ライフサイエンスコーパス: E-selectin

1 +/- 3.7 for P-selectin and 4.8% +/- 2.3 for E-selectin).

2 ace adhesion molecule expression (ICAM-1 and E-selectin).

3 kers von Willebrand factor (vWf) and soluble E selectin.

4 ing that CD43 alone is a dominant ligand for E-selectin.

5 hensive characterization of their binding to E-selectin.

6 city on human endothelial cells that express E-selectin.

7 ntegrin binding to RGD or sialyl Lewis(x) to E-selectin.

8 ndent on overlapping contributions of P- and E-selectin.

9 We observed no associations with ICAM-1 or E-selectin.

10 mia cells through the cell adhesion molecule E-selectin.

11 partial reduction in rolling interaction on E-selectin.

12 tory cytokines, followed by the induction of E-selectin.

13 More Th17 than Th1 cells interacted with E-selectin.

14 nhibitor of metalloproteinases (TIMP)-1, and E-selectin.

15 ase in the expression of both P-selectin and E-selectin.

16 the bloodstream, through down regulation of E-selectin.

17 droxyurea was abrogated in mice deficient in E-selectin.

18 s is responsible for rolling of the cells on E-selectin.

19 d proinflammatory cytokines MCP-1, IL-6, and E-selectin.

20 ls of matrix metalloproteinase-8 and soluble E-selectin.

21 l endothelial activation and the presence of E-selectin.

22 tion with PSGL-1 in Th1 cells for binding to E-selectin.

23 d endothelium in ischemic tissues, including E-selectin.

24 blockade of P (0.47 +/- 0.03, P < 0.05) and E selectin (0.49 +/- 0.1, P < 0.05) reduced the number o

25 The P- (93.3-fold, P < 0.05) and E-selectin (17.1-fold, P < 0.005) are upregulated in rej

26 : 1) high sensitivity C-reactive protein; 2) E-selectin; 3) tumor necrosis factor (TNF)-alpha; 4) vas

27 eviation] of vessels positive; P < .001) and E-selectin (31.2% +/- 25.7) in vessels in the bowel wall

28 pressure (-4.9 mm Hg, P = 0.019) and reduced E-selectin (-7.8%, P = 0.012).

29 not involuting phase, constitutively express E-selectin, a cell adhesion molecule not present in quie

30 ed to characterize their rolling behavior on E-selectin, a critical step in leukocyte recruitment dur

31 In this study, we performed E-selectin adherence assays under hemodynamic flow condi

32 ch using nanoscale liposomes conjugated with E-selectin adhesion protein and Apo2L/TRAIL (TNF-related

33 g ligand (TRAIL) on their surface along with E-selectin adhesion receptor.

34 luble intercellular adhesion molecule 1, and E-selectin all fell short of significance (after Bonferr

35 Patterning regions with and without E-selectin allows captured leukocytes, which also bind E

36 ctor pathway inhibitor-2 (TFPI2), as well as E-selectin, an unrelated protein possessing a potential

37 trophils expressing exogenous CD44 rolled on E-selectin and activated Src kinases after binding anti-

38 allows captured leukocytes, which also bind E-selectin and are unwanted impurities in CTC isolation,

39 Rivipansel antagonizes ligand recognition by E-selectin and blocks outside-in signaling of integrin-m

40 hat PCa cell rolling capacity is mediated by E-selectin and can be enhanced by stromal cell-derived f

41 Infected cells rolled on E-selectin and endothelial surfaces, and this rolling wa

42 shear, contact time, and the spacing between E-selectin and HA regions patterned on the substrate.

43 E-selectin and ICAM-1 expression are essential for leuko

44 Combined CD14 and C5 inhibition reduced E-selectin and ICAM-1 expression by 96 and 98% for E. co

45 aureus-induced EC activation was measured by E-selectin and ICAM-1 expression using flow cytometry.

46 egulation of cell-surface adhesion molecules E-selectin and ICAM-1.

47 ut not HU, and the expression of endothelial E-selectin and intercellular adhesion molecule 1 was dec

48 ssue endothelium and BMD-EPC to express both E-selectin and its ligands.

49 L), which is the most potent ligand for both E-selectin and L-selectin expressed on human cells.

50 tion of leukocyte adhesion molecules such as E-selectin and P-selectin.

51 culating monocytes are specialized to engage E-selectin and providing key insights into the molecular

52 ukocyte tethering and rolling on L-, P-, and E-selectin and slightly increased rolling velocity.

53 ciated significantly with progression of DR, E-selectin and tumor necrosis factor-alpha (TNF-alpha) l

54 f the EC-leukocyte adhesion molecules (ELAM) E-selectin and vascular cell adhesion molecule 1 (VCAM-1

55 ssion of endothelial cell adhesion molecules E-selectin and vascular cell adhesion molecule-1 in the

56 We also show that E-selectin and VCAM-1, but not ICAM-1, are upregulated i

57 iR-126* and miR-126 downregulation increased E-selectin and VCAM1, respectively, while miR-126 overex

58 human L-selectin is preferentially bound by E-selectin and, on ligation, initiates secretion of MRP8

59 By performing BM transplantation using E-selectin(-/-) and E-selectin(+/+) mice as the donors a

60 eased levels of tumor necrosis factor-alpha, E selectin, and P selectin, compared with controls.

61 ations of plasminogen activator inhibitor-1, E-selectin, and angiopoietin-2 as markers of endothelial

62 the BMP9/BMP10-induced surface expression of E-selectin, and both ALK1 and ALK2 in the up-regulation

63 ethering to and rolling on immobilized P- or E-selectin, and compromised E-selectin-induced activatio

64 igen, VWF collagen-binding activity, soluble E-selectin, and endothelin-1 levels by using ELISA and B

65 igen, VWF collagen-binding activity, soluble E-selectin, and endothelin-1) were significantly increas

66 rleukin 6, interleukin 8, VEGF, osteopontin, E-selectin, and HGF with continuous tumour shrinkage or

67 ations of intercellular adhesion molecule-1, E-selectin, and IL-6 and inhibited the expression of lym

68 n molecules, including VCAM-1, IL-6, ICAM-1, E-selectin, and monocyte chemoattractant protein (MCP)-1

69 e vascular cell adhesion molecule 1, soluble E-selectin, and monocyte chemoattractant protein 1 and c

70 ide synthase 2, NADPH oxidase (NOX) 2, NOX4, E-selectin, and monocyte chemotactic protein-1.

71 essions of TNFalpha, MCP1, IL1beta, MIP2 and E-Selectin, and neutrophil accumulation), oxidative/nitr

72 Plasma concentrations of ICAM-1, E-selectin, and soluble TNF receptor 2 (sTNF-R2), a mark

73 s VCAM-1, intercellular adhesion molecule-1, E-selectin, and tissue factor.

74 her serum intercellular adhesion molecule-1, E-selectin, and vascular cell adhesion molecule-1 (P < 0

75 lenged with LPS through an increase in TLR4, E-selectin, and VCAM-1 and ultimately through enhanced l

76 These data provide evidence that E-selectin- and ICAM-1-dependent adhesion of Th17 and Th

77 vascular cell adhesion molecule, and soluble-E-selectin are atherosclerosis-associated indicators of

78 atory adhesion molecules ICAM-1, VCAM-1, and E-selectin, as well as the proinflammatory cytokines IL1

79 alter plasminogen activator inhibitor-1 and E-selectin associations with delirium, suggesting that t

80 Neutrophil rolling over E-selectin at precise shear stress transmits tension and

81 Moreover, inhibition of E-selectin at this time point resulted in exacerbation o

82 hanced tethering and rolling interactions on E-selectin-bearing endothelium under flow conditions in

83 culating lymphocytes, which exhibit variable E-selectin binding among CD4(+) and CD8(+) T cells but n

84 lated with a prominent function of ESL-1 for E-selectin binding and for migration of hematopoietic pr

85 iformly express high levels of the canonical E-selectin binding determinant sialyl Lewis X (sLe(X)) a

86 ed for HSPCs (CD34(+) cells) display greater E-selectin binding than those obtained from mouse (lin(-

87 During inflammation, PSGL-1 dominated E-selectin binding, rolling, integrin activation, and ex

88 E-selectin blockade inhibited approximately 60% of CCR4(

89 selectin; both processes were neutralized by E-selectin-blocking antibodies.

90 Prostate cancer cells roll on E-selectin(+) BMEC through E-selectin ligand-binding int

91 we demonstrated that Malat1 binds to Bim and E-selectin both in vitro and in vivo Our study suggests

92 16,243 administration is also dependent upon E-selectin but not P-selectin.

93 ion and adhesion was enhanced by recombinant E-selectin but not P-selectin; both processes were neutr

94 ercellular adhesion molecule 1 (ICAM-1), and E-selectin by approximately 20% compared with stimulatio

95 m, CD44-mediated rolling of monocytes on the E-selectin-coated surfaces.

96 ng attachment to both human and mouse P- and E-selectin compared with MBControl in vitro (P </= .002)

97 ion of adhesion molecules such as ICAM-1 and E-selectin compared with the effect of either ligand alo

98 s that are responsible for binding to P- and E-selectins constitutively expressed by the marrow micro

99 These data suggest that endothelial E-selectin could be a major ligand for HemSCs and thereb

100 ized the distribution of lipid rafts and the E-selectin counterreceptor CD44 on the monocyte surface.

101 Intratumoral vascular E-selectin, critical for T-cell entry into skin, was dow

102 By using E-selectin cross-linking and beads coated with CD44 immu

103 ation) of 17.9 (99.5); ng/mL (P = 0.006) and E-selectin decreased by 2.33 (16.08) ng/mL (P = 0.03) in

104 than Th1 cells bound to TNF-alpha-activated E-selectin-deficient endothelial cells, and intravital m

105 In addition, E-selectin-deficient mice showed reduced hepatic express

106 than Th1 cells in wild-type mice but not in E-selectin-deficient mice.

107 thout E-selectin ligands, were attenuated in E-selectin-deficient mice.

108 All three glycan families contributed to E-selectin dependent cell adhesion with N-glycans contri

109 utrophil rolling and strongly reduced L- and E-selectin-dependent adhesion in airway postcapillary ve

110 tion of tumor cells through the induction of E-selectin-dependent endothelial retractions and a subse

111 IL-17 also led to a synergistic increase in E-selectin-dependent leukocyte rolling on microvascular

112 In an ex vivo flow chamber assay, P- and E-selectin-dependent leukocyte rolling was mildly reduce

113 found impaired P-selectin-dependent, but not E-selectin-dependent leukocyte rolling, whereas in doubl

114 and a microfluidic system, we evaluated how E-selectin-dependent rolling modulates hyaluronic acid (

115 Furthermore, E-selectin-dependent rolling promotes adhesion to HA by

116 e rolling, whereas in double-deficient mice, E-selectin-dependent rolling was almost completely absen

117 initiated by binding of blood-borne cells to E-selectin displayed at target endothelial beds.

118 ic oxide (NO) production is one mechanism of E-selectin downregulation and it can be tracked by quant

119 y targeting the early (P-selectin) and late (E-selectin) endothelial ischemic response.

120 inflamed venules, neutrophils roll on P- or E-selectin, engage P-selectin glycoprotein ligand-1 (PSG

121 R) was functionalized with recombinant human E-selectin (ES) and polyethylene glycol (PEG) to target

122 ow been identified for the adhesion molecule E-selectin expressed by bone marrow endothelial cells at

123 CC patients whose tumors had higher vascular E-selectin expression (P<0.05).

124 e within MCC tumors were associated with low E-selectin expression (P<0.05; n=45) and decreased CD8 l

125 cts could be partially attributed to reduced E-selectin expression after EP4 receptor stimulation.

126 Existing therapeutic agents that modulate E-selectin expression and/or RNS generation may restore

127 tor N(omega)-nitro-L-arginine(L-NNA) induced E-selectin expression at levels comparable to imiquimod-

128 ar results were observed when TLR4 dependent E-selectin expression by endothelial cells was determine

129 ta), and arginase, and inhibited endothelial E-selectin expression in vitro.

130 d that nitric oxide (NO) potently suppresses E-selectin expression on human endothelial cells and tha

131 tercellular adhesion molecule 1 (ICAM-1) and E-selectin expression on HUVECs by 3- and 1.5-fold, resp

132 V inside the bone marrow correlated with the E-selectin expression pattern.

133 hain reaction analyses revealed that hepatic E-selectin expression was up-regulated 10-fold, whereas

134 CCs and that NO inhibition restores vascular E-selectin expression, potentially enhancing T-cell recr

135 le release, but not endothelial cell surface E-selectin expression, was blocked by inhibiting RLC pho

136 production of NO in SCCs may impair vascular E-selectin expression.

137 ctivation, resulting in enhanced endothelial E-selectin expression.

138 le-1, vascular cell adhesion molecule-1, and E-selectin expressions are markedly up-regulated in the

139 E-selectin extends from the plasma membrane of inflamed

140 This work demonstrates that E-selectin functionalized L-DXR, sheared in suspension o

141 fficking to lymphoid tissue, and blockade of E-selectin has a modest effect on improving long-term gr

142 Tumor necrosis factor receptor 1, E-selectin, hK11, tumor necrosis factor-related activati

143 were associated with decreased expression of E-selectin, ICAM-1, CCL2, CXCL8, and IL-6.

144 ha-induced inflammatory cytokine production (E-selectin, ICAM-1, VCAM-1 and IL-6).

145 Flow cytometry using E-selectin-Ig chimera (E-Ig) shows that human marrow cel

146 Correlations among changes in E-selectin, IL-6, and DM-related variables suggest that

147 ted microspheres (the lack of actins) on the E-selectin-immobilized slides.

148 y flowing microspheres coated with CD24 onto E-selectin-immobilized surfaces further revealed that th

149 exhibit the rolling response selectively on E-selectin-immobilized surfaces.

150 ic stimulation acts through up-regulation of E-selectin in adipose tissue endothelial cells to induce

151 ocyte chemotactic protein-1, P-selectin, and E-selectin in DBD compared with LD and DCD kidneys.

152 genes such as adhesion molecules VCAM-1 and E-selectin in ECs in vitro and in vivo.

153 colitis and high expression levels of P- and E-selectin in mucosal capillaries (P = .014).

154 hemistry to investigate expression of P- and E-selectin in rejected versus accepted allografts and ly

155 ncident with significantly reduced levels of E-selectin in serum and on pulmonary epithelia.

156 localized activation of endothelial FAK and E-selectin in the lung vasculature mediates the initial

157 P-selectin were not required, deficiency of E-selectin in the recipient bone marrow endothelium sign

158 The second, E-selectin, increases CTC capture under shear.

159 mmobilized P- or E-selectin, and compromised E-selectin-induced activation of spleen tyrosine kinase

160 combination of two physiological processes: E-selectin-induced cell rolling and poly(amidoamine) (PA

161 they did not prevent Syk phosphorylation or E-selectin-induced leukocyte slow rolling.

162 n of Arg140 on HOXA9, an event essential for E-selectin induction.

163 trated in situ-like expression of cadherins, E-selectin, intercellular adhesion molecule 1 (ICAM-1),

164 10- to 15-fold increase in the expression of E-selectin, intercellular adhesion molecule 1, vascular

165 Here we show that E-selectin is a major receptor for monocyte recruitment

166 e findings provide evidence that endothelial E-selectin is a novel factor contributing to endothelial

167 E-selectin is a surface marker of endothelial cell (EC)

168 lished roles in mediating leukocyte rolling, E-selectin is emerging as a multifunctional receptor cap

169 cleaved less efficiently by mesotrypsin, and E-selectin is not cleaved at the anticipated site.

170 rolling ligand despite its weak affinity for E-selectin is unknown.

171 led that CD24 has a binding affinity against E-selectin (K(D) = 3.4 +/- 0.7 nM).

172 E-selectin ligand HCELL (hematopoietic cell E-selectin/L-selectin ligand) and, despite absence of CX

173 lymphocyte Ag, CD43E, and hematopoietic cell E-selectin/L-selectin ligand, respectively), and B cells

174 044), but there was no difference in soluble E selectin level (P = 0.278).

175 The decrease in E-selectin levels was also evident in human sickle cell

176 E-selectin levels were significantly correlated with DM-

177 ve was to determine the interaction of CCR4, E-selectin ligand (ESL), and alpha(4)beta(1) on memory a

178 ocyte-associated antigen (CLA), a functional E-selectin ligand (ESL), is selectively expressed on cir

179 press typical skin-homing receptors, such as E-selectin ligand and alpha-4 and beta-1 integrins, they

180 this study, we show that two such molecules, E-selectin ligand and alpha4beta1 integrin, enable activ

181 gs unveil distinct cell-specific patterns of E-selectin ligand expression among human PBMCs, indicati

182 ts suggest that strategies toward increasing E-selectin ligand expression could be applicable as part

183 n mesenchymal stem cells (hMSCs) creates the E-selectin ligand HCELL (hematopoietic cell E-selectin/L

184 ur findings demonstrate that CD43 is a major E-selectin ligand in Th17 cells that functions independe

185 nd report that CD43 functions as a Th17 cell E-selectin ligand in vitro that mediates Th17 cell rolli

186 Our studies show that this novel E-selectin ligand is a glycoform of the heavy chain comp

187 In both human and mouse cells, E-selectin ligand reactivity was observed at ~ 120- to 1

188 alized MPO glycovariant, referred to as "MPO-E-selectin ligand" (MPO-EL), is expressed on circulating

189 (HSPCs), our knowledge regarding the cognate E-selectin ligand(s) on HSPCs is incomplete.

190 rafficking to murine femurs was dependent on E-selectin ligand, beta1 integrin, and Rac1.

191 ood, Sreeramkumar and colleagues report that E-selectin ligand-1 (ESL-1) is a highly selective ligand

192 E-selectin ligand-1 (ESL-1), a Golgi apparatus-localized

193 We have characterized mice deficient in E-selectin ligand-1 (ESL-1), or in both P-selectin glyco

194 cer cells roll on E-selectin(+) BMEC through E-selectin ligand-binding interactions under shear flow,

195 Moreover, eliminating E-selectin ligand-synthesizing alpha1,3 fucosyltransfera

196 sm for BMD-EPC homing and indicate that dual E-selectin/ligand pairs may be effective targets/tools f

197 tively, we demonstrate that upregulated dual E-selectin/ligand pairs reciprocally expressed on ischem

198 captures native glycoforms of two well known E-selectin ligands (CD44/hematopoietic cell E-/L-selecti

199 traversed BMEC via sequential dependence on E-selectin ligands and beta1 and alphaVbeta3 integrins.

200 tein ligand-1, CD43, and CD44 (rendering the E-selectin ligands cutaneous lymphocyte Ag, CD43E, and h

201 ction and structural biology of glycoprotein E-selectin ligands expressed on human PBMCs.

202 acterize the expression and functionality of E-selectin ligands in Th type 17 lymphocytes (Th17 cells

203 of the expression and function of leukocyte E-selectin ligands is key to understanding the tempo and

204 integrin dimer VLA-4, but lack expression of E-selectin ligands that program HSPC trafficking to BM.

205 type (CCR7(int/+)CD62L(int)CD69(-)CD103(+/-) E-selectin ligands(+)) that is distinct from memory T ce

206 These results unify the requirement for E-selectin ligands, alpha1,3 fucosyltransferases, beta1

207 ammation by stimulating expression of potent E-selectin ligands, including an uncharacterized approxi

208 120- to 130-kDa region, which contained two E-selectin ligands, the P-selectin glycoprotein ligand-1

209 metastasis using murine tumor cells, without E-selectin ligands, were attenuated in E-selectin-defici

210 le for FUT9 during the biosynthesis of human E-selectin ligands.

211 , respectively), and B cells altogether lack E-selectin ligands.

212 n marked increases in levels of cell surface E-selectin ligands.

213 r circulating EPC, which express counterpart E-selectin ligands.

214 rmine whether platelet (P)- and endothelial (E)-selectin mediate T cell recruitment in corneal transp

215 n a model of corneal transplantation, P- and E-selectin mediate T cell recruitment to the graft, E-se

216 Thus, SLP-76 and ADAP are involved in E-selectin-mediated integrin activation and neutrophil r

217 n promoting adaptor protein) are involved in E-selectin-mediated integrin activation and slow leukocy

218 E-selectin-mediated rolling facilitates pancreatic cance

219 here all three fucosyltransferases conferred E-selectin-mediated rolling in HEK293T cells.

220 E-selectin-mediated rolling transmits signals into neutr

221 Rac1 is involved in E-selectin-mediated slow rolling and crawling.

222 ipansel is a glycomimetic drug that inhibits E-selectin-mediated vaso-occlusion induced by integrin-d

223 tin mediate T cell recruitment to the graft, E-selectin mediates APC trafficking to lymphoid tissue,

224 BM transplantation using E-selectin(-/-) and E-selectin(+/+) mice as the donors and recipients respec

225 intercellular adhesion molecule 1 (ICAM-1), E-selectin, monocyte chemoattractant protein 1 (MCP-1),

226 Using P- and E-selectin neutralizing antibodies, we evaluated the eff

227 ild type and P-selectin-null mice but not in E-selectin-null mice.

228 serum lipid biomarkers, blood pressure, and E-selectin offer a potential public health strategy for

229 Interactions of CD44 on neutrophils with E-selectin on activated endothelial cells mediate rollin

230 We propose that constitutively expressed E-selectin on endothelial cells in the proliferating pha

231 red that SDF-1alpha specifically upregulates E-selectin on endothelial cells, thus tethering circulat

232 d-1 (ESL-1) is a highly selective ligand for E-selectin on hematopoietic progenitors with unexpected

233 l recruitment, as well as the effect of anti-E-selectin on long-term allograft survival.

234 Although well recognized that expression of E-selectin on marrow microvessels mediates osteotropism

235 ruitment could be explained by regulation of E-selectin on the cocultured EC.

236 detection at least in part by downregulating E-selectin on tumor vessels, thereby restricting entry o

237 Elevated E-selectin on wound vasculature serve as docking sites f

238 , and the interactions between monocytes and E-selectin or aortic endothelium under flow were charact

239 othelial cells with monoclonal antibodies to E-selectin or ICAM-1 or treating neutrophils with wortma

240 Endothelial adhesion molecules, such as E-selectin or ICAM-1, are connected to the actin cytoske

241 t HOXA9 methylation with concomitant loss in E-selectin or VCAM-1 induction.

242 01), Na + K-ATPase activity (P < 0.001), and E-selectin (P < 0.001) in the perfusate.

243 and reduced C-reactive protein (P = 0.001), E-selectin (P = 0.0005), and vascular cell adhesion mole

244 asminogen activator inhibitor-1 (p = 0.002), E-selectin (p = 0.02), and S100B (p < 0.001) concentrati

245 sion was reversed by shedding of endothelial E-selectin, P-selectin, and alphavbeta3 integrin, and le

246 lecule-1, intracellular adhesion molecule-1, E-selectin, P-selectin, TAT (thrombin/antithrombin compl

247 ral atherosclerosis mediators in serum (e.g. E-selectin, PI3/elafin, CCL7, IL-16) correlated with SCO

248 Elevated E-selectin plays an important role in hepatic neutrophil

249 Our studies revealed that the CD31(+)E-selectin(+) population accounted for 20.8%, 26.4% and

250 E-selectin-positive HemECs also stimulated migration and

251 The genetic deletion of E-selectin prevented chronic-binge ethanol-induced hepat

252 ysis revealed that PRMT5 is recruited to the E-selectin promoter following transient HOXA9 binding to

253 In conclusion, targeting the overexpressed E-selectin provides an effective approach for tissue-spe

254 We show that E-selectin-PSGL-1 interaction during neutrophil rolling

255 In contrast to P- and L-selectin, the E-selectin/PSGL-1 binding does not exhibit significant c

256 ions, and mRNA expression of ICAM-1, VCAM-1, E-selectin, RANTES, IL-17, IL-33, thymic stromal lymphop

257 biology of G-CSF and MPO, and on the role of E-selectin receptor/ligand interactions in leukocyte mig

258 Anti-E-selectin reduced activated CD8 more than CD4 cell migr

259 Anti-E-selectin reduced the number of mature antigen-presenti

260 and endothelium, but the role of endothelial E-selectin remains unclear.

261 cular cell adhesion molecule-1 (VCAM-1), and E-selectin, resulting in a decreased adhesion of leukocy

262 vascular cell adhesion molecule-1 (sVCAM-1), E-selectin (sE-Selectin), thrombomodulin (sTM), tissue f

263 Thus, endothelial E-selectin shapes the tumor microenvironment through the

264 Knocking-down vascular E-selectin significantly inhibited SDF-1alpha-induced EP

265 the adhesion/migration cascade (e.g., mAb to E-selectin) significantly downregulated other steps of t

266 (LFA-1), which can be induced by rolling on E-selectin (slowly) or by exposure to the chemokine CXCL

267 ium chelating buffer effectively deactivates E-selectin so that leukocytes may be rinsed away 60% mor

268 , plasminogen activator inhibitor-1, soluble E-selectin, soluble intercellular adhesion molecule-1 (I

269 The E-selectin-specific SLC1 inhibited NF-kappaB by interfer

270 In vivo, neutralizing antibodies to E-selectin strongly inhibited formation of blood vessels

271 Crystal structures of P- and E-selectin suggest a two-state model in which ligand bin

272 nges on the mechanics of monocyte rolling on E-selectin surfaces at 1 dyn/cm(2) in microchannels.

273 rine NCGN model, prophylactic application of E-selectin-targeted immunoliposomes packed with p65 siRN

274 m was imaged with clinical-grade dual P- and E-selectin-targeted MBs (MBSelectin) at increasing doses

275 Dual P- and E-selectin-targeted microbubbles (MBs) have previously b

276 inant SLC1 consists of three modules: (i) an E-selectin targeting domain, (ii) a Pseudomonas exotoxin

277 of microRNA (miR)-146a and miR-181b with an E-selectin-targeting multistage vector (ESTA-MSV) to inf

278 markedly greater adhesive interactions with E-selectin than do circulating lymphocytes, which exhibi

279 ped a thioaptamer that specifically binds to E-selectin that is overexpressed in the vasculature of t

280 delivery of therapeutic siRNA loaded in the E-selectin thioaptamer-conjugated multistage vector (EST

281 core 2 O-glycans, which interact with P- and E-selectins to modulate trafficking to inflamed tissues.

282 e binding dynamics of selectins (P-, L-, and E-selectin) to P-selectin glycoprotein ligand-1 (PSGL-1)

283 that both ligands bind recombinant monomeric E-selectin transiently with fast on- and fast off-rates,

284 Anti-E-selectin treatment delayed graft rejection and increas

285 observed that engagement of hMSC HCELL with E-selectin triggers VLA-4 adhesiveness, resulting in she

286 GL-1(-/-)CD43(-/-) Th17 cells accumulated on E-selectin under shear flow conditions compared with wil

287 Cell-type differences on E-selectin upregulation were observed.

288 iated with up-regulated expression levels of E-selectin, vascular cell adhesion molecule (VCAM-1), an

289 les P-selectin, von Willebrand factor (VWF), E-selectin, vascular cell adhesion molecule 1, intercell

290 ivated WT PAEC, increasing the expression of E-selectin, vascular cell adhesion molecule-1, intercell

291 The binding kinetics between CD24 and E-selectin was directly measured using surface plasmon r

292 E-selectin was further increased when HemECs were expose

293 Finally, the expression of E-selectin was highly up-regulated in human alcoholic fa

294 CD43(-/-) Th17 cell accumulation on E-selectin was impaired as compared with wild-type and P

295 contrast, no cooperation effect on ICAM-1 or E-selectin was observed with a TLR2/TLR1 ligand.

296 No binding to E-selectin was observed.

297 Cell rolling on E-selectin was unaltered although the number of adherent

298 We show that tumor cells rolling on E-selectin were approximately 40-fold more likely to bin

299 ntial confounders, baseline plasma levels of E-selectin were associated significantly with progressio

300 nd fast off-rates, whereas they bind dimeric E-selectin with remarkably slow on- and off-rates.