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1 neutrophil adhesion to endothelial cells and transendothelial migration.
2 rins CD11b/CD18 (Mac-1), specifically during transendothelial migration.
3  of calcium fluxes and Rac1 during leukocyte transendothelial migration.
4 , S730, or S737 were necessary for leukocyte transendothelial migration.
5 RNA completely blocked bradykinin-stimulated transendothelial migration.
6 ancer cell-endothelial cell interactions and transendothelial migration.
7 L-selectin, function to facilitate leukocyte transendothelial migration.
8 ing sequentially induce PECAM-1-mediated PMN transendothelial migration.
9  cell adhesion molecule 1 (PECAM-1)-mediated transendothelial migration.
10 eceptors that bind to chemokines and trigger transendothelial migration.
11 tep 1) into firm adhesion (step 3), yielding transendothelial migration.
12 phosphorylation events are indispensable for transendothelial migration.
13  junction formation, leukocyte adhesion, and transendothelial migration.
14 f adhesion molecules, monocyte adhesion, and transendothelial migration.
15 ; and regulation of cellular recruitment via transendothelial migration.
16  necessary, but not sufficient for increased transendothelial migration.
17 resulted in increased E-cadherin and reduced transendothelial migration.
18 e endothelial surface for potential sites of transendothelial migration.
19  SIRPgamma, play an important role in T-cell transendothelial migration.
20 tion of early cellular processes involved in transendothelial migration.
21 esion molecule-1 (ICAM-1)-dependent monocyte transendothelial migration.
22 igration of PMN or evoke a role for JAM-C in transendothelial migration.
23 0.01) increase in IL-8-induced migration and transendothelial migration.
24 ssed ligand for PMN beta(2) integrins during transendothelial migration.
25 r transition to shear-resistant adhesion and transendothelial migration.
26 g monocyte adhesion to endothelial cells and transendothelial migration.
27 d the ability of CCL2 to stimulate monocytic transendothelial migration.
28 n molecule (JAM)-C plays a role in leukocyte transendothelial migration.
29 , compound 4 nonetheless inhibits lymphocyte transendothelial migration.
30 ells to endothelium from flow but also drove transendothelial migration.
31 s particularly important for steps involving transendothelial migration.
32 ial barrier function and reducing neutrophil transendothelial migration.
33 nt component in the regulation of neutrophil transendothelial migration.
34 s, aggregation, adhesion to endothelium, and transendothelial migration.
35 ll junctions is ligated by leukocytes during transendothelial migration.
36 d primarily to mediate stronger adhesion and transendothelial migration.
37 be an essential element in chemokine-induced transendothelial migration.
38 tent inducer of CXCR3 down-regulation and of transendothelial migration.
39 m tethering to firm adhesion, spreading, and transendothelial migration.
40 of RhoA, we found that RhoA was required for transendothelial migration.
41  receptors such as CXCR4, MMP-9, followed by transendothelial migration.
42 cell-cell contacts and facilitates leukocyte transendothelial migration.
43 t ~10% underwent spontaneous basal to apical transendothelial migration.
44 s a relevant negative regulator of leukocyte transendothelial migration.
45 hibited PMN adhesion, arrest under flow, and transendothelial migration.
46 ak through matrix barriers during tumor cell transendothelial migration.
47 ed human monocyte recruitment, adhesion, and transendothelial migration.
48 from the primary tumor, stromal invasion and transendothelial migration.
49 of CLL cell binding to PEX9, chemotaxis, and transendothelial migration.
50  catenins out of the junction at the site of transendothelial migration.
51 l ligands and support leukocyte adhesion and transendothelial migration.
52 ctins but impaired intraluminal crawling and transendothelial migration.
53 ls roll on the endothelium to initiate their transendothelial migration.
54 ty integrin activation and chemokine-induced transendothelial migration.
55 cruitment was assessed based on adhesion and transendothelial migration.
56 MMP-1 regulates endothelial permeability and transendothelial migration.
57 eir presentation to leukocytes and leukocyte transendothelial migration.
58                          In contrast, during transendothelial migration, a form of active deformation
59 stimulatory effect of platelets on leukocyte transendothelial migration, a key mediator of atheroprog
60 (INV) expression are required for tumor cell transendothelial migration, a necessary step during intr
61 are not inherently toxic to neurons but that transendothelial migration across IL-1-stimulated brain
62 , we demonstrated that monocyte adhesion and transendothelial migration across inflamed endothelium w
63                       In vitro, T lymphocyte transendothelial migration across PECAM-KO endothelial c
64 on the endothelial surface before undergoing transendothelial migration, also called diapedesis.
65 vidity to coordinate adhesion and subsequent transendothelial migration, although the sequential sign
66  in the processes of neutrophil and monocyte transendothelial migration, an analogous function of VE-
67 othelial cells and fibroblasts and prevented transendothelial migration, an effect rescued by the for
68 entation on endothelial cells and subsequent transendothelial migration, an essential step for lympho
69                                    Leukocyte transendothelial migration and adhesion to RA ST require
70 nts are inhibited by antibodies that prevent transendothelial migration and are reversed following tr
71 es that have been reported to play a role in transendothelial migration and asks why so many molecule
72 d to increased intravasation, the details of transendothelial migration and detachment into circulati
73 on of primary human monocytes promotes their transendothelial migration and differentiation into proi
74 60% of HIV-1-infected patients, to stimulate transendothelial migration and drive productively infect
75  early metastatic seeding, including arrest, transendothelial migration and early micrometastases for
76 il but endothelial LSP1 regulates neutrophil transendothelial migration and extravascular directional
77  sequential steps of lymphocyte adhesion and transendothelial migration and facilitates lymphocyte mi
78 ytoskeletal rearrangements abrogated CD34(+) transendothelial migration and impaired CD34(+) cell hom
79 ults extend the role of EMT in metastasis to transendothelial migration and implicate ZEB1 and N-cadh
80  regulates human polymorphonuclear leukocyte transendothelial migration and is anti-inflammatory.
81                                        Thus, transendothelial migration and lung metastasis developme
82  primary HCMV infection of monocytes induces transendothelial migration and monocyte-to-macrophage di
83  These results implicate defects in both PMN transendothelial migration and PMN DAG kinase alpha sign
84 stop human polymorphonuclear leukocyte (PMN) transendothelial migration and PMN infiltration in sever
85 n the regulation of Mena(INV) expression and transendothelial migration and provide mechanistic infor
86 treatment can potentially decrease leukocyte transendothelial migration and reduce angiogenesis assoc
87 sions that interacted with leukocytes before transendothelial migration and removal of HS reduced thi
88                             To this end, PMN transendothelial migration and superoxide anion generati
89 sions, important for tumor cell invasion and transendothelial migration and tumor cell dissemination.
90  APCs in draining lymph nodes as well as for transendothelial migration and tumor cell recognition at
91  foci formation, mechanotransduction, T cell transendothelial migration, and homing to lymph nodes, a
92 vage fluid cells, inhibited bone marrow cell transendothelial migration, and inhibited endothelial ce
93 le-1 expression, polymorphonuclear leukocyte transendothelial migration, and leukocyte sequestration
94 adhesion to microvascular endothelial cells, transendothelial migration, and metastatic retention in
95 activity including cell invasion, migration, transendothelial migration, and proliferation were incre
96 lly required for Axl-mediated cell invasion, transendothelial migration, and resistance against TGF-b
97 an occur without polymorphonuclear leukocyte transendothelial migration, and that polymorphonuclear l
98 bone marrow (BM) are recruited to tissues by transendothelial migration, and we found that CCL2 is ch
99  L-selectin; HEV expression of molecules for transendothelial migration; and metabolic programs for l
100       JAM-C has been implicated in leukocyte transendothelial migration, angiogenesis, cell adhesion,
101  integrin-mediated firm adhesion followed by transendothelial migration - are dependent on the activa
102 pecific cellular processes (phagocytosis and transendothelial migration) are enriched for transcripts
103                                            A transendothelial migration assay was used to determine t
104                             Angiogenesis and transendothelial migration assays were performed in cons
105 12 both in transwell migration assays and in transendothelial migration assays.
106 alysis, inflammatory stimulation assays, and transendothelial migration assays.
107  genes and other genes involved in leukocyte transendothelial migration at the vaccine injection site
108  tubulin binding returned cell migration and transendothelial migration back to control levels, indic
109 onocyte ADAM17 facilitates the completion of transendothelial migration by accelerating the rate of d
110 ge in vivo, despite interruption of in vitro transendothelial migration by CD177 ligation.
111     We conclude that Trio promotes leukocyte transendothelial migration by inducing endothelial docki
112  data show that annexin A2 limits neutrophil transendothelial migration by organizing the spatial dis
113 nts in understanding regulation of leukocyte transendothelial migration by small GTPase signaling.
114 d chemokine receptor expression and enhanced transendothelial migration capacity in patients with CKD
115 a-forming cell (CAFC) capacity and augmented transendothelial migration capacity, which was abrogated
116 s firm adhesion to the vascular endothelium, transendothelial migration, chemotaxis, and phagocytosis
117 alis-stimulated monocytes displayed enhanced transendothelial migration compared with monocytes stimu
118 is factor alpha, and supported higher immune transendothelial migration compared with PAECs.
119 esulting increase in lymphocyte and monocyte transendothelial migration could be blocked with soluble
120            Intravital imaging demonstrated a transendothelial migration defect into DAP12-deficient l
121 d diminished support for B16F10 adhesion and transendothelial migration, diminished B16F10-induced pe
122 egrins have been shown to mediate neutrophil transendothelial migration during systemic and local inf
123  by signaling through activating FcRs before transendothelial migration has occurred.
124 fficking by promoting the diapedesis step of transendothelial migration in a alpha4 integrin-dependen
125 romoting the adhesion of monocytes and their transendothelial migration in a Mac-1-dependent manner.
126 e candidate targets for inhibiting leukocyte transendothelial migration in heart disease and chronic
127                               Measurement of transendothelial migration in response to CCL5 demonstra
128 CR2 and CD62L levels and underwent efficient transendothelial migration in response to fractalkine (F
129 ng stathmin expression significantly reduced transendothelial migration in two different neuroblastom
130                                     Notably, transendothelial migration in vitro and extravasation in
131 y neutrophil arrest, adhesion, crawling, and transendothelial migration in vitro and in vivo.
132 ver, this mutant chemokine failed to promote transendothelial migration in vitro and inhibited the ha
133 Niflumic acid-treated PMNs also had impaired transendothelial migration in vitro, whereas migration i
134 d an increased chemotaxis, chemokinesis, and transendothelial migration in vitro.
135 priming impaired priming-enhanced eosinophil transendothelial migration in vitro.
136 mal cells and fibronectin along with reduced transendothelial migration in vitro.
137 nt role in mediating neutrophil and monocyte transendothelial migration in vivo.
138 ic interactions play a key role in leukocyte transendothelial migration, in allowing PECAM-1 to serve
139 ed permeability and increased naive monocyte transendothelial migration include the disruption of act
140 s have been shown to play a critical role in transendothelial migration including signals derived fro
141   Several mechanisms play a critical role in transendothelial migration, including signals derived fr
142                   ICAM-1 is also involved in transendothelial migration, independently of its role in
143 ers, proportionally fewer MO-MDSCs underwent transendothelial migration, indicating that the final st
144  (1 unit/mL) tumor necrosis factor-alpha and transendothelial migration induced by high-dose (100 uni
145 contacts culminate in cooperative, step-wise transendothelial migration into bone is not known.
146                                    Leukocyte transendothelial migration involves the active participa
147       The process of intravasation involving transendothelial migration is a key step in metastatic s
148 d in cell-cell interactions during leukocyte transendothelial migration is a prerequisite for designi
149 of metastasis (TMEM), facilitates tumor cell transendothelial migration is not completely understood.
150  a separate step in leukocyte extravasation, transendothelial migration is regulated by molecules tha
151                                              Transendothelial migration itself can be dissected into
152 t resolvins directly act on PMN to attenuate transendothelial migration, less is known about the infl
153                              Compared to PMN transendothelial migration, little is known about how PM
154 emained static before a proportion underwent transendothelial migration mediated by a combination of
155  migration, the effects of Pak1 knockdown on transendothelial migration (microinvasion), tumor growth
156 nd evidence suggests that initial neutrophil transendothelial migration modifies endothelial cell phe
157 ase-PI(3,4)P2 signaling axis while augmented transendothelial migration occurs in a vascular endothel
158 okine expression, proliferation, and delayed transendothelial migration of allogeneic memory, but not
159 ion that cognate recognition of ECs enhanced transendothelial migration of antigen-specific T lymphoc
160 CD40-stimulated tumor cells also support the transendothelial migration of autologous CCR4(+) antileu
161 ascular leakage in tumors, and inhibited the transendothelial migration of cancer cells.
162 igen was necessary for the firm adhesion and transendothelial migration of CD8+ effector T cells spec
163 estational age newborns, then minimizing the transendothelial migration of circulating cells by pharm
164                                              Transendothelial migration of effector memory CD4 T cell
165                        Bradykinin stimulated transendothelial migration of EPCs in a concentration-de
166              The ability of FNf to stimulate transendothelial migration of HIV-1-infected MNLs may he
167 reased endothelial permeability and elevated transendothelial migration of HIV-infected monocytes acr
168 -1 inhibition enhanced vitronectin-dependent transendothelial migration of human bone marrow-derived
169 -docosahexaenoic acid, and they both stopped transendothelial migration of human neutrophils (EC(50)
170   To study this process further, we analyzed transendothelial migration of human PC-3 prostate cancer
171 nce across the in vitro BBB and the enhanced transendothelial migration of immunocompetent cells acro
172 BBB permeability using TEER measurements and transendothelial migration of immunocompetent cells.
173 2 deficiency impaired the integrin-dependent transendothelial migration of innate leukocytes and rest
174 essed on the endothelial barrier can promote transendothelial migration of KSHV-infected cells.
175 lectin, and breakdown of the BRB, leading to transendothelial migration of leukocytes and recruitment
176 ressure, vascular permeability, clotting and transendothelial migration of leukocytes and tumor cells
177 on of blood-brain barrier (BBB) function and transendothelial migration of leukocytes are essential c
178 on endothelium and other cells as well as to transendothelial migration of leukocytes in the microcir
179 d flow shear modulate vascular adherence and transendothelial migration of leukocytes into inflamed t
180                                              Transendothelial migration of leukocytes is a critical e
181 g the molecules and mechanisms that regulate transendothelial migration of leukocytes, or diapedesis,
182 alysis suggests that ARHGEF26 influences the transendothelial migration of leukocytes.
183 own that stanniocalcin-1 (STC1) inhibits the transendothelial migration of macrophages and T cells, s
184 was reduced by blocking WASP binding to WIP, transendothelial migration of macrophages, the most cruc
185 osome formation, thereby mediating efficient transendothelial migration of macrophages.
186 duced proliferation and superantigen-induced transendothelial migration of memory T cells, indicating
187 ivation, which led us to investigate whether transendothelial migration of monocytes across HSECs inf
188  These data point to a role of MMP-14 during transendothelial migration of monocytes and T-cell attra
189                                              Transendothelial migration of monocytes is the process b
190                We found that MCP-1-dependent transendothelial migration of monocytes markedly acceler
191 nocyte adhesion to ECs, EC migration and the transendothelial migration of monocytes, while the over-
192 othelial cells increased the recruitment and transendothelial migration of monocytes.
193 thelial and BBB hyperpermeability as well as transendothelial migration of monocytic cells.
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
198                                              Transendothelial migration of neutrophils in postcapilla
199 se brain endothelial cells and supported the transendothelial migration of neutrophils in vitro.
200                   Furthermore, RAP inhibited transendothelial migration of neutrophils induced by fib
201           Conditioned medium harvested after transendothelial migration of neutrophils or supernatant
202 own that TSG-6 inhibits chemokine-stimulated transendothelial migration of neutrophils via a direct i
203 that is needed to facilitate the early-onset transendothelial migration of PMN.
204 d with cobra venom factor and intrapulmonary transendothelial migration of PMNs into the bronchoalveo
205 f TRPM2 expressed in ECs in the mechanism of transendothelial migration of PMNs.
206 lled F. tularensis LVS for 24 h promoted the transendothelial migration of subsequently added neutrop
207         Our results provide visualization of transendothelial migration of T cells into lymphatic sin
208 in reduced microvilli formation and impaired transendothelial migration of T cells.
209  costimulatory conditions, and inhibition of transendothelial migration of T cells.
210 xpress CXCR3 and reduced the IP-10-dependent transendothelial migration of T helper cells under condi
211 neutrophils would also modify the subsequent transendothelial migration of T lymphocytes across cytok
212 thway in brain EC is essential for efficient transendothelial migration of T lymphocytes into the bra
213 c G-protein-mediated signaling in supporting transendothelial migration of T lymphocytes.
214 examine the effects of B. burgdorferi on the transendothelial migration of T lymphocytes.
215 pression of VLA-4 also resulted in increased transendothelial migration of Tck cells, which could be
216 pain as a critical driver of T. b. gambiense transendothelial migration of the human BBB.
217 as well as on endothelial cells promoted the transendothelial migration of the melanoma cells.
218                                              Transendothelial migration of these cells depended on ex
219                           Monocytes promoted transendothelial migration of tumor cells through the in
220        Far less is known about the impact of transendothelial migration on eosinophil survival, in pa
221 /Rap1 GTPase signaling pathway, resulting in transendothelial migration on stimulated human umbilical
222 se VCAM-1 signals are required for leukocyte transendothelial migration on VCAM-1.
223 sion to HUVEC, but significantly reduced PMN transendothelial migration (P < 0.0001) and fMLP-induced
224             Here, we show that the leukocyte transendothelial migration pathway is activated in the o
225  resulting in enhanced monocyte motility and transendothelial migration, prolonged monocyte survival,
226 by expression of Rap1GAP increased leukocyte transendothelial migration, providing physiological rele
227  to the regulation of leukocyte adhesion and transendothelial migration remains poorly understood.
228 r, a complete mechanism governing tumor cell transendothelial migration remains unclear.
229 ell arrest on the EC surface, preventing the transendothelial migration response to IP-10.
230  cancer cell adhesion to the endothelium and transendothelial migration, resulting in reduced liver m
231                          Ex vivo analyses of transendothelial migration revealed that Nef disrupted T
232 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
234                In addition, we addressed the transendothelial migration (TEM) activity of bone marrow
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
237                       Leukocyte crawling and transendothelial migration (TEM) are potentiated by shea
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.
241                                    Leukocyte transendothelial migration (TEM) has been modeled as a m
242 e EM CD4+ T cells, but fail to support their transendothelial migration (TEM) in response to TCR enga
243                                    Leukocyte transendothelial migration (TEM) is a critical event dur
244                                              Transendothelial migration (TEM) is a tightly regulated
245                                    Leukocyte transendothelial migration (TEM) is a tightly regulated,
246                                   Lymphocyte transendothelial migration (TEM) is critically dependent
247                           In vivo, leukocyte transendothelial migration (TEM) occurs at endothelial c
248  essential role in the CXCL12/CXCR4-mediated transendothelial migration (TEM) of CXCR4(+)CXCR7(+) hum
249  ability of several C-C chemokines to induce transendothelial migration (TEM) of eosinophils in vitro
250 hat regulate the endothelial response during transendothelial migration (TEM) of invasive cancer cell
251                                              Transendothelial migration (TEM) of normal lymphocytes i
252                                              Transendothelial migration (TEM) of polymorphonuclear le
253                   This rapid process, called transendothelial migration (TEM) or diapedesis, is compl
254                                    Leukocyte transendothelial migration (TEM) requires two major even
255                                          The transendothelial migration (TEM) step is poorly understo
256  distributed chemokines and their effects on transendothelial migration (TEM) under hydrodynamic shea
257       PECAM-1/CD31 is required for leukocyte transendothelial migration (TEM) under most inflammatory
258 helial cells (ECs) lining the venular lumen (transendothelial migration (TEM)) in a luminal-to-ablumi
259 designated as chemokine-driven or TCR-driven transendothelial migration (TEM), respectively.
260 leukocytes and transmit signals required for transendothelial migration (TEM).
261 sion (TEP) by the T cell but fails to induce transendothelial migration (TEM).
262 tes subsequent signaling that promotes their transendothelial migration (TEM).
263 n, and azithromycin, in an in vitro model of transendothelial migration (TEM).
264 ecycling compartment (LBRC), is critical for transendothelial migration (TEM).
265 s primary human monocytes actively engage in transendothelial migration (TEM).
266  adhesion, crawling towards EC junctions and transendothelial migration (TEM).
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
273 ma cells highlighted that stathmin regulates transendothelial migration through ROCK signaling.
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                  We found that the increased transendothelial migration (TM) of MDA-MB-231 cells resu
277 i showed that inflammation-induced leukocyte transendothelial migration to peritoneum or lungs was si
278 )CD28- T cells enhanced their chemotaxis and transendothelial migration toward the chemokine CCL5.
279 d for the induction of monocyte motility and transendothelial migration, two biological events requir
280 integrins, leading to defective adhesion and transendothelial migration under conditions of physiolog
281 n of CXCR 3 promotes lymphocyte adhesion and transendothelial migration under flow and that human hep
282 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
288                    Furthermore, T lymphocyte transendothelial migration was inhibited by treatment of
289                                              Transendothelial migration was not observed in CD14(dim)
290                The reduction in T lymphocyte transendothelial migration was not observed using a diff
291                      In vitro chemotaxis and transendothelial migration were examined in a Transwell
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

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