ライフサイエンスコーパス: selectin

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

2 sed microparticles of iron oxide targeting P-selectin.

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

4 of matrix metalloproteinase-8 and soluble E-selectin.

5 o decreased the upregulation of ICAM-1 and P-selectin.

6 n also increasing cell rolling velocity on L-selectin.

7 endothelial activation and the presence of E-selectin.

8 on with PSGL-1 in Th1 cells for binding to E-selectin.

9 We focused on Efb interaction with P-selectin.

10 mbrane domain of the cell adhesion protein l-selectin.

11 endothelium in ischemic tissues, including E-selectin.

12 g that CD43 alone is a dominant ligand for E-selectin.

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

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

15 tion in tethering and rolling density on all selectins.

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

17 24.4 +/- 13.3 ng/mL, P < 0.0001), soluble p-selectin (14.2 +/- 4.05 versus 33.2 +/- 15.2 ng/mL, P <

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

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

20 Platelet count and P-selectin (a ubiquitous cargo of alpha-granules) were not

21 to characterize their rolling behavior on E-selectin, a critical step in leukocyte recruitment durin

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

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

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

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

26 ld monitor the subcellular distribution of L-selectin and better understand how ectodomain shedding m

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

28 Infected cells rolled on E-selectin and endothelial surfaces, and this rolling was

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

30 E-selectin and ICAM-1 expression are essential for leukocy

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

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

33 ulation of cell-surface adhesion molecules E-selectin and ICAM-1.

34 ue endothelium and BMD-EPC to express both E-selectin and its ligands.

35 s including peripheral node addressin, E-, L-selectin and Mac-1 but not P-selectin or LFA-1.

36 ndothelial cells constitutively synthesize P-selectin and mobilize it to the plasma membrane to media

37 followed by immunoblotting, we identified P-selectin and multimerin-1 as novel Efb interaction partn

38 The interaction of both P-selectin and multimerin-1 with Efb is independent of fib

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

40 te basal and inducible expression of human P-selectin and reveal human-specific differences in P-sele

41 Soluble endothelial selectin and soluble intercellular adhesion molecule con

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

43 -126* and miR-126 downregulation increased E-selectin and VCAM1, respectively, while miR-126 overexpr

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

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

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

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

48 culation of healthy individuals are CD41(+)P-selectin(+)and that distinct binding of patient plasma P

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

50 sed by shedding of endothelial E-selectin, P-selectin, and alphavbeta3 integrin, and leukocyte CD44 a

51 ions of plasminogen activator inhibitor-1, E-selectin, and angiopoietin-2 as markers of endothelial a

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

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

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

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

56 rface CD42b, unstimulated platelet surface P-selectin, and platelet forward light scatter (FSC) were

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

58 nged with LPS through an increase in TLR4, E-selectin, and VCAM-1 and ultimately through enhanced leu

59 tivating peptide (TRAP)-stimulated percent P-selectin- and activated glycoprotein (GP)IIb-IIIa-positi

60 tically, FGF23 binding to FGFR2 counteracted selectin- and chemokine-triggered beta2 integrin activat

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

62 Selectins are carbohydrate-binding adhesion molecules th

63 Selectins are vascular receptors facilitating interactio

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

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

66 lter plasminogen activator inhibitor-1 and E-selectin associations with delirium, suggesting that the

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

68 Activated platelets that expressed P-selectin attached to vascular endothelium and macrophage

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

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

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

72 fb-N interaction with P-selectin inhibited P-selectin binding to its physiological ligand, P-selectin

73 L-selectin blockade also demonstrated significant hepatopr

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

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

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

77 oxylin-eosin staining) and for expression of selectins (by using quantitative immunofluorescence anal

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

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

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

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

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

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

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

85 mor necrosis factor-alpha, E selectin, and P selectin, compared with controls.

86 ents diabetes-induced increases in soluble P-selectin concentrations and limits the impact of the dis

87 that are responsible for binding to P- and E-selectins constitutively expressed by the marrow microva

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

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

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

91 ion) 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 t

92 out E-selectin ligands, were attenuated in E-selectin-deficient mice.

93 ignificantly enhanced, indicating that the P-selectin(DeltaCT/DeltaCT) neutrophils were primed for NE

94 All three glycan families contributed to E-selectin dependent cell adhesion with N-glycans contribu

95 rophil rolling and strongly reduced L- and E-selectin-dependent adhesion in airway postcapillary venu

96 lasticity consisted of rapid and selective P-selectin-dependent binding of PMPs to a CCR6(+)HLA-DR(+)

97 on of tumor cells through the induction of E-selectin-dependent endothelial retractions and a subsequ

98 NA during contact hypersensitivity reduced P-selectin-dependent inflammation in Selp(KI) (/-) mice.

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

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

101 However, TNF-alpha did not further reduce P-selectin-dependent rolling velocities.

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

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

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

105 ating platelet-monocyte aggregates (PMAs), p-selectin expression (P-SEL), and integrin alphaIIbbeta3

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

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

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

109 ificant reductions in stimulated (ex vivo) P-selectin expression compared with the placebo group (P <

110 Even moderate deficits in L-selectin expression disrupt T cell trafficking to distan

111 elet integrin alphaIIbbeta3 activation and P-selectin expression in a Toll-like receptor 2 (TLR2)-dep

112 inhibition reduced fibrinogen binding and P-selectin expression of d12 platelet-like particles (PLPs

113 Interestingly, L-selectin expression was decreased on CLL cells from pati

114 ima) and endothelial activation (increased P-selectin expression).

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

116 ivation, resulting in enhanced endothelial E-selectin expression.

117 -1, vascular cell adhesion molecule-1, and E-selectin expressions are markedly up-regulated in the en

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

119 Excess of P-selectin extracellular domain significantly impaired Efb

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

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

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

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

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

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

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

127 n and reveal human-specific differences in P-selectin function.

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

129 We demonstrate Th17 cells express CD44, P-selectin glycoprotein ligand (PSGL)-1, and CD43.

130 with neutrophil activation, rolling ligand P-selectin glycoprotein ligand 1 (PSGL-1) expression, as w

131 and rejected grafts express high levels of P-selectin glycoprotein ligand 1 and glycosylated CD43.

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

133 P-selectin glycoprotein ligand-1 (PSGL-1) and its glycostr

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

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

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

137 ectin binding to its physiological ligand, P-selectin glycoprotein ligand-1 (PSGL-1), both in cell ly

138 ted the function of the adhesion molecule, P-selectin glycoprotein ligand-1 (PSGL-1), that is upregul

139 travascular neutrophils through P-selectin/P-selectin glycoprotein ligand-1 (PSGL-1)-mediated binding

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

141 s was induced in female wild-type (WT) and P-selectin glycoprotein ligand-1 deficient (Psgl-1(-/-)) m

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

143 regs, forming the Sialyl Lewis X moiety on P-selectin glycoprotein ligand-1, would improve their traf

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

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

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

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

148 Correlations among changes in E-selectin, IL-6, and DM-related variables suggest that t2

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

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

151 mistry to investigate expression of P- and E-selectin in rejected versus accepted allografts and lymp

152 Higher basal P-selectin in Selp(KI) (/) (KI) mice compensated for this

153 pression, leukocytes rolled more slowly on P-selectin in trauma-stimulated venules of Selp(KI) (/) (K

154 ts in significant elevation of circulating L-selectin in tumor-bearing mice.

155 ferences in expression of human and murine P-selectin in vivo.

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

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

158 Efb-N interaction with P-selectin inhibited P-selectin binding to its physiologic

159 Selectin interactions with fucosylated glycan ligands me

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

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

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

163 findings provide evidence that endothelial E-selectin is a novel factor contributing to endothelial r

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

165 dies show that leukocyte rolling on P- and L-selectin is ablated in cells lacking O-glycans, with N-g

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

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

168 ng by activated platelets, suggesting that P-selectin is the main receptor for Efb on the surface of

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

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

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

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

173 E-selectin levels were significantly correlated with DM-re

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

175 and Gcnt1, glycosyltransferases critical for selectin ligand biosynthesis, but they were not required

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

177 nal mechanisms that underlie cytokine-driven selectin ligand expression are poorly understood.

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

179 iate upstream activator of p38 MAPK, induced selectin ligand expression equivalent to that of cytokin

180 demethylation within the fut7 gene controls selectin ligand expression in mice and humans, including

181 d2/Smad3 doubly deficient CD4 cells restored selectin ligand expression to wild-type levels.

182 he FUT7 gene whereas hepatocytes, which lack selectin ligand expression, exhibited extensive methylat

183 findings demonstrate that CD43 is a major E-selectin ligand in Th17 cells that functions independent

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

185 tly required via Runx2 for TGF-beta1-induced selectin ligand induction on murine CD4 T cells.

186 ld of TGF-beta1 signal strength required for selectin ligand induction.

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

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

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

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

191 vely, we demonstrate that upregulated dual E-selectin/ligand pairs reciprocally expressed on ischemic

192 E- and P-selectin ligands (E- and P-ligs) guide effector memory T

193 node flow cytometry to assess expression of selectin ligands by effector T cells.

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

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

196 regulating the biosynthesis of E-, P-, and L-selectin ligands in humans.

197 terize the expression and functionality of E-selectin ligands in Th type 17 lymphocytes (Th17 cells)

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

199 rs Smad2, Smad3, or Smad4, that induction of selectin ligands on CD4 cells in response to TGF-beta1 r

200 Induction of selectin ligands on T cells is controlled primarily by c

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

202 tastasis using murine tumor cells, without E-selectin ligands, were attenuated in E-selectin-deficien

203 ory processes by interacting with lymphocyte selectin ligands.

204 circulating EPC, which express counterpart E-selectin ligands.

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 MDSC-induced L-selectin loss occurs through a contact-dependent, post-t

209 suppression by reducing expression of the L-selectin lymph node (LN) homing receptor on naive T and

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

211 geting lymphocyte CD4 (MBCD4), endothelial P-selectin (MBPSel), or isotype control antibody (MBIso) a

212 Thus, L-selectin mechanochemistry limits premature activation of

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

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

215 Endothelial E- and P-selectins mediate lymphocyte trafficking in inflammatory

216 E-selectin-mediated rolling facilitates pancreatic cancer

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

218 E-selectin-mediated rolling transmits signals into neutrop

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

220 n mediate T cell recruitment to the graft, E-selectin mediates APC trafficking to lymphoid tissue, an

221 transplantation using E-selectin(-/-) and E-selectin(+/+) mice as the donors and recipients respecti

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

223 RNA in tissues but only slightly increased P-selectin mRNA after injection of TNF-alpha or LPS.

224 Blunted up-regulation of P-selectin mRNA during contact hypersensitivity reduced P-

225 rease P-selectin mRNA in mice but decrease P-selectin mRNA in humans.

226 terleukin 1beta, and LPS markedly increase P-selectin mRNA in mice but decrease P-selectin mRNA in hu

227 ssed more P-selectin on platelets and more P-selectin mRNA in tissues but only slightly increased P-s

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

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

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

231 Using P- and E-selectin neutralizing antibodies, we evaluated the effec

232 Immunohistochemical staining for ICAM-1, P-selectin, nitrotyrosine, and poly(ADP)ribose showed a po

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

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

235 /) (KI) mice constitutively expressed more P-selectin on platelets and more P-selectin mRNA in tissue

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

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

238 (-/-) platelets displayed no difference in P-selectin or alphaIIbbeta3 activation upon stimulation wi

239 and the interactions between monocytes and E-selectin or aortic endothelium under flow were character

240 ddressin, E-, L-selectin and Mac-1 but not P-selectin or LFA-1.

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

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

243 sion molecules (CD49d, CD18, CD11a, CD11b, L-selectin) or of the chemokine receptor CCR3, but decreas

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

245 on was reversed by shedding of endothelial E-selectin, P-selectin, and alphavbeta3 integrin, and leuk

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

247 dhere to intravascular neutrophils through P-selectin/P-selectin glycoprotein ligand-1 (PSGL-1)-media

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

249 strongly correlated with plasma levels of P-selectin, platelet factor 4, and platelet basic protein

250 o additional receptor-ligand interactions, P-selectin &PSGL-1 and Notch &DLL1.

251 Because of the importance of P-selectin-PSGL-1 binding in the interaction between plate

252 an immunoregulatory role via inhibition of P-selectin-PSGL-1-dependent formation of platelet-leukocyt

253 Anti-E-selectin reduced the number of mature antigen-presenting

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

255 L-selectin regulates leukocyte adhesion and rolling along

256 d endothelium, but the role of endothelial E-selectin remains unclear.

257 lar cell adhesion molecule-1 (VCAM-1), and E-selectin, resulting in a decreased adhesion of leukocyte

258 rend for a reduction of sVCAM-1, sICAM-1, sP-selectin, SBP, and DBP after 6 wk of hesperidin treatmen

259 Thus, endothelial E-selectin shapes the tumor microenvironment through the r

260 mechanism that is independent of the major L-selectin sheddase, ADAM17, but results in significant el

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

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

263 lar adhesion molecule-1 (sICAM-1), soluble P-selectin (sP-selectin), systolic blood pressure (SBP), a

264 mbrane-labeled mouse neutrophils rolled on P-selectin substrate at 10 dyn/cm(2).

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

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

267 molecule-1 (sICAM-1), soluble P-selectin (sP-selectin), systolic blood pressure (SBP), and diastolic

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

285 f microRNA (miR)-146a and miR-181b with an E-selectin-targeting multistage vector (ESTA-MSV) to infla

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

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

288 Anti-E-selectin treatment delayed graft rejection and increased

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

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

291 -1(-/-)CD43(-/-) Th17 cells accumulated on E-selectin under shear flow conditions compared with wild-

292 es regulating human myeloid cell adhesion to selectins under physiological shear-flow observed during

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

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

295 ated WT PAEC, increasing the expression of E-selectin, vascular cell adhesion molecule-1, intercellul

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

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

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

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

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