ライフサイエンスコーパス: selectin

1 hesion molecule-1, soluble E-Selectin, and P-Selectin).

2 lls do not express sLe (X) and do not bind E-selectin.

3 old increase over T cells unable to cleave L-selectin.

4 f the WPB cargos von Willebrand factor and P-selectin.

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

6 gand by using a ridged channel coated with P selectin.

7 eric adipose tissues is partly mediated by L-selectin.

8 sed microparticles of iron oxide targeting P-selectin.

9 cks AP-1-dependent retrograde transport of L-selectin.

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

11 he capacity of human CAR T-cells to engage E-selectin.

12 in non-ICU patients; p<0.0001) and soluble P-selectin (15.9 ng/mL [4.8] vs 11.2 ng/mL [3.1]; p=0.0014

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

14 elets to lymphocytes was blocked with anti-P-selectin Abs, and when this occurred we observed higher

15 In this study, we performed E-selectin adherence assays under hemodynamic flow conditi

16 ble intercellular adhesion molecule 1, and E-selectin all fell short of significance (after Bonferron

17 In neutrophils, selectins also trigger an immunoreceptor-like signaling

18 trophils enter the lymph node entirely via L-selectin and actively exit via efferent lymphatics via a

19 vipansel antagonizes ligand recognition by E-selectin and blocks outside-in signaling of integrin-med

20 Cooperative selectin and chemokine signaling in Th1 cells promoted a

21 ells expressing cleavable or non-cleavable L-selectin and determined the impact of L-selectin proteol

22 oncogenesis enhances AML blast binding to E-selectin and enable promotion of pro-survival signaling

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

24 to recirculate, much like lymphocytes via L-selectin and high endothelial venules in lymph nodes and

25 Circulating levels of E-selectin and ICAM-1 and increases in ICAM-1 over the cou

26 E-selectin and ICAM-1 partially mediated the associations

27 to assess the longitudinal associations of E-selectin and ICAM-1 with subclinical alterations in card

28 However, the temporal associations between E-selectin and ICAM-1 with subclinical cardiac dysfunction

29 f inflammatory marker expression (PECAM-1, E-selectin and ICAM-1).

30 g adults, we evaluated the associations of E-selectin and ICAM-1, obtained at year (Y) 7 (Y7) and Y15

31 ti-G-CSFR, as was the level of circulating P-selectin and ICAM-1.

32 E-selectin and intercellular adhesion molecule (ICAM)-1 ar

33 od, PAR1-AP-triggered TF exposure required P-selectin and PGSL-1.

34 lating monocytes are specialized to engage E-selectin and providing key insights into the molecular e

35 Soluble endothelial selectin and soluble intercellular adhesion molecule con

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

37 M-1 and induced cell surface expression of P-selectin and VCAM-1.

38 -126* and miR-126 downregulation increased E-selectin and VCAM1, respectively, while miR-126 overexpr

39 uman L-selectin is preferentially bound by E-selectin and, on ligation, initiates secretion of MRP8/1

40 dPGS is able to cross the BBB, bind to P/L-selectins and accumulate selectively in intracranial tum

41 a to induce the up-regulation of endothelial selectins and adhesion molecules, ultimately resulting i

42 phils in venules relies on capturing through selectins and chemokine-induced integrin activation.

43 Despite the broad role of both selectins and fucosyltransferases in various inflammator

44 ntary assays to compare ligand binding to WT selectins and to E88D selectins that replaced Glu-88 wit

45 molecules relevant for leukocyte rolling (P-selectin) and platelet capture (von Willebrand factor [V

46 r adhesion molecule-1, soluble E-Selectin, P-Selectin, and angiopoietin-2 (p < 0.0001 for all).

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

48 L2/MIP-2, MCP-1/CCL2, CXCR2, IL-6, ICAM-1, P-selectin, and C5aR) was suppressed by anti-G-CSFR, as wa

49 levels of the prothrombotic proteins vWF, P-selectin, and ICAM1 and high levels of the antithromboti

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

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

52 sions of TNFalpha, MCP1, IL1beta, MIP2 and E-Selectin, and neutrophil accumulation), oxidative/nitrat

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

54 ) antigen, soluble thrombomodulin, soluble P-selectin, and soluble CD40 ligand, as well as coagulatio

55 nto four major groups: cadherins, integrins, selectins, and immunoglobulins.

56 evaluations indicate improved activity as P-selectin antagonists for the axially configured analogue

57 fucoidan (from Fucus vesiculosus) or anti-P-selectin antibody (Rb40.34) during Days 21-35.

58 /-) ) and CD4(-/-) mice along with CD8 and L-selectin antibody-treated mice were fed an HFD, and hepa

59 nique insights into the functional role of E-selectin as a component of the vascular niche critical f

60 e expressed the entire ectodomain of mouse P-selectin as a monomer (sP-selectin) or as a disulfide-li

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

62 use model, we identified brain endothelial P-selectin as a potential biomarker for transient ischaemi

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

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

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

66 peutic potential of targeting the fucoidan/P-selectin axis in PH.

67 The effects of the fucoidan/P-selectin axis on vascular remodeling and pulmonary hyper

68 nced tethering and rolling interactions on E-selectin-bearing endothelium under flow conditions in vi

69 ve shown that activated T-cells re-express L-selectin before lymph node egress and use L-selectin to

70 E-selectin binding activity mediated by the alpha1-3 fucos

71 lating lymphocytes, which exhibit variable E-selectin binding among CD4(+) and CD8(+) T cells but no

72 ormly express high levels of the canonical E-selectin binding determinant sialyl Lewis X (sLe(X)) and

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

74 urface fucosylation, with resultant robust E-selectin binding under hemodynamic shear.

75 F-beta resulted in a gradual loss of E- or P-selectin-binding central and peripheral memory populatio

76 L-selectin blockade also demonstrated significant hepatopr

77 P-selectin blockade by an antibody prevented complement de

78 P-selectin blockage resulted in a marked reduction of PASM

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

80 structure of the lectin and EGF domains of L-selectin bound to a fucose mimetic; that is, a terminal

81 Blockade of CD8 and L-selectin, but not CD4, ameliorated hepatocellular injury

82 Blockage of P-selectin by administration of anti-P-selectin Rb40.34 an

83 Rivipansel effectively blocked formation of selectin catch-bonds, revealing a novel mechanotransduct

84 signs of increased reactivity: shedding of l-selectin, CD11b upregulation, increased oxidative burst,

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

86 tients with CML at diagnosis expressed low l-selectin (CD62L) levels, which was not a result of propo

87 Leukocyte adhesion is mediated mainly by selectins, cell adhesion molecules and chemokines induce

88 s demonstrated increased CD8(+) /CD62L(+) (L-selectin) cells in HFD-fed mice after IRI.

89 This doubles the efficiency of selectin-chemokine driven neutrophil arrest by PILR-beta

90 n in mouse and human T cells and show that L-selectin cleavage does not regulate T cell activation me

91 L-selectin cleavage enhances integrin-mediated outside-in

92 Mechanistically, L-selectin cleavage from the neutrophil surface triggered

93 age inflammatory protein 1, interleukin-1, P-selectin, cluster of differentiation 45-positive cells);

94 DBTA using selectin-coated probes is able to detect functional sele

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

96 ail peptide, and the intracellular pool of L-selectin colocalizes with AP-1 at the trans-Golgi networ

97 aled the critical impact of the triad TLR4/P-selectin/complement in the liver damage and its relevanc

98 t thromboembolism was comparable to plasma P-selectin concentrations (thromboembolism, 78.3 ng/mL vs

99 ed the distribution of lipid rafts and the E-selectin counterreceptor CD44 on the monocyte surface.

100 uble recombinant P-selectin had no effect, P-selectin coupled to 2 um beads triggered TF exposure.

101 We used L-selectin cytoplasmic tail peptide pulldown assays combin

102 TF ELISA, soluble P-selectin, d-dimer, FVIII, and C-reactive protein were as

103 We demonstrate that L-selectin-deficient mice are prone to pulmonary infection

104 Studies in P-selectin-deficient mice confirmed a mechanistic role for

105 on of anti-P-selectin Rb40.34 antibody and P-selectin-deficient mice improved vascular remodeling and

106 uced VAT inflammation in response to HFMs, P-selectin-deficient mice still developed glucose intolera

107 a HFD for 24 h quickly induces a transient P-selectin-dependent inflammatory phenotype in the VAT but

108 nd a microfluidic system, we evaluated how E-selectin-dependent rolling modulates hyaluronic acid (HA

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

110 nsgenic mice that overexpressed monomeric sP-selectin did not exhibit increased inflammation or throm

111 We now report in contrast, E-selectin directly triggers signaling pathways that promo

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

113 endothelial cells induces shedding of the P-selectin ectodomain into the circulation.

114 accharidic ligand of the adhesion molecule P-selectin, exhibits antiproliferative properties.

115 lood and further demonstrate that platelet P-selectin exposure is necessary and sufficient.

116 ignalling to integrin alpha(IIb)beta(3) or P-selectin exposure upon agonist-induced activation in pla

117 Cell adhesion mediated by selectins (expressed by activated endothelium, activated

118 ngs and PASMCs were used for assessment of P-selectin expression and function.

119 regulation of circulating platelet surface P-selectin expression and the formation of platelet-leukoc

120 Compound 6b also inhibited platelet P-selectin expression and thus may diminish atherosclerosi

121 elets from COVID-19 patients had increased P-selectin expression basally and upon activation.

122 P-selectin expression by the endothelium may enhance VTE b

123 Clinical imaging of P-selectin expression for disease characterization could h

124 C3a and C5a generation, endothelial P-selectin expression, and adhesion of human primary and i

125 ediators that upregulate endothelial niche E-selectin expression.

126 ytokines, vascular activation markers, and E-selectin expression.

127 E-selectin extends from the plasma membrane of inflamed en

128 is known regarding how tumor cell rolling on selectins facilitates adhesion to a distinct substrate-b

129 induced oligomerization of sP-selectin or sP-selectin-Fc was required to trigger formation of neutrop

130 the Fc portion of mouse immunoglobulin G (sP-selectin-Fc).

131 Dimeric sP-selectin-Fc, but not monomeric sP-selectin, triggered in

132 Injecting sP-selectin-Fc, but not sP-selectin, into mice augmented in

133 tor 1, monocyte chemoattractant protein-1, P-selectin, fibrinogen, receptor activator of nuclear fact

134 The leukocyte adhesion receptor L-selectin forms bonds with P-selectin glycoprotein ligand

135 in and metalloproteinase 17 (ADAM17) sheds L-selectin from the neutrophil surface in an IRhom2-depend

136 he cytoplasmic tail of L-selectin regulate L-selectin functions.

137 We identified P-selectin glycoprotein ligand 1 (PSGL-1) as an HIV-1 rest

138 with a supporting role for the P-selectin/P-selectin glycoprotein ligand 1 axis, followed by (2) fir

139 P-selectin glycoprotein ligand-1 (PSGL-1) has long been st

140 horylated myosin L chain, flotillin-2, and P-selectin glycoprotein ligand-1 (PSGL-1) in the uropod.

141 minus as an extension of membrane-anchored P-selectin glycoprotein ligand-1 (PSGL-1) inhibited integr

142 esion receptor L-selectin forms bonds with P-selectin glycoprotein ligand-1 (PSGL-1) on other leukocy

143 We find that targeting the BMME with P-selectin glycoprotein ligand-1 (PSGL-1)-targeted BTZ and

144 pod, the "nucleopod," which is capped with P-selectin glycoprotein ligand-1 (PSGL-1).

145 to the adhesion and co-inhibitory receptor P-selectin glycoprotein ligand-1 (PSGL-1).

146 n an array of protein scaffolds, including P-selectin glycoprotein ligand-1, CD43, and CD44 (renderin

147 ed monocytes, although soluble recombinant P-selectin had no effect, P-selectin coupled to 2 um beads

148 Soluble P-selectin has been identified as a biomarker of cancer-as

149 The adhesion molecule L-selectin has recently been implicated in integrin activa

150 Tumor necrosis factor receptor 1, E-selectin, hK11, tumor necrosis factor-related activation

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

152 tion in endothelial cell adhesion molecule E-selectin, (ii) transmigration through TNF-alpha-activate

153 strated variation in expression of IL-1ra, P-Selectin, IL-4 and IL-5; ZIKV-infected donors demonstrat

154 strated variation in expression of IL-1ra, P-Selectin, IL-4, RANK-L, CD40L and C3a.

155 ed the amount of mu1A associated with anti-L-selectin immunoprecipitates.

156 on of FUT6 p.Glu274Lys with higher soluble E-selectin in an independent population of 748 AAs from th

157 e of this review is to outline the role of P-selectin in cardiovascular inflammatory conditions and i

158 The up-regulation of P-selectin in endothelial cells and platelets contributes

159 ) expression including VCAM-1, ICAM-1, and E-selectin in human aortic endothelial cells (HAoECs), we

160 n promoter and transcriptionally activated P-selectin in hypoxia.

161 e for ADAM17 in TCR-induced proteolysis of L-selectin in mouse and human T cells and show that L-sele

162 ient mice confirmed a mechanistic role for P-selectin in the initiation of leukocyte trafficking, mye

163 Chronic hypoxia caused an upregulation of P-selectin in the medial layer of the small pulmonary arte

164 indicate a previously unrecognized role of P-selectin in the proliferative response of PASMCs associa

165 ication increased plasma levels of soluble P-selectin in wild-type but not in MC-deficient mice.

166 Our data support a two-state model for selectins in which Glu-88 must engage ligand to trigger

167 ulation of monocyte recruitment genes (eg, L-selectin) in the macrophage compartment in wild-type mic

168 It is not known whether selectins induce similar signaling events in T cells.

169 Selectin-induced cell rolling facilitates surface recrui

170 Selectin interactions with fucosylated glycan ligands me

171 mmunohistochemistry of eNOS, endothelin-1, P-selectin, intercellular adhesion molecule 1, and vascula

172 ke tyrosine kinase, von Willebrand factor, E-selectin, intercellular adhesion molecule, vascular cell

173 lial growth factor, von Willebrand factor, E-selectin, intercellular adhesion molecule, vascular cell

174 Injecting sP-selectin-Fc, but not sP-selectin, into mice augmented integrin-dependent adhesio

175 We conclude that elevated plasma sP-selectin is a consequence rather than a cause of cardiov

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

177 P-selectin is an adhesion molecule translocated to the sur

178 ual targeting properties, as we found that P-selectin is not only expressed on tumor endothelium but

179 demonstrate that sLe(x) expressed on human L-selectin is preferentially bound by E-selectin and, on l

180 Circulating sP-selectin is thought to trigger signaling in leukocytes t

181 Our findings indicate that L-selectin is transported constitutively by the AP-1 compl

182 Plasma soluble P-selectin (sP-selectin) is elevated threefold to fourfold in patients

183 mphocyte Ag, CD43E, and hematopoietic cell E-selectin/L-selectin ligand, respectively), and B cells a

184 the lung endothelium; and reduced surface P-selectin levels in IL-13-stimulated endothelial cells.

185 Surface P-selectin levels were measured by using flow cytometry.

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

187 e identified the ABO locus associated with E-selectin levels.

188 ined genome-wide associations with soluble E-selectin levels.

189 yte-associated antigen (CLA), a functional E-selectin ligand (ESL), is selectively expressed on circu

190 unveil distinct cell-specific patterns of E-selectin ligand expression among human PBMCs, indicating

191 suggest that strategies toward increasing E-selectin ligand expression could be applicable as part o

192 L-selectin ligand MECA-79 was increased in HFD-fed mice un

193 D22 ligand-modified NK-92MI cells with the E-selectin ligand sialyl Lewis X to promote trafficking to

194 ed microbubbles (MB) functionalized with the selectin ligand sialyl Lewis(a) individually (MBsLea) or

195 , CD43E, and hematopoietic cell E-selectin/L-selectin ligand, respectively), and B cells altogether l

196 n flow, the FMCR assay was used to analyze E-selectin-ligand interactions following the addition (fuc

197 and leukocytes) binding to their resepective selectin ligands (expressed by cancer cells) may be invo

198 in ligand-1, CD43, and CD44 (rendering the E-selectin ligands cutaneous lymphocyte Ag, CD43E, and hem

199 ion and structural biology of glycoprotein E-selectin ligands expressed on human PBMCs.

200 Therefore, methods of characterizing selectin ligands expressed on human tissue may serve as

201 n innovative method for detecting functional selectin ligands expressed on human tissue that uses a d

202 n-coated probes is able to detect functional selectin ligands expressed on tissue from multiple cance

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

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

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

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

207 However, sP-selectin likely circulates as a monomer, and in vitro st

208 Future molecular MRI targeting P-selectin may be used to improve diagnosis, follow-up of

209 n of key inflammatory factors (eg, ICAM-1, E-selectin, MCP-1) in endothelial cells or vascular smooth

210 Thus, L-selectin mechanochemistry limits premature activation of

211 After selectin-mediated braking, neutrophils migrate along the

212 E-selectin-mediated rolling facilitates pancreatic cancer

213 Although the mechanics of selectin-mediated rolling have been extensively studied,

214 E-selectin-mediated rolling transmits signals into neutrop

215 ansel is a glycomimetic drug that inhibits E-selectin-mediated vaso-occlusion induced by integrin-dep

216 E-selectin mediates the rolling of circulating leukocytes

217 cular magnetic resonance imaging targeting P-selectin might aid in the diagnosis of transient ischaem

218 les that contain von Willebrand factor and P-selectin, molecules that regulate hemostasis and inflamm

219 onomer, and in vitro studies suggest that sP-selectin must dimerize to induce signaling in leukocytes

220 Here we show that mice expressing an L-selectin mutant (N138G) have altered catch bonds and pro

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

222 riming requires signals transduced through L-selectin N138G after it engages PSGL-1 or PNAd.

223 ing GTPase, which localizes to a subset of P-selectin-negative WPBs.

224 phenomenon that was inhibited by platelet P-selectin neutralization or integrin alphaIIb/beta3 block

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

226 Leukocyte adhesion to P-selectin on activated platelets and endothelial cells in

227 These data show that P-selectin on activated platelets rapidly triggers TF expo

228 L-selectin on T-cells is best known as an adhesion molecul

229 itment could be explained by regulation of E-selectin on the cocultured EC.

230 ndent of its reported cognate ligands vWF, P-selectin or Mac-1, offering a potential target against N

231 Antibody-induced oligomerization of sP-selectin or sP-selectin-Fc was required to trigger forma

232 odomain of mouse P-selectin as a monomer (sP-selectin) or as a disulfide-linked dimer fused to the Fc

233 al cells (expressing homing molecules, e.g., selectins) or a surface (expressing recombinant homing m

234 ent of NADPH oxidase activity, shedding of l-selectin, or mobilization of CD11b.

235 We anticipate that blockade of TLR4, P-selectin, or the complement system could prevent liver i

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

237 rand factor with a supporting role for the P-selectin/P-selectin glycoprotein ligand 1 axis, followed

238 However, the molecular mechanism by which L-selectin participates in host defense against Klebsiella

239 l atherosclerosis mediators in serum (e.g. E-selectin, PI3/elafin, CCL7, IL-16) correlated with SCORA

240 reasing endothelial cell adhesion molecule E-Selectin production, (ii) transmigration through HUVEC m

241 lls modified with glycan ligands to CD22 and selectins promote both targeted killing of B lymphoma ce

242 cible factor 1alpha) directly bound to the P-selectin promoter and transcriptionally activated P-sele

243 skipping and soluble versus transmembrane P-selectin protein production.

244 the ratio of transmembrane versus soluble P-selectin protein production.

245 Therefore, we considered other roles for L-selectin proteolysis during T cell activation.

246 le L-selectin and determined the impact of L-selectin proteolysis on T cell activation in virus-infec

247 Following virus infection of mice, L-selectin proteolysis promoted early clonal expansion of

248 ge of P-selectin by administration of anti-P-selectin Rb40.34 antibody and P-selectin-deficient mice

249 t was independent of the platelet GPIb and P-selectin receptors.

250 roteins binding to the cytoplasmic tail of L-selectin regulate L-selectin functions.

251 L-selectin regulates leukocyte adhesion and rolling along

252 ocking their association to fibrinogen and P-selectin, respectively.

253 helial cell adhesion molecule (PECAM1) and L-selectin (SELL) were particularly significant in patient

254 on ex vivo and in vitro, including reduced l-selectin shedding, oxidative burst, chemotaxis, neutroph

255 opose that ADAM17-dependent proteolysis of L-selectin should be considered a regulator of T-cell acti

256 T cells unable to cleave L-selectin showed delayed proliferation in vitro which cor

257 The selectin signaling cascade resembled that used by the TC

258 Plasma soluble P-selectin (sP-selectin) is elevated threefold to fourfold

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

260 d by alphaIIbbeta3 integrin activation and P-selectin surface exposure.

261 contributes to the inhibition of platelet P-selectin surface expression.

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

263 ctors expressing high levels of binding to P-selectin, T-bet, and Blimp-1, and that more of them secr

264 and to explain how phosphorylation of the L-selectin tail abrogates mu1A interaction.

265 mu1A is required for interaction with the L-selectin tail and that L-selectin tail phosphorylation m

266 entify the mu1A surface domain binding the L-selectin tail and to explain how phosphorylation of the

267 3)) in the membrane-proximal domain of the L-selectin tail as well as a doublet of aspartic acid resi

268 serve pool and that phosphorylation of the L-selectin tail blocks AP-1-dependent retrograde transport

269 DD(370)) in the membrane-distal end of the L-selectin tail involved in mu1A binding.

270 ength GST-mu1A did not bind to the phospho-L-selectin tail or phospho-mimetic S364D L-selectin tail.

271 ot the GST-mu1A N-terminal domain, bind to L-selectin tail peptide, and the intracellular pool of L-s

272 eraction with the L-selectin tail and that L-selectin tail phosphorylation may regulate this interact

273 teraction in vivo Molecular docking of the L-selectin tail to mu1A was used to identify the mu1A surf

274 Incubation of the L-selectin tail with cell extracts from phorbol 12-myrista

275 graphy/mass spectrometry to identify novel L-selectin tail-binding proteins.

276 o-L-selectin tail or phospho-mimetic S364D L-selectin tail.

277 ne NCGN model, prophylactic application of E-selectin-targeted immunoliposomes packed with p65 siRNA

278 By encapsulating BYL719 into P-selectin-targeted nanoparticles, we achieve specific acc

279 arkedly greater adhesive interactions with E-selectin than do circulating lymphocytes, which exhibit

280 e ligand binding to WT selectins and to E88D selectins that replaced Glu-88 with Asp.

281 miR-1 recruited P-selectin, thymic stromal lymphopoietin, eotaxin-3, and t

282 -selectin before lymph node egress and use L-selectin to locate to virus-infected tissues.

283 n, both neutrophils and effector T cells use selectins to roll and integrins to arrest in postcapilla

284 ally, TLR4-dependent surface expression of P-selectin triggered an unconventional mechanism of comple

285 ound that mouse Th1 cells rolling on P- or E-selectin triggered signals that promoted alphaLbeta2-dep

286 Dimeric sP-selectin-Fc, but not monomeric sP-selectin, triggered integrin-dependent adhesion of mouse

287 her levels of endotoxin, soluble endothelial selectin, triglycerides, and insulin resistance (r > 0.6

288 e cluster of differentiation 40 ligand and p-selectin (two markers of platelet activation), and zonul

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

290 argeting the endothelial adhesion molecule P-selectin unmasks the pathological events that take place

291 ele(-/-) hosts) or therapeutic blockade of E-selectin using small molecule mimetic GMI-1271/Uprolesel

292 ted with up-regulated expression levels of E-selectin, vascular cell adhesion molecule (VCAM-1), and

293 rdin, and VCAM-1 among African-Americans, sE-selectin, VCAM-1, BFL-1 and Hemopexin among Caucasians,

294 mits tension and catch-bond formation with L-selectin via sLe(x), resulting in focal clusters that de

295 P-selectin was persistently upregulated in PASMCs of human

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

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

298 l damage (syndecan-1, thrombomodulin, and sE-selectin) were measured and demography, injury type and

299 an antibody against the adhesion molecule P-selectin, were evaluated in patients with sickle cell di

300 the release of the proinflammatory ligand, P-selectin, while diverting WPBs carrying non-inflammatory

301 r cells is provided by bone vascular niche E-selectin, whose direct binding to cancer cells promotes