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1 n of Cdc42 activity, increased invasion, and transendothelial migration.
2 of CLL cell binding to PEX9, chemotaxis, and transendothelial migration.
3 catenins out of the junction at the site of transendothelial migration.
4 l ligands and support leukocyte adhesion and transendothelial migration.
5 ctins but impaired intraluminal crawling and transendothelial migration.
6 ls roll on the endothelium to initiate their transendothelial migration.
7 ty integrin activation and chemokine-induced transendothelial migration.
8 cruitment was assessed based on adhesion and transendothelial migration.
9 MMP-1 regulates endothelial permeability and transendothelial migration.
10 leukocyte rolling, adhesion, and ultimately transendothelial migration.
11 eir presentation to leukocytes and leukocyte transendothelial migration.
12 neutrophil adhesion to endothelial cells and transendothelial migration.
13 rins CD11b/CD18 (Mac-1), specifically during transendothelial migration.
14 ry signature with concomitant attenuation of transendothelial migration.
15 of calcium fluxes and Rac1 during leukocyte transendothelial migration.
16 , S730, or S737 were necessary for leukocyte transendothelial migration.
17 RNA completely blocked bradykinin-stimulated transendothelial migration.
18 ancer cell-endothelial cell interactions and transendothelial migration.
19 L-selectin, function to facilitate leukocyte transendothelial migration.
20 ing sequentially induce PECAM-1-mediated PMN transendothelial migration.
21 cell adhesion molecule 1 (PECAM-1)-mediated transendothelial migration.
22 tep 1) into firm adhesion (step 3), yielding transendothelial migration.
23 phosphorylation events are indispensable for transendothelial migration.
24 junction formation, leukocyte adhesion, and transendothelial migration.
25 f adhesion molecules, monocyte adhesion, and transendothelial migration.
26 ; and regulation of cellular recruitment via transendothelial migration.
27 necessary, but not sufficient for increased transendothelial migration.
28 resulted in increased E-cadherin and reduced transendothelial migration.
29 e endothelial surface for potential sites of transendothelial migration.
30 o the glomerular vasculature did not undergo transendothelial migration.
31 SIRPgamma, play an important role in T-cell transendothelial migration.
32 tion of early cellular processes involved in transendothelial migration.
33 esion molecule-1 (ICAM-1)-dependent monocyte transendothelial migration.
34 igration of PMN or evoke a role for JAM-C in transendothelial migration.
35 0.01) increase in IL-8-induced migration and transendothelial migration.
36 ssed ligand for PMN beta(2) integrins during transendothelial migration.
37 g monocyte adhesion to endothelial cells and transendothelial migration.
38 d the ability of CCL2 to stimulate monocytic transendothelial migration.
39 n molecule (JAM)-C plays a role in leukocyte transendothelial migration.
40 , compound 4 nonetheless inhibits lymphocyte transendothelial migration.
41 ells to endothelium from flow but also drove transendothelial migration.
42 s particularly important for steps involving transendothelial migration.
43 ial barrier function and reducing neutrophil transendothelial migration.
44 nt component in the regulation of neutrophil transendothelial migration.
45 eceptors that bind to chemokines and trigger transendothelial migration.
46 r transition to shear-resistant adhesion and transendothelial migration.
47 cell-cell contacts and facilitates leukocyte transendothelial migration.
48 n, epithelial-to-mesenchymal transition, and transendothelial migration.
49 t ~10% underwent spontaneous basal to apical transendothelial migration.
50 s a relevant negative regulator of leukocyte transendothelial migration.
51 hibited PMN adhesion, arrest under flow, and transendothelial migration.
52 ak through matrix barriers during tumor cell transendothelial migration.
53 ed human monocyte recruitment, adhesion, and transendothelial migration.
54 from the primary tumor, stromal invasion and transendothelial migration.
56 stimulatory effect of platelets on leukocyte transendothelial migration, a key mediator of atheroprog
57 (INV) expression are required for tumor cell transendothelial migration, a necessary step during intr
58 are not inherently toxic to neurons but that transendothelial migration across IL-1-stimulated brain
59 , we demonstrated that monocyte adhesion and transendothelial migration across inflamed endothelium w
62 othelial cells and fibroblasts and prevented transendothelial migration, an effect rescued by the for
63 entation on endothelial cells and subsequent transendothelial migration, an essential step for lympho
65 es that have been reported to play a role in transendothelial migration and asks why so many molecule
66 d to increased intravasation, the details of transendothelial migration and detachment into circulati
67 on of primary human monocytes promotes their transendothelial migration and differentiation into proi
68 60% of HIV-1-infected patients, to stimulate transendothelial migration and drive productively infect
69 early metastatic seeding, including arrest, transendothelial migration and early micrometastases for
70 il but endothelial LSP1 regulates neutrophil transendothelial migration and extravascular directional
71 sequential steps of lymphocyte adhesion and transendothelial migration and facilitates lymphocyte mi
72 ytoskeletal rearrangements abrogated CD34(+) transendothelial migration and impaired CD34(+) cell hom
73 ults extend the role of EMT in metastasis to transendothelial migration and implicate ZEB1 and N-cadh
76 primary HCMV infection of monocytes induces transendothelial migration and monocyte-to-macrophage di
77 istration resulted in inhibition of monocyte transendothelial migration and monocyte/macrophage accum
78 These results implicate defects in both PMN transendothelial migration and PMN DAG kinase alpha sign
79 stop human polymorphonuclear leukocyte (PMN) transendothelial migration and PMN infiltration in sever
80 n the regulation of Mena(INV) expression and transendothelial migration and provide mechanistic infor
81 treatment can potentially decrease leukocyte transendothelial migration and reduce angiogenesis assoc
82 sions that interacted with leukocytes before transendothelial migration and removal of HS reduced thi
85 sions, important for tumor cell invasion and transendothelial migration and tumor cell dissemination.
86 APCs in draining lymph nodes as well as for transendothelial migration and tumor cell recognition at
88 foci formation, mechanotransduction, T cell transendothelial migration, and homing to lymph nodes, a
89 vage fluid cells, inhibited bone marrow cell transendothelial migration, and inhibited endothelial ce
90 le-1 expression, polymorphonuclear leukocyte transendothelial migration, and leukocyte sequestration
91 adhesion to microvascular endothelial cells, transendothelial migration, and metastatic retention in
92 activity including cell invasion, migration, transendothelial migration, and proliferation were incre
93 lly required for Axl-mediated cell invasion, transendothelial migration, and resistance against TGF-b
94 an occur without polymorphonuclear leukocyte transendothelial migration, and that polymorphonuclear l
95 bone marrow (BM) are recruited to tissues by transendothelial migration, and we found that CCL2 is ch
96 L-selectin; HEV expression of molecules for transendothelial migration; and metabolic programs for l
98 integrin-mediated firm adhesion followed by transendothelial migration - are dependent on the activa
99 pecific cellular processes (phagocytosis and transendothelial migration) are enriched for transcripts
104 genes and other genes involved in leukocyte transendothelial migration at the vaccine injection site
105 tubulin binding returned cell migration and transendothelial migration back to control levels, indic
106 onocyte ADAM17 facilitates the completion of transendothelial migration by accelerating the rate of d
108 We conclude that Trio promotes leukocyte transendothelial migration by inducing endothelial docki
109 data show that annexin A2 limits neutrophil transendothelial migration by organizing the spatial dis
110 nts in understanding regulation of leukocyte transendothelial migration by small GTPase signaling.
111 d chemokine receptor expression and enhanced transendothelial migration capacity in patients with CKD
112 a-forming cell (CAFC) capacity and augmented transendothelial migration capacity, which was abrogated
113 s firm adhesion to the vascular endothelium, transendothelial migration, chemotaxis, and phagocytosis
114 alis-stimulated monocytes displayed enhanced transendothelial migration compared with monocytes stimu
116 esulting increase in lymphocyte and monocyte transendothelial migration could be blocked with soluble
118 endothelial R-Ras facilitates TNF-dependent transendothelial migration (diapedesis) of naive T cells
119 d diminished support for B16F10 adhesion and transendothelial migration, diminished B16F10-induced pe
121 egrins have been shown to mediate neutrophil transendothelial migration during systemic and local inf
122 regulated markers associated with leukocyte transendothelial migration, extracellular matrix injury
124 tigen processing and presentation, Leukocyte transendothelial migration, IL-17 signaling, Chemokine s
125 fficking by promoting the diapedesis step of transendothelial migration in a alpha4 integrin-dependen
126 romoting the adhesion of monocytes and their transendothelial migration in a Mac-1-dependent manner.
127 e candidate targets for inhibiting leukocyte transendothelial migration in heart disease and chronic
129 CR2 and CD62L levels and underwent efficient transendothelial migration in response to fractalkine (F
130 ng stathmin expression significantly reduced transendothelial migration in two different neuroblastom
132 ndothelial barrier and to support neutrophil transendothelial migration in vitro and in vivo in the s
134 ver, this mutant chemokine failed to promote transendothelial migration in vitro and inhibited the ha
135 Niflumic acid-treated PMNs also had impaired transendothelial migration in vitro, whereas migration i
139 ic interactions play a key role in leukocyte transendothelial migration, in allowing PECAM-1 to serve
140 ed permeability and increased naive monocyte transendothelial migration include the disruption of act
141 s have been shown to play a critical role in transendothelial migration including signals derived fro
142 Several mechanisms play a critical role in transendothelial migration, including signals derived fr
144 ers, proportionally fewer MO-MDSCs underwent transendothelial migration, indicating that the final st
145 (1 unit/mL) tumor necrosis factor-alpha and transendothelial migration induced by high-dose (100 uni
149 d in cell-cell interactions during leukocyte transendothelial migration is a prerequisite for designi
150 of metastasis (TMEM), facilitates tumor cell transendothelial migration is not completely understood.
151 a separate step in leukocyte extravasation, transendothelial migration is regulated by molecules tha
153 t resolvins directly act on PMN to attenuate transendothelial migration, less is known about the infl
155 emained static before a proportion underwent transendothelial migration mediated by a combination of
156 migration, the effects of Pak1 knockdown on transendothelial migration (microinvasion), tumor growth
157 nd evidence suggests that initial neutrophil transendothelial migration modifies endothelial cell phe
158 ase-PI(3,4)P2 signaling axis while augmented transendothelial migration occurs in a vascular endothel
159 okine expression, proliferation, and delayed transendothelial migration of allogeneic memory, but not
160 ion that cognate recognition of ECs enhanced transendothelial migration of antigen-specific T lymphoc
162 igen was necessary for the firm adhesion and transendothelial migration of CD8+ effector T cells spec
166 reased endothelial permeability and elevated transendothelial migration of HIV-infected monocytes acr
167 -1 inhibition enhanced vitronectin-dependent transendothelial migration of human bone marrow-derived
168 -docosahexaenoic acid, and they both stopped transendothelial migration of human neutrophils (EC(50)
169 To study this process further, we analyzed transendothelial migration of human PC-3 prostate cancer
170 nce across the in vitro BBB and the enhanced transendothelial migration of immunocompetent cells acro
171 BBB permeability using TEER measurements and transendothelial migration of immunocompetent cells.
172 2 deficiency impaired the integrin-dependent transendothelial migration of innate leukocytes and rest
174 lectin, and breakdown of the BRB, leading to transendothelial migration of leukocytes and recruitment
175 ressure, vascular permeability, clotting and transendothelial migration of leukocytes and tumor cells
176 on of blood-brain barrier (BBB) function and transendothelial migration of leukocytes are essential c
177 on endothelium and other cells as well as to transendothelial migration of leukocytes in the microcir
178 d flow shear modulate vascular adherence and transendothelial migration of leukocytes into inflamed t
180 g the molecules and mechanisms that regulate transendothelial migration of leukocytes, or diapedesis,
182 own that stanniocalcin-1 (STC1) inhibits the transendothelial migration of macrophages and T cells, s
183 was reduced by blocking WASP binding to WIP, transendothelial migration of macrophages, the most cruc
185 duced proliferation and superantigen-induced transendothelial migration of memory T cells, indicating
186 ivation, which led us to investigate whether transendothelial migration of monocytes across HSECs inf
187 These data point to a role of MMP-14 during transendothelial migration of monocytes and T-cell attra
189 nocyte adhesion to ECs, EC migration and the transendothelial migration of monocytes, while the over-
194 tactic Protein 1 (MCP-1), play a key role in transendothelial migration of mononuclear cells during t
195 ecruitment with a predominant enhancement of transendothelial migration of neutrophilic granulocytes.
196 is an adhesion molecule believed to mediate transendothelial migration of neutrophils and other leuk
197 9 regulate distinct, sequential steps in the transendothelial migration of neutrophils during inflamm
199 se brain endothelial cells and supported the transendothelial migration of neutrophils in vitro.
202 own that TSG-6 inhibits chemokine-stimulated transendothelial migration of neutrophils via a direct i
205 lled F. tularensis LVS for 24 h promoted the transendothelial migration of subsequently added neutrop
208 xpress CXCR3 and reduced the IP-10-dependent transendothelial migration of T helper cells under condi
209 neutrophils would also modify the subsequent transendothelial migration of T lymphocytes across cytok
211 pression of VLA-4 also resulted in increased transendothelial migration of Tck cells, which could be
217 /Rap1 GTPase signaling pathway, resulting in transendothelial migration on stimulated human umbilical
219 he subsets was studied in in vitro models of transendothelial migration or interstitial chemokinesis
220 ted that P5 peptide does not affect monocyte transendothelial migration or macrophage efflux from the
221 sion to HUVEC, but significantly reduced PMN transendothelial migration (P < 0.0001) and fMLP-induced
223 resulting in enhanced monocyte motility and transendothelial migration, prolonged monocyte survival,
224 by expression of Rap1GAP increased leukocyte transendothelial migration, providing physiological rele
225 to the regulation of leukocyte adhesion and transendothelial migration remains poorly understood.
228 cancer cell adhesion to the endothelium and transendothelial migration, resulting in reduced liver m
231 ost defense cell responsiveness to GM-CSF at transendothelial migration sites while suppressing it in
233 through a dense three-dimensional matrix and transendothelial migration, suggesting that tyrosine pho
235 lecule, is required for CLL cells to undergo transendothelial migration (TEM) and enter the prolifera
236 e and clustering) is required for lymphocyte transendothelial migration (TEM) and entry into lymph no
238 trol efflux of small molecules and leukocyte transendothelial migration (TEM) between blood and tissu
239 previously reported that the TCR-stimulated transendothelial migration (TEM) depends on fractalkine
240 ar requirements of chemokine- and TCR-driven transendothelial migration (TEM) differ significantly.
242 e EM CD4+ T cells, but fail to support their transendothelial migration (TEM) in response to TCR enga
248 essential role in the CXCL12/CXCR4-mediated transendothelial migration (TEM) of CXCR4(+)CXCR7(+) hum
249 hat regulate the endothelial response during transendothelial migration (TEM) of invasive cancer cell
256 distributed chemokines and their effects on transendothelial migration (TEM) under hydrodynamic shea
259 helial cells (ECs) lining the venular lumen (transendothelial migration (TEM)) in a luminal-to-ablumi
267 to form short-lived "gaps" during leukocyte transendothelial migration (TEM); however, whether these
268 ss endothelium [referred to as diapedesis or transendothelial migration (TEM)] is a critical step in
269 nocyte-to-myeloid fibroblast formation after transendothelial migration (TEM; 3-fold, P < 0.01).
270 cells were found to be independent of VEGF, transendothelial migration through CNS microvascular end
271 wice as many CD14++CD16+ monocytes underwent transendothelial migration through hepatic endothelial c
272 easured using in vitro chemotaxis assays and transendothelial migration through human umbilical vein
274 ion pathways may lead to PECAM-1-independent transendothelial migration through the pulmonary or the
275 nderlying mechanisms that regulate leukocyte transendothelial migration through the vascular endothel
276 i showed that inflammation-induced leukocyte transendothelial migration to peritoneum or lungs was si
277 )CD28- T cells enhanced their chemotaxis and transendothelial migration toward the chemokine CCL5.
278 d for the induction of monocyte motility and transendothelial migration, two biological events requir
279 integrins, leading to defective adhesion and transendothelial migration under conditions of physiolog
280 n of CXCR 3 promotes lymphocyte adhesion and transendothelial migration under flow and that human hep
281 results in increased neutrophil adhesion and transendothelial migration under flow conditions and red
283 okines, promote mononuclear leukocytes (MNL) transendothelial migration, up-regulate monocyte CD11b a
284 diated both leukocyte adhesion and leukocyte transendothelial migration upon oxLDL treatment of endot
285 the lung, but acted by inhibiting neutrophil transendothelial migration upstream of interstitial migr
286 , which facilitates endothelial adhesion and transendothelial migration via an ICAM1-fibrinogen-ICAM1
287 cell proliferation, migration, adhesion, and transendothelial migration via increased expression of I
292 within endothelial cells decreased leukocyte transendothelial migration, whereas inhibiting Rap1 acti
293 and P3/P3a/P3b peptides inhibited B-CLL cell transendothelial migration, whereas the mutated peptide
294 hocytes, the malignant cells did not undergo transendothelial migration, which could explain why lymp
295 l gap formation, the first step during tumor transendothelial migration, which is mediated by both ad
296 ed breast cancer cell adhesion to HUVECs and transendothelial migration, which were repressed by ET-1
297 ing leaves open a possible role in leukocyte transendothelial migration, which would be consistent wi
298 resence of activated neutrophils and reduces transendothelial migration without affecting adhesion of
299 neutrophils, with alpha2-agonists decreased transendothelial migration, without affecting neutrophil
300 (SDF-1alpha [CXCL12])-mediated T lymphocyte transendothelial migration, without reducing accumulatio