ライフサイエンスコーパス: VCAM-1

1 VCAM-1 and ICAM-1 were the endothelial adhesion molecule

2 VCAM-1 and osteopontin demonstrated sustained upregulati

3 VCAM-1 expression by cholangiocytes contributes to persi

4 VCAM-1 expression correlated with tumor stage.

5 VCAM-1 peaked at 2 dynes/cm(2) and decreased to below st

6 VCAM-1 was detected on BDs in CLDs (primary biliary cirr

7 VCAM-1 was expressed and secreted by murine and human pa

8 maging of vascular cell adhesion molecule-1 (VCAM 1) P-selectin, and platelet glycoprotein-1balpha (G

9 n ligands vascular cell adhesion molecule 1 (VCAM-1) and fibronectin, whereas inhibition of MEK/ERK b

10 f soluble vascular cell adhesion molecule 1 (VCAM-1) and osteoprotegerin were significantly associate

11 n between vascular cell adhesion molecule 1 (VCAM-1) and very late antigen-4 (VLA-4) played an integr

12 dependent vascular cell adhesion molecule 1 (VCAM-1) expression on lung endothelial cells.

13 Vascular cell adhesion molecule 1 (VCAM-1) expression, however, was unaffected by the disea

14 tegrin to vascular cell adhesion molecule 1 (VCAM-1) on neurons in the inflammatory context.

15 Vascular cell adhesion molecule 1 (VCAM-1) plays a major role in the chronic inflammatory p

16 inding to vascular cell adhesion molecule 1 (VCAM-1) upregulated on inflamed arterial endothelium.

17 l (HUVEC) vascular cell adhesion molecule 1 (VCAM-1) upregulation.

18 red pulp vascular cell adhesion molecule 1 (VCAM-1)(+) macrophages are essential to extramedullary m

19 captures vascular cell adhesion molecule 1 (VCAM-1)(+) metastatic tumor cells, thereby promoting lym

20 y marker, vascular cell adhesion molecule 1 (VCAM-1), in atherosclerotic plaques.

21 including vascular cell adhesion molecule 1 (VCAM-1), intercellular adhesion molecule 1 (ICAM-1), E-s

22 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), platelet-endothelial cell adhesion molecule 1 (

23 or human vascular cell adhesion molecule 1 (VCAM-1), recently has been proposed as a new imaging age

24 (ICAM-1)/vascular cell adhesion molecule 1 (VCAM-1)-mediated adhesion of both macrophages and neutro

25 d a novel vascular cell adhesion molecule 1 (VCAM-1)-targeted magnetic resonance imaging (MRI) contra

26 AM-1) and vascular cell adhesion molecule 1 (VCAM-1).

27 ectin and vascular cell adhesion molecule 1 (VCAM-1).

28 Vascular cell adhesion molecule 1 (VCAM-1; CD106), a member of the immunoglobulin superfami

29 P = .02); vascular cell adhesion molecule-1 (VCAM-1) (Group I: 0.34 (0.67) ng/mL, Group II: 0.11 (0.1

30 ocytes to vascular cell adhesion molecule-1 (VCAM-1) activates signals in endothelial cells, includin

31 ession of vascular cell adhesion molecule-1 (VCAM-1) and could be mimicked by knockdown of mammalian

32 proteins vascular cell adhesion molecule-1 (VCAM-1) and endothelial nitric oxide synthase, whereas P

33 ession of vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1),

34 on of the vascular cell adhesion molecule-1 (VCAM-1) and monocyte adhesion to coronary artery endothe

35 sensitive vascular cell adhesion molecule-1 (VCAM-1) and monocyte chemotactic protein-1 (MCP-1) in is

36 n markers vascular cell adhesion molecule-1 (VCAM-1) and vascular adhesion protein-1 (VAP-1).

37 hMSCs and vascular cell adhesion molecule-1 (VCAM-1) blockade on HSECs.

38 lation of vascular cell adhesion molecule-1 (VCAM-1) expression in a PKCepsilon- and NF-kappaB-depend

39 ce global vascular cell adhesion molecule-1 (VCAM-1) expression.

40 (TF) and vascular cell adhesion molecule-1 (VCAM-1) in diabetic apoE(-/-)hAR mice aortas and in high

41 ession of vascular cell adhesion molecule-1 (VCAM-1) in primary culture of tumour endothelial cells.

42 Vascular cell adhesion molecule-1 (VCAM-1) is expressed on the mesothelium of ovarian cance

43 Vascular cell adhesion molecule-1 (VCAM-1) plays important roles in development and inflamm

44 First, vascular adhesion molecule-1 (VCAM-1) was evaluated as a vascular target of inflammati

45 ), and soluble vascular adhesion molecule-1 (VCAM-1)) using baseline data from 668 participants (age,

46 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin, resulting in a decreased adhesi

47 AM-1) and vascular cell adhesion molecule-1 (VCAM-1), are expressed.

48 (MCP-1), vascular cell adhesion molecule-1 (VCAM-1), nuclear factor kappaB (NF-kappaB), endothelial

49 le-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1), P-selectin, and L-selectin, function to facilit

50 dothelial vascular cell adhesion molecule-1 (VCAM-1), which is required for eosinophil accumulation.

51 inding to vascular cell adhesion molecule-1 (VCAM-1), which is upregulated in inflamed endothelial ce

52 ession of vascular cell adhesion molecule-1 (VCAM-1), which regulates leukocyte extravasation.

53 lesional vascular cell adhesion molecule-1 (VCAM-1).

54 diated by vascular cell adhesion molecule-1 (VCAM-1).

55 dothelial vascular cell adhesion molecule-1 (VCAM-1).

56 AM-1) and vascular cell adhesion molecule-1 (VCAM-1).

57 CAM-1) and vascular cell adhesion protein 1 (VCAM-1) under flow conditions.

58 iostin and vascular cell adhesion protein 1 (VCAM-1), molecules that mediate leukocyte infiltration a

59 olecules (vascular cell adhesion molecule 1 [VCAM-1] and intracellular adhesion molecule 1 [ICAM-1]).

60 es 1; and vascular cell adhesion molecule 1 [VCAM-1]) were measured by using enzyme-linked immunosorb

61 kines, such as CD31, BDNF, TFF3, Serpin E-1, VCAM-1, Vitamin D BP, and PDGF-AA, were significantly up

62 (4.4-folds); decreased expression of ICAM-1, VCAM-1 (3.2-fold), along with reduced levels of cytokine

63 F-beta, NFkappaB, MCP-1, IL-1, IL-6, ICAM-1, VCAM-1 and CD68 macrophages.

64 ory cytokine production (E-selectin, ICAM-1, VCAM-1 and IL-6).

65 The expression of ICAM-1, VCAM-1 and of MCP-1 was elevated and apoptosis was incre

66 emic and vascular inflammation (CRP, ICAM-1, VCAM-1), and SAA (all P < .001).

67 e proinflammatory adhesion molecules ICAM-1, VCAM-1, and E-selectin, as well as the proinflammatory c

68 ung sections, and mRNA expression of ICAM-1, VCAM-1, E-selectin, RANTES, IL-17, IL-33, thymic stromal

69 g and activation proteins, including ICAM-1, VCAM-1, HLA class I and II, and interferon gamma recepto

70 lial, and/or vascular CAMs (ICAM-1, PECAM-1, VCAM-1).

71 1-targeted nanocarriers outperformed PECAM-1/VCAM-1 in control and disease-like conditions, and tripl

72 AM-1-targeted nanocarriers surpassed PECAM-1/VCAM-1 in control, but showed lower selectivity toward d

73 In endothelial cells, binding of PECAM-1/VCAM-1-targeted nanocarriers was intermediate to single-

74 rmed cells, and targeting NF-kappaB or VLA-4/VCAM-1 signaling could be a clinically relevant mechanis

75 High concentrations of MMP-7, ICAM-1, IL-8, VCAM-1, and S100A12 predicted poor overall survival, poo

76 We exemplified this strategy by generating a VCAM-1-targeted perfluorocarbon nanoparticle for in vivo

77 Recruitment from blood to a VCAM-1 substrate under shear stress was assessed ex vivo

78 inhibition of endothelial activation with a VCAM-1 blocking antibody or a VAP-1 small molecule inhib

79 ta extract, or rIL-33 was used to induce AAI/VCAM-1 expression in wild-type (WT) and RAGE-knockout (R

80 1 and Hemopexin among Caucasians, and ALCAM, VCAM-1, TFPI and PF-4 among Asians.

81 ADAP, and Pyk2, the strength of alpha4beta1-VCAM-1 interaction and cell spreading on VCAM-1 are targ

82 ion of sepsis-induced endothelial ICAM-1 and VCAM-1 expression in this model.

83 hosphorylation and an increase in ICAM-1 and VCAM-1 expression.

84 C4 upregulated the expressions of ICAM-1 and VCAM-1 in an aspirin-sensitive and TP receptor-dependent

85 and macrophage chemoattractant protein-1 and VCAM-1 levels in insulin-resistant LMCs indicated activa

86 signals, showing upregulation of ICAM-1 and VCAM-1 on their surface, as well as release of CCL2, sol

87 ulation of the adhesion molecules ICAM-1 and VCAM-1 resulted in an increased adhesion of peripheral b

88 their putative counter receptors ICAM-1 and VCAM-1 significantly attenuated CCL3-, CXCL1-, or PAF-el

89 ctional expression of endothelial ICAM-1 and VCAM-1 was confirmed by T-cell interaction with EECM-BME

90 xpression of the integrin ligands ICAM-1 and VCAM-1, as well as the T cell chemokines CXCL9, CXCL10,

91 ry molecules such as IL-6, MCP-1, ICAM-1 and VCAM-1.

92 cells, as well as to immobilized ICAM-1 and VCAM-1.

93 NF-kappaB-dependent expression of ICAM-1 and VCAM-1.

94 F-alpha-activated endothelium and ICAM-1 and VCAM-1.

95 ed, namely the adhesion molecules ICAM-1 and VCAM-1; the chemokines CCL5, CCL20, CXCL1, CXCL3, CXCL5,

96 s, stromal cell-derived factor 1 (SDF-1) and VCAM-1, which could be selectively blocked using a speci

97 as CXCL-9, CCL-20, CCL-4, CCL-2, ICAM-1, and VCAM-1 in HUVECs.

98 the greater expression of CCL19, ICAM-1, and VCAM-1 in the mucosal tip compared with the neuroepithel

99 38(++) PCs through secreted CXCL10/IP-10 and VCAM-1 contact.

100 Mechanistically, MMP-9 and VCAM-1 appear to be involved downstream of PDGF-PDGFRbet

101 tion, and inflammatory markers TNF-alpha and VCAM-1 expression.

102 the secretion of VCAM-1; both TNF-alpha and VCAM-1 were significantly associated with lower placenta

103 gnate endothelial receptors (alphaVbeta3 and VCAM-1).

104 In this study, we show that CCRL2 and VCAM-1 are upregulated on cultured human and mouse vascu

105 G myocardium had more inflammatory cells and VCAM-1-positive vessels than did wild-type myocardium af

106 appropriately in response to fibronectin and VCAM-1 binding.

107 ion and decreased CNS T cell infiltrates and VCAM-1+ endothelial cells.

108 roglia, Th1 and Th17 T cell infiltrates, and VCAM-1+ endothelial cells and improved neurocognitive ac

109 nic factors, which enhanced inflammation and VCAM-1 expression.

110 ent MSCs did not induce T cell migration and VCAM-1 expression, resulting in insufficient cell-cell c

111 Osteopontin and VCAM-1 demonstrated sustained upregulation at all time p

112 s indicated that the source of periostin and VCAM-1 was the inflamed sheep liver tissue.

113 tive disease are ALCAM, PF-4, properdin, and VCAM-1 among African-Americans, sE-selectin, VCAM-1, BFL

114 We also show that E-selectin and VCAM-1, but not ICAM-1, are upregulated in response to B

115 ed cell surface expression of P-selectin and VCAM-1.

116 through an increase in TLR4, E-selectin, and VCAM-1 and ultimately through enhanced leukocyte recruit

117 ited the BMP9-induced expression of TLR4 and VCAM-1 and inhibited BMP9-induced human neutrophil recru

118 Increased ERK1/2 activity antagonizes VCAM-1 expression by repressing TNF induction of the tra

119 Anti-VCAM-1 coated rods exhibited a 3.5-fold increase in the

120 crease in binding affinity and restored anti-VCAM-1 binding in tissue sections from ApoE(-)/(-) mice

121 Intravenous (i.v.) anti-VCAM-1 or intraperitoneal (i.p.) beta7 blocking antibody

122 dhesion, nanoparticles were coated with anti-VCAM-1 and tested under static conditions in cell cultur

123 ce expression of adhesion molecules (such as VCAM-1 the ligand for VLA-4), and leukocyte adhesion to

124 pression or knock-down of VCAM-1, as well as VCAM-1-blocking treatment in the spontaneous mouse model

125 ly significant associations between baseline VCAM-1 or tumor necrosis factor alpha receptor 1 levels

126 ral and dermal MVECs, and CXCL8, CCL3, CCL4, VCAM-1, and cyclooxygenase 2 (COX-2) in cerebral MVECs.

127 asting cellular contacts by enhancing T cell VCAM-1 expression in a CCL2-dependent manner.

128 Early up-regulation of cerebrovascular VCAM-1 expression was evident on tumor-associated vessel

129 Chronic VCAM-1 expression reflected the effect of platinum-based

130 AGEs N(epsilon)-(carboxymethyl)lysine (CML), VCAM-1, neutrophilic granulocytes, lymphocytes, and macr

131 surgical indication in the presence of CML, VCAM-1 expression, inflammatory cells, and fibrosis.

132 In a third set (n = 21), we compared VCAM-1 expression with (99m)Tc-cAbVCAM1-5 uptake in vari

133 In contrast, VCAM-1 was essential only for promoting endothelial-leuk

134 re distinct functional sites that coordinate VCAM-1 activation of calcium fluxes and Rac1 during leuk

135 murine cremasteric arterioles and decreased VCAM-1 and ICAM-1 expression.

136 on by blood endothelial cells, and decreased VCAM-1 while increasing CXCL1, CXCL2, CXCL12, CCL5, CCL2

137 ECFCs transfusion dramatically decreased VCAM-1 and NF-kappaB expression, increased eNOS expressi

138 Insulin decreased VCAM-1 expression and leukocyte adhesion in quiescent tu

139 lone, whereas antiatherogenic TGRL decreased VCAM-1 expression by approximately 20% while still upreg

140 We detected VCAM-1 on cholangiocytes in chronic liver disease (CLD)

141 ct of antiatherogenic TGRL by downregulating VCAM-1 expression.

142 When we silenced either VCAM-1 or M-CSFR in mice with myocardial infarction or i

143 platinum-resistant tumors retained elevated VCAM-1 expression and tumor burden after treatment.

144 Endothelial VCAM-1 surface expression stimulated by TNFalpha provide

145 s beta1-integrin (VLA-4) to bind endothelial VCAM-1.

146 cts produced TGRL that increased endothelial VCAM-1 expression by >=35%, and exhibited impaired fasti

147 ed with an impaired induction of endothelial VCAM-1 and led to a significantly reduced number of matu

148 y required for VEGF-A-stimulated endothelial VCAM-1 gene expression.

149 Enhanced VCAM-1 expression in the lungs by HDM, AA, or rIL-33 exp

150 These results establish VCAM-1 and VAP-1 as mediators of myeloid cell recruitmen

151 titis C), and human cholangiocytes expressed VCAM-1 in response to tumor necrosis factor alpha alone

152 women with advanced stage disease expressed VCAM-1, the incidence of expression was reduced among wo

153 monocytes to inflamed endothelium expressing VCAM-1 contributes to the development of plaque during a

154 a 2-fold increase in P-selectin expression, VCAM-1 expression, and platelet adhesion between 30 and

155 ng antibodies against von Willebrand factor, VCAM-1, and alpha-smooth muscle actin, were measured for

156 37, but not S728 or Y729, were necessary for VCAM-1 activation of Rac1.

157 Finally, FAK/Pyk2 activity is required for VCAM-1 expression and macrophage recruitment to the vess

158 uce cytokines and/or chemokines required for VCAM-1 upregulation on the lung endothelium, which in tu

159 IP-10, GM-CSF, M-CSF, TNF-alpha, IFN-gamma, VCAM-1, ICAM-1, PD-L1 and ICOS-L.

160 reduced expression of NF-kappaB target genes VCAM-1, intercellular adhesion molecule-1, E-selectin, a

161 tigen-positive vasculature displayed greater VCAM-1 intensity in patients with short duration of untr

162 bition concentration [IC50 ] 4 nM) and HUVEC VCAM-1 up-regulation (IC50 12 nM) in a dose-dependent ma

163 vant VCAM-1-specific imaging probes identify VCAM-1 expression as an indicator of ovarian cancer peri

164 ian cancer peritoneal metastasis to identify VCAM-1 as a viable imaging target.

165 boplatin resulted in a transient decrease in VCAM-1 expression 4 h after treatment that returned to b

166 il As was associated with a 1.7% increase in VCAM-1 (95% CI: 0.2, 3.2).

167 evented this response as well as increase in VCAM-1, ICAM-1, IL-6, and IL-8 levels.

168 receptors and partly prevented increases in VCAM-1 and leukocyte adhesion after treatment with tumou

169 adhesion molecule (CAM) expression including VCAM-1, ICAM-1, and E-selectin in human aortic endotheli

170 chemokines and adhesion molecules, including VCAM-1, IL-6, ICAM-1, E-selectin, and monocyte chemoattr

171 caused decreased NOS activity and increased VCAM-1 expression in RAECs.

172 Toll-like receptor (TLR) 4 pathway increased VCAM-1 and ICAM-1 dependent binding of leukocytes.

173 ammatory Paigen diet significantly increased VCAM-1 expression with respect to the control group in v

174 nt BMSCs greatly compromised their increased VCAM-1 protein expression and IL-6 and RANKL secretion i

175 y, this change was correlated with increased VCAM-1 and phospho-IkBalpha immunoreactivity along the e

176 down-regulation is associated with increased VCAM-1 in both muscle and blood, suggesting that VCAM-1

177 se lung endothelial cells with IL-33 induced VCAM-1 expression in WT, but not RAGE-KO cells.

178 XR agonists also prevented TNF-alpha-induced VCAM-1 and ICAM-1 expression, as well as endothelial gro

179 -GTP selectively decreased TNF-alpha-induced VCAM-1 but not ICAM-1 protein levels.

180 iption factor required for TNF-alpha-induced VCAM-1 production.

181 nstrates that allergen- and cytokine-induced VCAM-1 expression is RAGE-dependent and contributes to l

182 n, these molecules suppressed ox-LDL-induced VCAM-1 expression and monocyte adhesion onto human endot

183 BI3 subunit with IL-35, promoted LPS-induced VCAM-1 in human aortic ECs and that EBI3-deficient mice

184 ability of rapamycin to inhibit TNF-induced VCAM-1 expression.

185 educed endothelial expression of TNF-induced VCAM-1, which was restored via pharmacological inhibitio

186 n inhibitor of epoxide hydrolysis, inhibited VCAM-1 and ICAM-1 expression and protein levels; convers

187 We investigated VCAM-1 expression as a marker of peritoneal metastasis a

188 mary progenitor cells to alpha4beta1 ligands VCAM-1 and CS1 under both static and flow conditions.

189 y roles for kinase-inhibited FAK in limiting VCAM-1 production via nuclear localization and promotion

190 or IFN regulatory factor 1, promoted maximum VCAM-1 expression.

191 activation by suppressing MAPK-AP1-mediated VCAM-1 expression and attenuates LPS-induced secretion o

192 The effects of carboplatin on mesothelial VCAM-1 expression were determined in cultured cells by W

193 ssion of the endothelial activation molecule VCAM-1 but increased expression of the endothelial tight

194 n of endothelial cell (EC) adhesion molecule VCAM-1 through IL-35 receptors gp130 and IL-12Rbeta2 via

195 these macrophages use the adhesion molecule VCAM-1 to retain HSCs in the spleen.

196 ariation in vascular cell adhesion molecule (VCAM-1) expression correlates with the wall shear stress

197 E-selectin, vascular cell adhesion molecule (VCAM-1), and intercellular adhesion molecule 1 (ICAM-1)

198 ma vascular and cellular adhesion molecules (VCAM-1 and ICAM-1, respectively), matrix metalloproteina

199 ptoglobin and CRP), cell adhesion molecules (VCAM-1), endothelial growth factors (VEGF) and VDBP.

200 zer p47phox, thereby increasing ROS-NFkappaB-VCAM-1/ICAM-1 expression and monocyte adhesion in ECs in

201 a consequence of artery ligation, whereas no VCAM-1 expression was detected in the contralateral caro

202 Administration of VCAM-1 and beta7-integrin blocking antibodies reduced IL

203 c cells induced the high-affinity binding of VCAM-1/CD106 Fc chimeric protein and promoted VCAM-1-dep

204 Depletion of VCAM-1 interrupted the binding of macrophages to GBM cel

205 n reported whether the cytoplasmic domain of VCAM-1 is necessary for these signals.

206 tumors with overexpression or knock-down of VCAM-1, as well as VCAM-1-blocking treatment in the spon

207 ly attenuated TNFalpha-induced expression of VCAM-1 and ICAM-1, and thus reduced monocyte adherence t

208 Differential expression of VCAM-1 and intercellular adhesion molecule 1 (ICAM-1) wa

209 and hypothesized that biliary expression of VCAM-1 contributes to the persistence of liver inflammat

210 Expression of VCAM-1 in the ligated and contralateral carotid arteries

211 examined whether cholangiocyte expression of VCAM-1 promotes the survival of intrahepatic alpha4beta1

212 Importantly, expression of VCAM-1 was shown in human brain tissue containing both e

213 Proatherogenic TGRL increased expression of VCAM-1, intercellular adhesion molecule 1 (ICAM-1), and

214 itive area and intensity/high power field of VCAM-1 expression than did juvenile DM patients with lon

215 In vivo imaging of VCAM-1 also demonstrated an acute decrease in expression

216 vatives might allow the molecular imaging of VCAM-1 expression in an experimental model of atheroscle

217 io was suboptimal for the in vivo imaging of VCAM-1 expression in atherosclerotic lesions.

218 otracer for the in vivo molecular imaging of VCAM-1 expression in atherosclerotic plaques.

219 Induction of VCAM-1 is dependent on tumor cell-clot formation, decrea

220 ed medium further increased the induction of VCAM-1.

221 Simultaneous inhibition of VCAM-1 and VAP-1 does not result in further reduction in

222 patobiliary inflammation where inhibition of VCAM-1 decreased liver inflammation by reducing lymphocy

223 Moreover, the pharmacological inhibition of VCAM-1 in Phc2-deficient mice reverses the symptoms.

224 lerotic lesions correlated with the level of VCAM-1 expression (P < 0.05).

225 First, the relationship between the level of VCAM-1 expression and (99m)Tc-cAbVCAM1-5 uptake was eval

226 EDE levels of VCAM-1, von Willebrand factor, platelet-derived growth f

227 these metabolites was strongly predictive of VCAM-1 expression.

228 ensitive, and reproducible quantification of VCAM-1 expression in mouse atherosclerotic lesions.

229 sions of HO-1 and VEGF, and the reduction of VCAM-1.

230 d both ALK1 and ALK2 in the up-regulation of VCAM-1 and ICAM-1.

231 Endothelial up-regulation of VCAM-1 at susceptible sites in arteries modulates the re

232 mental role for EGF-induced up-regulation of VCAM-1 expression in EGFR activation-promoted macrophage

233 y ER stress genes abrogated SS regulation of VCAM-1 transcription and monocyte recruitment.

234 atherogenic or antiatherogenic regulation of VCAM-1.

235 The miRNA miR-126, a negative regulator of VCAM-1 expression, was significantly decreased (3.39-fol

236 nistration was used to determine the role of VCAM-1 in IL-33-induced AAI.

237 We examined the role of VCAM-1/alpha4beta1 integrin interaction in T cell recrui

238 alpha, which then triggered the secretion of VCAM-1; both TNF-alpha and VCAM-1 were significantly ass

239 lyzed VEGF-A isoform-specific stimulation of VCAM-1 gene expression, which controls endothelial-leuko

240 observations support testing the utility of VCAM-1 imaging probes to monitor treatment response in o

241 ooperation in shear-resistant cell arrest on VCAM-1 are ill defined.

242 itated the rolling and spreading of cells on VCAM-1 and the migration of cells toward SDF-1alpha.

243 of lymphatic endothelial cells; dependent on VCAM-1 and non-canonical NFkappaB signalling via LTbetaR

244 ta1-VCAM-1 interaction and cell spreading on VCAM-1 are targets of regulation by these three proteins

245 by 1-NM-PP1 enhanced eosinophil spreading on VCAM-1 but inhibited eotaxin-1 (CCL11)-mediated eosinoph

246 ignificant inhibition of T cell spreading on VCAM-1.

247 (PF-228 or Dasatinib), which inhibited only VCAM-1 expression.

248 ein expression of PECAM-1, but not ICAM-1 or VCAM-1.

249 ological blockade of integrin alpha4beta1 or VCAM-1 inhibits it.

250 diated firm adhesion involving ICAM-1 and/or VCAM-1 and demonstrated ICAM-1-dependent shape-change an

251 in 2 genetic models lacking either Spi-C or VCAM-1 with impaired native macrophage proliferative exp

252 alized with antibodies to MAdCAM-1 (MB-M) or VCAM-1 (MB-V), biomarkers of gut endothelial cell inflam

253 ation with concomitant loss in E-selectin or VCAM-1 induction.

254 n, gauged by higher levels of IkBalpha, p65, VCAM-1, ICAM-1, CXCL10, CCL2, TNF, and IL-6 (mostly loca

255 In AF patients, VCAM-1 expression in blood vessels and the numbers of in

256 p38 specifically abrogated the rise to peak VCAM-1 at low SS (2 dyn/cm(2)), whereas inhibition of ER

257 ocked by Abs against human LFA-1 and porcine VCAM-1.

258 c cells, necrotic cores, and proinflammatory VCAM-1 (vascular cell adhesion molecule) and MCP-1 (mono

259 CAM-1/CD106 Fc chimeric protein and promoted VCAM-1-dependent arrest to immobilized ligands under she

260 Radiolabeled VCAM-1-specific peptide imaging probes and SPECT were us

261 the integrin alpha4 and its counter-receptor VCAM-1, respectively; expression of the latter was upreg

262 ith platinum-sensitive tumors showed reduced VCAM-1 expression, which correlated with reduced tumor b

263 aked at 2 dynes/cm(2), where IRF-1-regulated VCAM-1 expression and monocyte recruitment also rose to

264 othelial CREB and significantly up-regulated VCAM-1, ICAM-1, and CXCL8.

265 esting a role for chemotherapy in regulating VCAM-1 expression.

266 Clinically relevant VCAM-1-specific imaging probes identify VCAM-1 expressio

267 Robust VCAM-1 immunostaining was observed in the left carotid a

268 VCAM-1 among African-Americans, sE-selectin, VCAM-1, BFL-1 and Hemopexin among Caucasians, and ALCAM,

269 lpha (P=0.0085); Fas-R (P=0.0354), and serum VCAM-1 (P=0.0007) were highly significant.

270 macrophages in CD169 iDTR mice or silencing VCAM-1 in macrophages released HSCs from the spleen.

271 lasminogen activator inhibitor-1 and soluble VCAM-1 associated with arsenic exposure were stronger am

272 se of CCL2, soluble fractalkine, and soluble VCAM-1.

273 as alpha4beta1 integrin affinity for soluble VCAM-1 was not.

274 The HR for a 1-SD higher soluble VCAM-1 level was 1.34 (95% CI, 1.11-1.62; Bonferroni-cor

275 riable odds ratios for a 1-SD higher soluble VCAM-1 level, 1.91; 95% CI, 1.24-2.96, P = .003; and 2.5

276 Levels of soluble VCAM-1, but not other inflammation markers, are signific

277 rsenic (ln mug/g creatinine), plasma soluble VCAM-1 was 1.02 (95% confidence interval: 1.01, 1.03) an

278 uture studies should address whether soluble VCAM-1 is capable of improving AF risk classification be

279 -stimulation by CXCL12 together with soluble VCAM-1 potentiated integrin immobilization with a 5-fold

280 lenic macrophage maturation, reduced splenic VCAM-1 expression and compromised splenic HSC retention.

281 ATF-2 knockdown blocked VEGF-A-stimulated VCAM-1 expression and endothelial-leukocyte interactions

282 riptional regulation of TNF-alpha-stimulated VCAM-1 expression.

283 ric of EC orientation, markers of ER stress, VCAM-1 and ICAM-1 expression, and monocyte recruitment.

284 t increase in the expression of cell surface VCAM-1 (Akt-dependent) and ICAM-1 in Akt-dependent and e

285 on and tumor cell invasion and indicate that VCAM-1 is a potential molecular target for improving can

286 These results indicate that VCAM-1/alpha4beta1 integrin interaction is crucial for p

287 -1 in both muscle and blood, suggesting that VCAM-1 plays a critical role early in juvenile DM diseas

288 he VCAM-1 cytoplasmic domain, we deleted the VCAM-1 cytoplasmic domain or mutated the cytoplasmic dom

289 computational model of the structure of the VCAM-1 cytoplasmic domain as an alpha-helix with S728 an

290 restingly, the 19-amino acid sequence of the VCAM-1 cytoplasmic domain is 100% conserved among many m

291 To examine the function of the VCAM-1 cytoplasmic domain, we deleted the VCAM-1 cytopla

292 hyaluronan but had no effect on adhesion to VCAM-1 (alpha4beta1 integrin ligand), confirming its spe

293 to enhancement of VLA-4-mediated adhesion to VCAM-1.

294 by alpha4beta1 integrin-mediated adhesion to VCAM-1.

295 is, (99m)Tc-cAbVCAM1-5 specifically bound to VCAM-1-positive lesions, thereby allowing their identifi

296 , Swap-70(-/-) eosinophils adhered poorly to VCAM-1 and ICAM-1 and exhibited inefficient leading edge

297 n on foamy monocytes competent to recruit to VCAM-1 on inflamed arterial endothelium.

298 derived peptide B2702p bound specifically to VCAM-1 and allowed the ex vivo imaging of atheroscleroti

299 vation of endothelial cells (EC) upregulates VCAM-1 receptors that target monocyte recruitment to ath

300 from cytokinestimulated HBEC to T cells was VCAM-1 and ICAM-1 dependent.