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 l endothelial activation and the presence of E-selectin.

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

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

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

6 hensive characterization of their binding to E-selectin.

7 ll surface expression of ICAM-1, ICAM-2, and E-selectin.

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

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

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

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

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

13 partial reduction in rolling interaction on E-selectin.

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

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

16 the capacity of human CAR T-cells to engage E-selectin.

17 cells do not express sLe (X) and do not bind E-selectin.

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

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

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

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

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

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

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

25 o illustrate the glycan-dependent binding of E-selectin, a central molecule in cell migration, to its

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

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

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

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

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

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

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

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

34 th oncogenesis enhances AML blast binding to E-selectin and enable promotion of pro-survival signalin

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

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

37 Circulating levels of E-selectin and ICAM-1 and increases in ICAM-1 over the c

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

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

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

41 E-selectin and ICAM-1 partially mediated the association

42 t to assess the longitudinal associations of E-selectin and ICAM-1 with subclinical alterations in ca

43 However, the temporal associations between E-selectin and ICAM-1 with subclinical cardiac dysfuncti

44 of inflammatory marker expression (PECAM-1, E-selectin and ICAM-1).

45 ung adults, we evaluated the associations of E-selectin and ICAM-1, obtained at year (Y) 7 (Y7) and Y

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

47 E-selectin and intercellular adhesion molecule (ICAM)-1

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

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

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 levels of IL-12, IL-17, IL-10, IL-5, CXCL9, E-Selectin and ST2/IL-1R4; and decreased levels of IL-13

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

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

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

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

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

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

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

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

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

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

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 was a reduction in gene expression of IL1B, E-selectin, and monocyte attachment.

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

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

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

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

73 e vascular cell adhesion molecule-1, soluble E-Selectin, and P-Selectin).

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

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

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

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

78 Barbier and colleagues uncover (E)-selectin as a novel mediator of malignant cell surviv

79 unique insights into the functional role of E-selectin as a component of the vascular niche critical

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

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

82 atriuretic peptide), interleukin (IL)-6, and E-selectin at age 60 to 64 years with performance at age

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

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

85 After multivariable adjustment, higher E-selectin at Y7 (beta coefficient per 1 SD higher: 0.22

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

87 E-selectin binding activity mediated by the alpha1-3 fuc

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

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

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

91 In vivo AML blasts with highest E-selectin binding potential are 12-fold more likely to

92 surface fucosylation, with resultant robust E-selectin binding under hemodynamic shear.

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

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

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

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

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

98 16,243 administration is also dependent upon E-selectin but not P-selectin.

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

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

101 ndered via binding of the endothelial lectin E-selectin (CD62E) to its cognate ligand, sialyl Lewis-X

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

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

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

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

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

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

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

109 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

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

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

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

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

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

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

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

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

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

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

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

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

122 We now report in contrast, E-selectin directly triggers signaling pathways that pro

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

139 cytokines, vascular activation markers, and E-selectin expression.

140 mediators that upregulate endothelial niche E-selectin expression.

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

142 E-selectin extends from the plasma membrane of inflamed

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

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

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

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

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

148 uction in endothelial cell adhesion molecule E-selectin, (ii) transmigration through TNF-alpha-activa

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

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

151 tion of FUT6 p.Glu274Lys with higher soluble E-selectin in an independent population of 748 AAs from

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

153 AM) expression including VCAM-1, ICAM-1, and E-selectin in human aortic endothelial cells (HAoECs), w

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

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

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

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

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

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

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

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

162 10- to 15-fold increase in the expression of E-selectin, intercellular adhesion molecule 1, vascular

163 like tyrosine kinase, von Willebrand factor, E-selectin, intercellular adhesion molecule, vascular ce

164 helial growth factor, von Willebrand factor, E-selectin, intercellular adhesion molecule, vascular ce

165 The endothelial cell adhesion molecule E-selectin is a key component of the bone marrow hematop

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

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

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

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

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

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

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

173 E-selectin levels were significantly correlated with DM-

174 ave identified the ABO locus associated with E-selectin levels.

175 amined genome-wide associations with soluble E-selectin levels.

176 74Lys, P = 9.02 x 10-24) with higher soluble E-selectin levels.

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

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

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

186 CD22 ligand-modified NK-92MI cells with the E-selectin ligand sialyl Lewis X to promote trafficking

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

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

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

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

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

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

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

194 in flow, the FMCR assay was used to analyze E-selectin-ligand interactions following the addition (f

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

212 ion of key inflammatory factors (eg, ICAM-1, E-selectin, MCP-1) in endothelial cells or vascular smoo

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

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

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

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

217 E-selectin-mediated rolling facilitates pancreatic cance

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

219 E-selectin-mediated rolling transmits signals into neutr

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

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

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

223 E-selectin mediates the rolling of circulating leukocyte

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 Higher E-selectin (n = 1,810) and ICAM-1 (n = 1,548) at Y7 were

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

228 Neither E-selectin nor ICAM-1 was associated with measures of LV

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

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

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

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

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

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

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 e intercellular adhesion molecule-1, soluble E-Selectin, P-Selectin, and angiopoietin-2 (p < 0.0001 f

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

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

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

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

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

252 ecreasing endothelial cell adhesion molecule E-Selectin production, (ii) transmigration through HUVEC

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

283 found that mouse Th1 cells rolling on P- or E-selectin triggered signals that promoted alphaLbeta2-d

284 th undifferentiated levels of CTC-recruiting E-selectin under DF vs UF conditions.

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

286 Sele(-/-) hosts) or therapeutic blockade of E-selectin using small molecule mimetic GMI-1271/Uproles

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

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

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

290 E-selectin was further increased when HemECs were expose

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

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

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

294 No binding to E-selectin was observed.

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

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

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

298 Cystatin C, NT-proBNP, and IL-6 (but not E-selectin) were inversely associated with all outcomes,

299 our cells is provided by bone vascular niche E-selectin, whose direct binding to cancer cells promote

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