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1 of caveolin-1, and endocytosis of albumin in human umbilical vein endothelial cell.
2 0 blocked S100b-induced monocyte adhesion to human umbilical vein endothelial cell.
3 encing, and chromatin immunoprecipitation in human umbilical vein endothelial cells.
4 sion of a subset of TNFalpha target genes in human umbilical vein endothelial cells.
5 expression, and led to apoptosis in HK-2 and human umbilical vein endothelial cells.
6 s can block VEGF-stimulated proliferation of human umbilical vein endothelial cells.
7 NS1 colocalized with eNOS in living human umbilical vein endothelial cells.
8 e of the underlying cytoskeleton in cultured human umbilical vein endothelial cells.
9 id not induce release of sFlt1 from cultured human umbilical vein endothelial cells.
10 targeting of miR-92a precursor/KLF2 mRNA in human umbilical vein endothelial cells.
11 -like tube formation and caused apoptosis of human umbilical vein endothelial cells.
12 ficantly increased the level of ER stress in human umbilical vein endothelial cells.
13 ctor-induced chemotaxis and morphogenesis of human umbilical vein endothelial cells.
14 cular myocytes, and proangiogenic effects on human umbilical vein endothelial cells.
15 and ROCK2 to adhesion molecule expression in human umbilical vein endothelial cells.
16 med at the protein level and functionally in human umbilical vein endothelial cells.
17 sGC in context of a primary cell culture of human umbilical vein endothelial cells.
18 nd Weibel-Palade body exocytosis in cultured human umbilical vein endothelial cells.
19 high-glucose-induced reduction of GTPCH I in human umbilical vein endothelial cells.
20 tes activated VEGFR2 immunoprecipitates from human umbilical vein endothelial cells.
21 36 (ie, to a CD36 low phenotype) in cultured human umbilical vein endothelial cells.
22 anges and to colocalize with microtubules in human umbilical vein endothelial cells.
23 nd enhances association of HDAC7 with PML in human umbilical vein endothelial cells.
24 cells, Madin-Darby canine kidney cells, and human umbilical vein endothelial cells.
25 dothelial growth factor-induced migration of human umbilical vein endothelial cells.
26 lial electrical resistance of the nonbarrier human umbilical vein endothelial cells.
27 effect of exosomes on cytokine release from human umbilical vein endothelial cells.
28 ted during primary KSHV infection of primary human umbilical vein endothelial cells.
29 ans of luciferase reporter gene assays using human umbilical vein endothelial cells.
30 nhibits the VEGF165-induced proliferation of human umbilical vein endothelial cells.
31 e obtained ChIP-seq data from widely studied human umbilical vein endothelial cells.
32 1 and Cav1 colocalized and coprecipitated in human umbilical vein endothelial cells.
33 Falpha-induced oxidative/nitrative stress in human umbilical vein endothelial cells.
34 against methylglyoxal-induced cell deaths in human umbilical vein endothelial cells.
35 sion, and colony formation when expressed in human umbilical vein endothelial cells.
36 t by hemangioma-derived endothelial cells or human umbilical-vein endothelial cells.
37 one marrow and skin) and macrovascular (from human umbilical vein) endothelial cells.
38 p53 activation and G(1) cell cycle arrest in human umbilical vein endothelial cells after 4 days.
39 Moreover, VEGF-A/VEGFR2-induced migration of human umbilical vein endothelial cells also depends on E
40 tor-mediated endothelial cell proliferation (human umbilical vein endothelial cell and choroidal vasc
42 cytoskeletal stress fiber formation in both human umbilical vein endothelial cell and human lung mic
43 coagulation times were measured on cultured human umbilical vein endothelial cells and a syncytializ
44 e may act as a ligand for these receptors in human umbilical vein endothelial cells and activate intr
45 triculture model that embeds hiPSC-HPCs with human umbilical vein endothelial cells and adipose-deriv
47 adherent MCF-7 and A549 cell lines, primary human umbilical vein endothelial cells and both differen
48 y, we identified its interacting proteins in human umbilical vein endothelial cells and HeLa cells us
49 n addition, 2E8 inhibits JY cell adhesion to human umbilical vein endothelial cells and homotypic agg
50 e South American ZIKV strains readily infect human umbilical vein endothelial cells and human ECs der
51 ry and transformed cells, including T cells, human umbilical vein endothelial cells and human embryon
52 her bolstered by the expression of UBIAD1 in human umbilical vein endothelial cells and human heart t
53 vascular activity in both cell-based models (human umbilical vein endothelial cells and human umbilic
55 blocked directed but not random migration of human umbilical vein endothelial cells and led to an inc
56 ppaB (p50 and p65) were examined in cultured human umbilical vein endothelial cells and mouse aortas
58 nd to tumor necrosis factor-alpha-stimulated human umbilical vein endothelial cells and murine caroti
59 ctivated protein kinase (MAPK) activation in human umbilical vein endothelial cells and rodent fibrob
60 normalities were measured on the surfaces of human umbilical vein endothelial cells and syncytialized
61 s a receptor for factor Xa on the surface of human umbilical vein endothelial cells and that annexin
62 thrombin-induced barrier permeabilization in human umbilical vein endothelial cells and their immorta
63 capillary endothelial cell line hCMEC/D3 and human umbilical vein endothelial cells), and without int
64 human microvascular brain endothelial cells, human umbilical vein endothelial cells, and a mouse endo
65 and examined their activity on plasmid DNA, human umbilical vein endothelial cells, and human embryo
66 al changes induced by preeclamptic plasma on human umbilical vein endothelial cells, and identified,
67 ubation results in phosphorylation of Akt in human umbilical vein endothelial cells, and inhibition o
68 types, including PC-12 neuronal-like cells, human umbilical vein endothelial cells, and murine adult
69 ssion of cytokine production in THP-1 cells, human umbilical vein endothelial cells, and RASFs was st
71 of antibodies in combination with lysates of human umbilical vein endothelial cells as a source of ta
72 ted by siRNA knockdown of Hipk1 and Hipk2 in human umbilical vein endothelial cells, as well as in en
73 WF) secreted from and anchored to stimulated human umbilical vein endothelial cells, as well as to im
74 inally, these effects were not restricted to human umbilical vein endothelial cells, because similar
75 nergetic capacity were also observed in that human umbilical vein endothelial cells belonging to hapl
76 (mtDNA) damage were assessed in single-donor human umbilical vein endothelial cells belonging to mtDN
77 w blood vessel formation was determined with human umbilical vein endothelial cells by culturing with
78 DLL4-NOTCH-dependent regulation of FABP4 in human umbilical vein endothelial cells by gene/protein e
79 inhibits the tubular structure formation of human umbilical vein endothelial cells by regulating the
81 vivo, and decreased the viability of HUVEC (Human Umbilical Vein Endothelial Cells) cells in vitro a
83 ith sunitinib enhanced angiogenesis in 786-0/human umbilical vein endothelial cell co-culture models.
84 ed that up to 40% of endogenous G alpha12 in human umbilical vein endothelial cells colocalize with m
86 all interfering RNA knockdown experiments in human umbilical vein endothelial cell cultures indicate
88 istically, SphK1 down-regulation by siRNA in human umbilical vein endothelial cells decreased cytokin
90 chicken chorioallantoic membrane assay and a human umbilical vein endothelial cell differentiation as
92 active and VEGF dose-dependent in triggering human umbilical vein endothelial cells (ECs) migration i
93 in glioma cells prevented tube formation of human umbilical vein endothelial cells elicited by the s
94 g RNA rescued survival and tube formation of human umbilical vein endothelial cell exposed to C2238-a
97 owth as assessed by time-lapse microscopy of human umbilical vein endothelial cell expressing fluorop
98 othelial cells from AMPKalpha2(-/-) mice and human umbilical vein endothelial cells expressing domina
100 hed STAT3 target microRNA17-92 expression in human umbilical vein endothelial cells from patients wit
101 hosphate (SK/S1P) pathway and showed that in human umbilical vein endothelial cells, histamine rapidl
102 ion and formation of capillary structures by human umbilical vein endothelial cells (HUV-EC-Cs) in in
103 U50,488H and TRK820, significantly inhibited human umbilical vein endothelial cell (HUVEC) migration
104 re we show that Kp-10 significantly inhibits human umbilical vein endothelial cell (HUVEC) migration,
105 a biochemical assay of ACE inhibition and a human umbilical vein endothelial cell (HUVEC) model.
106 mediator of thrombin-stimulated increases in human umbilical vein endothelial cell (HUVEC) monolayer
107 f varying physiologic stiffness, plated with human umbilical vein endothelial cell (HUVEC) monolayers
108 or (TNF)-alpha-mediated hyperpermeability in human umbilical vein endothelial cell (HUVEC) monolayers
109 rinsic KDR activity (IC 50 < 0.1 microM) and human umbilical vein endothelial cell (HUVEC) proliferat
110 d low nanomolar inhibition of VEGF-dependent human umbilical vein endothelial cell (HUVEC) proliferat
112 osarcoma cell line KYM-1D4 cytotoxicity, and human umbilical vein endothelial cell (HUVEC) vascular c
115 neumoniae D39 with FH increased adherence to human umbilical vein endothelial cells (HUVEC) 5-fold an
117 inal capillary endothelial cells (HRCEC) and human umbilical vein endothelial cells (HUVEC) by stimul
118 , microvascular endothelial cells (MEC), and human umbilical vein endothelial cells (HUVEC) cultured
120 we measured alterations in Ca(2+) levels in human umbilical vein endothelial cells (HUVEC) following
123 C treatment caused a decrease in survival of human umbilical vein endothelial cells (HUVEC) in a conc
124 ositively affects vascular tube formation of human umbilical vein endothelial cells (HUVEC) in vitro.
125 red to be 4.1 x 10(-5) M, while that against human umbilical vein endothelial cells (HUVEC) was more
129 l lines (HepG2 and LX2 cells, respectively), human umbilical vein endothelial cells (HUVEC), as well
136 active oxidative species (ROS) production in human umbilical vein endothelial cell (HUVECs), challeng
137 exosomes promoted tube formation activity in human umbilical vein endothelial cell (HUVECs), which wa
138 ificantly inhibited the tubular formation of human umbilical vein endothelial cells (HUVECs) (p<0.01)
139 glyoxal and AGE accumulation were studied in human umbilical vein endothelial cells (HUVECs) and C57
140 ionality being capable of co-localizing with human umbilical vein endothelial cells (HUVECs) and enha
141 how that both Robo1 and Robo4 are present in human umbilical vein endothelial cells (HUVECs) and have
142 ity of rapamycin to inhibit the migration of human umbilical vein endothelial cells (HUVECs) and huma
143 the OGF-OGFr axis on cell cycle activity in human umbilical vein endothelial cells (HUVECs) and huma
145 nt, death, migration, and differentiation of human umbilical vein endothelial cells (HUVECs) and neov
146 tially associated signaling mechanisms using human umbilical vein endothelial cells (HUVECs) as a mod
147 ransporter and stimulate angiogenesis, using human umbilical vein endothelial cells (HUVECs) as model
148 s (iPSCs), mesenchymal stem cells (MSCs) and human umbilical vein endothelial cells (HUVECs) as previ
149 n of these complement components in cultured human umbilical vein endothelial cells (HUVECs) by real-
150 scent human primary preadipocytes as well as human umbilical vein endothelial cells (HUVECs) develope
152 th human dental pulp stem cells (hDPSCs) and human umbilical vein endothelial cells (HUVECs) encapsul
153 ing an in vitro angiogenesis model, in which human umbilical vein endothelial cells (HUVECs) formed c
157 clarify these relationships using polarized human umbilical vein endothelial cells (HUVECs) grown on
158 ow that ADP stimulates migration of cultured human umbilical vein endothelial cells (HUVECs) in both
159 l pulp stem cells (DPSCs) prevascularized by human umbilical vein endothelial cells (HUVECs) in pulp
160 Previously, we found that KSHV infection of human umbilical vein endothelial cells (HUVECs) induces
161 e show that histamine-evoked Ca(2+) entry in human umbilical vein endothelial cells (HUVECs) is sensi
164 energetic function and oxidant generation in human umbilical vein endothelial cells (HUVECs) obtained
167 2 siRNA- and Hey2 vector plasmid-transfected human umbilical vein endothelial cells (HUVECs) resembli
173 y human aortic endothelial cells (HAECs) and human umbilical vein endothelial cells (HUVECs) using ge
176 ethod to enhance the angiogenic potential of human umbilical vein endothelial cells (HUVECs) was inve
179 n vitro angiogenesis model systems employing human umbilical vein endothelial cells (HUVECs) were use
182 e von Willebrand factor (VWF) secretion from human umbilical vein endothelial cells (HUVECs), and Stx
183 inase, is the primary ZIKV entry cofactor on human umbilical vein endothelial cells (HUVECs), and tha
185 egulates PML protein accumulation in primary human umbilical vein endothelial cells (HUVECs), HEK 293
186 hough similar results were obtained by using human umbilical vein endothelial cells (HUVECs), only a
188 calization of tTG(V1,2) compared with tTG in human umbilical vein endothelial cells (HUVECs), VSMC, a
205 A2 gain- and loss-of-function experiments in human umbilical vein endothelial cells identified a key
207 ccinate caused increased (18)F-FDG uptake by human umbilical vein endothelial cells in a concentratio
208 II (FVIIa) directly affect HSV1 infection of human umbilical vein endothelial cells in a manner that
209 rmal and LBS mutant forms of apo(a) bound to human umbilical vein endothelial cells in a similar mann
210 Functional PDI is rapidly secreted from human umbilical vein endothelial cells in culture upon a
216 Firstly, selective activation of EPAC in human umbilical vein endothelial cells increased C/EBP D
218 generations, and reduced ROS productions in human umbilical vein endothelial cells incubated with H2
220 Here, we show that KSHV infection of primary human umbilical vein endothelial cells induced the expre
221 invasive breast cancer cells (MDA-MB-231) to human umbilical vein endothelial cells induced tyrosine
222 as adenoviral-mediated CSE overexpression in human umbilical vein endothelial cells inhibited their r
223 (S1P) cooperatively initiate the invasion of human umbilical vein endothelial cells into collagen mat
224 Here, we show that expression of HuR in human umbilical vein endothelial cells is regulated by s
225 nts demonstrate that the virus replicates in human umbilical vein endothelial cells less efficiently
227 exes effectively inhibit angiogenesis in the human umbilical vein endothelial cell line EA.hy926 at 0
228 exes effectively inhibit angiogenesis in the human umbilical vein endothelial cell line EA.hy926.
231 In models of angiogenesis, CX-4945 inhibited human umbilical vein endothelial cell migration, tube fo
232 RI977143 promoted carcinoma cell invasion of human umbilical vein endothelial cell monolayers and fib
235 lial growth factor-induced cell migration of human umbilical vein endothelial cells more strongly tha
236 4 strain of F. tularensis was incubated with human umbilical vein endothelial cells, neither species
237 duced whereas knockdown of miR-155 inhibited human umbilical vein endothelial cell network formation,
238 d the effect of transient FABP4 knockdown in human umbilical vein endothelial cells on fatty acid met
242 arly, binding of properdin to the surface of human umbilical vein endothelial cells or Neisseria meni
244 of TLR2-dependent inflammatory signaling in human umbilical vein endothelial cells, primary human lu
245 R-2-treated pancreatic cancer cells enhanced human umbilical vein endothelial cell proliferation and
246 AR, beta(1) integrin, and the EGFR to induce human umbilical vein endothelial cell proliferation, gro
247 nal-deletion mutant (TEF3-DeltaNLS), induces human umbilical vein endothelial cell proliferation, mig
248 ompounds show modest to high potency against human umbilical vein endothelial cell proliferation.
249 of VEGF-A-stimulated ERK phosphorylation in human umbilical vein endothelial cells, providing eviden
251 ithelial cells, human dental pulp cells, and human umbilical vein endothelial cells (recell-dTBs); 3)
252 Overexpression of Y297A and D320A NRP1 in human umbilical vein endothelial cells reduced high-affi
255 Here we show that Sema3d and Sema3e affect human umbilical vein endothelial cells similarly but thr
257 and HMGB1-mediated inflammatory signaling in human umbilical vein endothelial cells specifically thro
259 % TF activity and protein level induction in human umbilical vein endothelial cells stimulated by the
260 rease in mitochondrial membrane potential in human umbilical vein endothelial cells stored in trophic
261 mouse model of ischemic AKI and in cultured human umbilical vein endothelial cells subjected to hypo
262 nockdown increased the level of KLF2 mRNA in human umbilical vein endothelial cells, suggesting that
265 in athymic rats and injected 5 million ECs (human umbilical vein endothelial cells) suspended in Mat
266 nd 8x more efficient (P=0.016) to stimulated human umbilical vein endothelial cells than to unstimula
267 ion, we xeno-grafted telomerase-immortalized human umbilical vein endothelial cells that are infected
269 ed tube formation were evaluated in vitro in human umbilical vein endothelial cells that were exposed
273 l surface as well as increasing adherence of human umbilical vein endothelial cells to the active pep
274 lts monitoring the cleavage rate of PAR-1 on human umbilical vein endothelial cells, transfected with
277 ow cytotoxicity in vitro when tested against human umbilical vein endothelial cells up to a concentra
278 alization of endogenous H2S produced in live human umbilical vein endothelial cells upon stimulation
279 rtantly, SNX-2112 inhibits tube formation by human umbilical vein endothelial cells via abrogation of
280 mation in Matrigel and increases invasion of human umbilical vein endothelial cells via the PI3K/Akt
281 MEF2C in human retinal endothelial cells and human umbilical vein endothelial cells was assayed by re
282 n the regulation of a subset of genes in the human umbilical vein endothelial cells was confirmed by
283 d Gas6 in human aortic endothelial cells and human umbilical vein endothelial cells was monitored by
287 hance the recruitment of perivascular cells, human umbilical vein endothelial cells were genetically
288 established in vitro when beads coated with human umbilical vein endothelial cells were placed at on
290 e-mediated eNOS phosphorylation at Ser-1177, human umbilical vein endothelial cells were treated with
291 , primary mouse aortic endothelial cells and human umbilical vein endothelial cells were used as a mo
292 lls impaired migration of endothelial cells (human umbilical vein endothelial cells), whereas an N-te
293 allogeneic human leukocyte antigen (HLA)-DR+ human umbilical vein endothelial cells (which lack B7 mo
294 ignificantly increased the tube formation of human umbilical vein endothelial cells, which was inhibi
295 pesvirus (KSHV) lytic replication in primary human umbilical vein endothelial cells while KSHV infect
296 ey cDNA and overexpressed in COS-7 cells and human umbilical vein endothelial cells with a C-terminal
298 tor in COS-7 cells or prolonged treatment of human umbilical vein endothelial cells with thrombin con
300 in transendothelial migration on stimulated human umbilical vein endothelial cells without chemokine
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