilitating leukocyte diapedesis at inflammatory sites and controlling periphe
59 herin, known to selectively affect leukocyte diapedesis, but not the induction of vascular permeabili
60 pothesized that VECs facilitate paracellular diapedesis by opening their cell-cell junctions in respo
63 or ADAM17 or monocyte ADAM10, reproduces the diapedesis delay observed with metalloproteinase inhibit
64 ial migration and cell polarization, but not diapedesis, depended on Nef's ability to inhibit host ce
67 ptor (uPAR; CD87) in neutrophil adhesion and diapedesis has been demonstrated with uPAR-knockout mice
69 eukocytes and endothelial cells critical for diapedesis have been identified, but the mechanisms unde
70 use monocyte adhesion to the endothelium and diapedesis in lesion-prone regions of the vasculature is
71 (i.e., through individual endothelial cells) diapedesis in vitro and demonstrate that virtually all,
77 recognition triggers effector functions in a diapedesis-independent manner and is inhibited by the pr
78 migration appeared to be responsible for the diapedesis induced by interaction between CCR5 on Th1-ty
82 chemokine signaling, leukocyte adhesion and diapedesis, invasive cell type-specific markers, and com
87 , called transendothelial migration (TEM) or diapedesis, is completed within 90 s after a leukocyte a
88 recycling compartment (LBRC) is required for diapedesis, is mediated by kinesin family molecular moto
90 junctions, where it functions to facilitate diapedesis, maintain vascular integrity, and transmit su
92 virtually all, both para- and transcellular, diapedesis occurs in the context of a novel "cuplike" tr
94 the principal MAPKs involved in facilitating diapedesis of CD4(+) lymphocytes across both types of MV
95 histamine release is known to promote rapid diapedesis of inflammatory cells, we evaluated the possi
98 agocytosis of bacteria), despite accelerated diapedesis of leukocytes into peripheral tissue, as well
100 ntibody to CD99, hec2, selectively inhibited diapedesis of monocytes across endothelial cells by >90%
101 olecules (CAMs) involved in the adhesion and diapedesis of monocytes and the adherence of SS reticulo
103 ant stress leading to increased adhesion and diapedesis of monocytes, as well as heightened adherence
105 mice, and correspondingly, there was reduced diapedesis of peripheral macrophages in the IL-1R1 null
106 nin-positive cells, consistent with a faster diapedesis of peripheral monocytes and neutrophils.
108 ition of the endothelium results in enhanced diapedesis of T cells into the tissue, while not affecti
109 ation is driven by excessive transmigration (diapedesis) of leukocytes from the blood to the tissue a
110 ime required for human monocytes to complete diapedesis on unactivated or inflamed human endothelium,
111 eukocytes across endothelium [referred to as diapedesis or transendothelial migration (TEM)] is a cri
112 endothelial MAPKs ERK, p38, and JNK mediate diapedesis-related and diapedesis-unrelated functions of
113 dothelial barrier integrity during leukocyte diapedesis requires local endothelial RhoA cycling.
114 ctivated T-cell trafficking by promoting the diapedesis step of transendothelial migration in a alpha
115 ial cell junctions, indicating that only the diapedesis step was blocked by interference with CD99.
116 M is a molecule used specifically during the diapedesis step when neutrophils and monocytes leave the
117 that precede it, transendothelial migration (diapedesis), the step in which leukocytes migrate betwee
120 has been shown to be important for leukocyte diapedesis through brain microvessels and subsequent bin
122 the cell will spread and will either undergo diapedesis through individual vascular endothelial cells
123 clude that specifically targeting neutrophil diapedesis through the endothelial barrier may represent
124 l inflammatory models, that it is neutrophil diapedesis through the endothelial barrier that is respo
125 se, which involves intraluminal crawling and diapedesis to the extravascular space, remains elusive.
127 p38, and JNK mediate diapedesis-related and diapedesis-unrelated functions of ICAM-1 in cerebral and
130 y, the hypothesis that systemic LPS inhibits diapedesis was tested by injection of LPS ip and ivt sim
132 steps: adhesion, junctional recognition, and diapedesis; we further demonstrate that ICAM-2 is expres
133 A-4 may serve to facilitate transendothelial diapedesis, whereas late and prolonged activation of VLA
134 cell-cell junction remodeling, adhesion, and diapedesis, which corresponded with lower plasma levels
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