ライフサイエンスコーパス: L-selectin

1 late the function and ectodomain shedding of l-selectin.

2 this interaction and the cytoplasmic tail of L-selectin.

3 rotein calmodulin to the cytoplasmic tail of L-selectin.

4 tail and part of the transmembrane domain of L-selectin.

5 of CaM with two peptides derived from human L-selectin.

6 -1 (PSGL-1), the leukocyte ligand for P- and L-selectin.

7 ion in the cremaster muscle are dependent on L-selectin.

8 ire transmembrane and cytoplasmic domains of l-selectin.

9 d their peritoneal influx was independent of L-selectin.

10 P-selectin under flow, which is dependent on L-selectin.

11 inase to elevate MDSC have reduced levels of L-selectin.

12 ios similar to each other but lower than for L-selectin.

13 ng rolling due to the mechanical shedding of L-selectin.

14 ncorporating the shear-dependent shedding of L-selectin.

15 7), an enzyme that cleaves the ectodomain of L-selectin.

16 this hypothesis for neutrophils adhering via L-selectin.

17 ith the increased CEA avidity for E- but not L-selectin.

18 locks AP-1-dependent retrograde transport of L-selectin.

19 ion also increasing cell rolling velocity on L-selectin.

20 membrane domain of the cell adhesion protein l-selectin.

21 The aged subset also expresses low levels of L-selectin.

22 ate expression of the T-cell homing receptor L-selectin.

23 lectin glycoprotein ligand-1 (PSGL-1) and of L-selectin.

24 enesis rescued by coexpression of chimeric E/L-selectin.

25 ncreased expression of the adhesion molecule L-selectin.

26 molecules is constitutively associated with L-selectin.

27 ultured with tumor-induced MDSC have reduced L-selectin; 2) T cells in tumor-free aged mice with elev

28 udies reveal a ligand-specific modulation of L-selectin affinity by DREG-55 mAb, resulting in a drama

29 ells from both groups expressed CXCR3, CCR5, L-selectin, alpha4 integrins, and cutaneous lymphocyte a

30 Importantly, L-selectin also functions as a signaling molecule.

31 nt with this, activation-induced shedding of L-selectin also mediated decreased lubricin binding to P

32 T(reg) cell subsets differentially express L-selectin, an adhesion molecule mediating lymphocyte mi

33 Strikingly, bonds between L-selectin and 6-sulfo-sialyl Lewis X were impervious to

34 ad an effector phenotype because they lacked L-selectin and a higher proportion in diseased mice prod

35 ould monitor the subcellular distribution of L-selectin and better understand how ectodomain shedding

36 talk" in the signaling pathways initiated by L-selectin and CCR7 provides a novel mechanism for funct

37 morphology and localize to T cell areas via L-selectin and CCR7.

38 experiments, the basal surface expression of L-selectin and CD11b was modified neither in murine nor

39 Mac-1 expression, enhanced cell adhesion via L-selectin and CD18 integrins, and degranulation of seco

40 ls isolated from MF skin lesions lacked CCR7/L-selectin and CD27 but strongly expressed CCR4 and CLA,

41 ymph node B cells due to lower expression of L-selectin and failed class-switch recombination due to

42 ed phenotypically by increased expression of L-selectin and functionally by enhanced antitumor immuni

43 lling duration, suggesting a gradual loss of L-selectin and is mediated by p38 mitogen-activated prot

44 curately recreate the mechanical shedding of L-selectin and its effect on the rolling behavior of neu

45 isolated lymphocytes for homing phenotypes (L-selectin and LPAM-1) and state of activation (CD25, CD

46 s (CD4 and CD8) along with homing phenotype (L-selectin and LPAM-1) in naive B (IgD) and antigen-acti

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

48 Heparin prevents mucin binding to P- and L-selectin and mucin-induced microthrombi.

49 he first report, to our knowledge, comparing L-selectin and P-selectin bond formation frequencies in

50 bead system was utilized to measure relative L-selectin and P-selectin bond formation rates on their

51 Dissociation of bonds between L-selectin and P-selectin glycoprotein ligand-1 (PSGL-1)

52 e migratory pattern to LNs, neutrophils used L-selectin and P-selectin glycoprotein ligand-1, macroph

53 mucin-triggered cathepsin G release requires L-selectin and PSGL-1 on neutrophils, P-selectin on plat

54 re the known lectin-like interaction between L-selectin and PSGL-1, the signaling output is dependent

55 Expression of L-selectin and the CCR2 chemokine receptor, both critica

56 otherwise monomeric transmembrane domain of L-selectin and the cytoplasmic domain of ADAM10 produces

57 e force-lifetime relationship between P- and L-selectin and their endogenous ligands have underscored

58 Notably, ligation of L-selectin and/or CCR7 did not result in increased CCR7

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

60 The key lymph node-homing receptors CD62L (L-selectin) and CCR7 were highly expressed on naive T ly

61 expressing lymphoid homing molecules (CCR7, L-selectin) and homeostatic cytokine receptors (IL-7alph

62 elial cells (E- and P-selectin), leukocytes (L-selectin), and platelets (P-selectin) play crucial rol

63 ce with elevated levels of MDSC have reduced L-selectin, and 3) peritoneal exudate T cells of tumor-f

64 The expression of alpha4beta7, L-selectin, and cutaneous lymphocyte antigen (CLA) on S.

65 i activate ectodomain shedding of TNF-alpha, L-selectin, and other transmembrane proteins.

66 d near the tips of microvilli in the case of L-selectin, and sequestered away from the microvillus ti

67 ermal growth factor receptor (EGFR) ligands, l-selectin, and TNF, from the cell surface, thus regulat

68 also elicited neutrophil shedding of surface L-selectin, another indicator of leukocyte activation.

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

70 mmunoreceptors, the extracellular domains of L-selectin are rapidly shed, a process negatively contro

71 sed the lymph node homing molecules CCR7 and L-selectin as well as the differentiation marker CD27, a

72 ligand(s) that mediate binding to lymphocyte L-selectin at conspicuously low shear stress levels of 0

73 iate colon carcinoma cell adhesion to E- and L-selectin at elevated shear stresses.

74 We show phosphorylation of L-selectin at Ser 364 is critical for CaM dissociation,

75 re Ly-6C(hi) monocytes rolled on P-, E-, and L-selectin at slower velocities than Ly-6C(lo) cells.

76 nic shear thresholding was not detected with L-selectin beads rolling on PSGL-1.

77 d the number of rolling leukocytes on P- and L-selectin-bearing substrates by ~85%, and increased med

78 This effect was specific for L-selectin, because vascular cell adhesion molecule 1 (V

79 loyed a chemistry approach to engineer P- or L-selectin binding nucleic acid aptamers onto mesenchyma

80 ding of E- and P-selectin to neutrophils and L-selectin binding to lymph node high endothelial venule

81 L-selectin blockade also demonstrated significant hepato

82 low generated compressive forces may enhance L-selectin bond formation relative to that of P-selectin

83 tion relative to that of P-selectin and that L-selectin bonds with PSGL-1 may be tuned for the compre

84 crovilli was cleaved by force exerted on the L-selectin bonds, the cell detached from the reactive pl

85 e structure of the lectin and EGF domains of L-selectin bound to a fucose mimetic; that is, a termina

86 atelet-rich microthrombi dependent on P- and L-selectin but not thrombin.

87 Blockade of CD8 and L-selectin, but not CD4, ameliorated hepatocellular inju

88 In contrast, L-selectin/CaM interaction remained intact in nontransmi

89 lucidated the molecular basis for the moesin/l-selectin/CaM ternary complex and suggested an importan

90 odeling that the force-dependent shedding of L-selectin can explain the rolling behavior of neutrophi

91 e force probe measurements of various P- and L-selectin catch bonds faithfully predict differences in

92 The transition force for the L-selectin catch-slip transition of 44 pN/bond agreed we

93 ll population and maintain the expression of L-selectin, CCR7, and IL-7R molecules.

94 g signs of increased reactivity: shedding of l-selectin, CD11b upregulation, increased oxidative burs

95 L-selectin (CD62L) is an important molecule in these pro

96 revealed that the lymphocyte homing receptor L-selectin (CD62L) is the key factor controlling the bin

97 patients with CML at diagnosis expressed low l-selectin (CD62L) levels, which was not a result of pro

98 The adhesion molecule L-selectin (CD62L), critical for this process, is highly

99 et by high expression of the homing molecule L-selectin (CD62L).

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

101 ysteine-X-X-cysteine motifs are critical for L-selectin cleavage.

102 ant transmembrane and cytoplasmic domains of l-selectin (CLS) reconstituted in model phospholipid lip

103 neutrophils and slower rolling velocities of L-selectin-coated microspheres, respectively.

104 tail peptide, and the intracellular pool of L-selectin colocalizes with AP-1 at the trans-Golgi netw

105 The PSGL-1-L-selectin complex signals through Src family kinases, I

106 The PSGL-1-L-selectin complex-induced signaling effects on neutroph

107 When most of the L-selectin concentrated on the tips of deformable microv

108 essing surface markers of neutrophils (Ly6G, L-selectin, CXC chemokines receptor 2, and 7/4) and DCs

109 phospholipid bilayer, the positively charged L-selectin cytoplasmic domain of CLS is associated with

110 an bind to ARR18 in aqueous solutions or the L-selectin cytoplasmic domain of CLS reconstituted in th

111 We used L-selectin cytoplasmic tail peptide pulldown assays comb

112 Antibody to L-selectin decreased the engraftment of BCR-ABL1-transdu

113 Intratracheal instillation of L-selectin-deficient (L-Sel(-/-)) mice with an adenoviru

114 BCR-ABL1-expressing L-selectin-deficient progenitors were also defective in

115 Flow augments L-selectin-dependent adhesion by increasing the initial

116 y affects lymphocyte membrane topography and L-selectin-dependent adhesion, which may be linked to de

117 that lubricin is able to bind to PMN via an L-selectin-dependent and -independent manner and may pla

118 uxiliary L-selectin ligand, which stabilizes L-selectin-dependent cell rolling against fluid shear.

119 L-selectin-dependent leukocyte rolling was completely ab

120 of N-glycan-linked 6-sulfo sialyl Lewis X in L-selectin-dependent lymphocyte homing and recruitment.

121 lymph nodes and 2.5-fold increased rates of L-selectin-dependent lymphocyte migration from the blood

122 ng of head and neck squamous cancer cells to L-selectin displays canonical biochemical features, such

123 ical for the resolution of inflammation, and L-selectin downregulation is induced during this process

124 eath receptor-mediated neutrophil apoptosis, L-selectin downregulation occurs primarily by ADAM17-med

125 eatment of microparticles with antibodies to L-selectin (DREG-200) or PSGL-1 (PL-1) significantly (P

126 Although the A108H substitution in L-selectin eliminated the ramp rate responsiveness of it

127 ing PMN and that it partly co-localized with L-selectin expressed by these cells.

128 e most potent ligand for both E-selectin and L-selectin expressed on human cells.

129 Even moderate deficits in L-selectin expression disrupt T cell trafficking to dist

130 ell frequency, FoxP3 expression, and altered L-selectin expression during infection.

131 Interestingly, L-selectin expression was decreased on CLL cells from pa

132 ponses to T-dependent and T-independent Ags, L-selectin expression, and expression of RelA, RelB, and

133 n is not due to CD11/CD18-mediated adhesion, L-selectin expression, or platelet adhesion to neutrophi

134 This was not because of defects in L-selectin expression, shedding, cytoskeletal anchorage,

135 s a mechanism for regulating the shedding of L-selectin following neutrophil stimulation.

136 The leukocyte adhesion receptor L-selectin forms bonds with P-selectin glycoprotein liga

137 mportant role of phospholipids in modulating l-selectin function and shedding.

138 dhesion molecule-1 (VCAM-1), P-selectin, and L-selectin, function to facilitate leukocyte transendoth

139 L-selectin functions as an important adhesion molecule t

140 the cytoplasmic tail of L-selectin regulate L-selectin functions.

141 These cells coexpress CD44 and L-selectin, giving them a surface phenotype similar to t

142 The L-selectin glycoprotein receptor mediates the initial st

143 shear-resistant adhesion to the vessel wall, L-selectin has frequently been reported to be rapidly cl

144 n molecules on human neutrophils reveal that L-selectin has the highest ratio of total internal refle

145 cialized carbohydrate ligands for lymphocyte L-selectin; HEV expression of molecules for transendothe

146 f T1D was associated with an increase in the L-selectin(high) T cell frequencies and enhanced suppres

147 nted the amount of mu1A associated with anti-L-selectin immunoprecipitates.

148 bricin was capable of binding to recombinant L-selectin in a glycosylation-dependent manner.

149 Consistent with the expression levels of L-selectin in different lymphocyte subsets, L-selectin-m

150 lts suggest that the association of CaM with L-selectin in the cell can be influenced by the membrane

151 tly associate with the cytoplasmic domain of l-selectin in the cell to modulate the function and ecto

152 ost likely due to an increased population of L-selectin in the high-affinity conformation as pH decre

153 oth calcium and the transmembrane segment of L-selectin in the interaction between these two proteins

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

155 rolling behavior of neutrophils mediated by L-selectin in vitro.

156 one residue (A108H) in the lectin domain of L-selectin increased its force-free affinity for a glyco

157 L-selectin initiates lymphocyte interactions with high e

158 Selectins (E-, P-, and L-selectins) interact with glycoprotein ligands to media

159 eosinophil surface proteins, including CD69, L-selectin, intercellular adhesion molecule-1 (ICAM-1, C

160 L-selectin is a cell adhesion molecule that tethers free

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

162 L-selectin is an adhesion molecule expressed by neutroph

163 eviously shown that constitutively expressed L-selectin is cleaved from the neutrophil surface during

164 L-selectin is constitutively expressed by neutrophils an

165 During formation of the lamellipod, L-selectin is distributed on microvilli tips along the t

166 It is well established that L-selectin is efficiently shed from the surface of neutr

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

168 Upon neutrophil activation, L-selectin is rapidly and efficiently down-regulated fro

169 Our findings indicate that L-selectin is transported constitutively by the AP-1 com

170 CD62L (L-selectin) is a key regulator of T cell trafficking, an

171 (x), a sulfated carbohydrate determinant for L-selectin, is carried on core 2 and extended core 1 O-g

172 in MDP-induced vascular inflammation because L-selectin knockout mice showed a significant decrease i

173 When compared with microspheres bearing L-selectin, L-selectinA108H microspheres rolled more slo

174 alysis of mixed chimeras shows that enhanced L-selectin levels and accelerated influx were both cell-

175 In contrast, L-selectin levels are elevated up to 10-fold in Adam17-n

176 explanation for the lack of diminished serum L-selectin levels in ADAM17-null mice, and suggests a me

177 m for the homeostatic maintenance of soluble L-selectin levels in the blood of healthy individuals.

178 Therefore, MDSC down-regulate L-selectin levels on naive T cells, decreasing their abi

179 m on MSCs into hematopoietic cell E-selectin/L-selectin ligand (HCELL), which conferred potent E-sele

180 D44 glycoform known as hematopoietic cell E-/L-selectin ligand (HCELL), which functions as a high aff

181 oform of CD44 known as hematopoietic cell E-/L-selectin ligand (HCELL), which is the most potent liga

182 selectin ligands (CD44/hematopoietic cell E-/L-selectin ligand and P-selectin glycoprotein ligand-1)

183 N-glycans bearing the 6-sulfo sialyl Lewis X L-selectin ligand in high endothelial venules.

184 The novel finding that CEA is an E- and L-selectin ligand may explain the enhanced metastatic po

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

186 e found that EG, previously implicated as an L-selectin ligand on endothelial cells, was present on h

187 ), which functions as a high affinity E- and L-selectin ligand on these cells.

188 Selective disruption of L-selectin ligand production did not reduce atherosclero

189 p(I294T) mutation failed to roll normally on L-selectin ligand under flow.

190 cancer cells express heretofore unrecognized L-selectin ligand(s) that mediate binding to lymphocyte

191 ligand HCELL (hematopoietic cell E-selectin/L-selectin ligand) and, despite absence of CXCR4, system

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

193 demonstrate that CEA serves as an auxiliary L-selectin ligand, which stabilizes L-selectin-dependent

194 s exhibited altered dynamic interaction with L-selectin ligand, with a significantly reduced rate of

195 orms (CD44v) as functional P-, but not E- or L-, selectin ligands on colon carcinoma cells.

196 These data define a novel class of L-selectin ligands and expand the scope of function for

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

198 es to assess the functions of O-glycan-borne L-selectin ligands in vivo.

199 nal shear threshold differing from all other L-selectin ligands, including those expressed on colon c

200 he roles of E- and P-selectin ligands versus L-selectin ligands, respectively, in diet-induced athero

201 lymphocyte homing, yet they lacked O-glycan L-selectin ligands.

202 Mechanistically, L-selectin loses association with calmodulin (CaM; a neg

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

204 ne suppression by reducing expression of the L-selectin lymph node (LN) homing receptor on naive T an

205 Of these, Lin(-)Sca-1(+)c-Kit(Hi)Thy1.1(-)L-selectin(+) lymphoid progenitors (LSPs) were the best

206 In this study, we show that the anti-human L-selectin mAbs DREG-55 and LAM1-5 but not DREG-56, DREG

207 Thus, L-selectin mechanochemistry limits premature activation

208 , catch-slip bonds have been shown to govern L-selectin-mediated cell rolling.

209 Pharmacologic inhibitor studies showed that L-selectin-mediated enhanced chemotaxis to SLC required

210 L-selectin in different lymphocyte subsets, L-selectin-mediated enhancement of chemotaxis to SLC was

211 L-selectin-mediated leukocyte rolling has been proposed

212 f T. cruzi, AgC10, is able to interfere with L-selectin-mediated monocyte adhesion.

213 e able to reconstruct the characteristics of L-selectin-mediated neutrophil rolling observed in the e

214 Interference with L-selectin-mediated trafficking in HEVs could represent

215 tonsils), adding to our understanding of how L-selectin mediates lymphocyte homing.

216 lymphoid tissues and effector memory (CCR7-, L-selectin-) mediating immune response in peripheral org

217 low cytometric quantitation of integrins and l-selectin membrane expression.

218 cell adhesion molecule-1, and P-selectin and L-selectin mRNA expression.

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

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

221 tes trafficking of both normal and malignant L-selectin-negative cells to the draining lymph nodes.

222 initiated by an adhesive interaction between L-selectin on lymphocytes and peripheral node addressin

223 is mediated by specific interaction between L-selectin on lymphocytes and the carbohydrate ligand 6-

224 lymph node migration assays, the absence of L-selectin on lymphocytes significantly attenuated both

225 elial cells of efferent lymphatics, it binds L-selectin on lymphocytes.

226 demonstrate that MDSC directly down-regulate L-selectin on naive T cells: 1) naive T cells cocultured

227 sialyl Lewis(X) present on salival mucins to l-selectin on neutrophils.

228 -selectin to regulate ectodomain shedding of L-selectin on the other side of the plasma membrane.

229 BALB/c mice and mice deficient in L-selectin or NOD2 received intravitreal injection of MD

230 and not an increase in microparticle surface L-selectin or PSGL-1 expression.

231 Antibodies to L-selectin or PSGL-1 had no effect on IL-8-induced migra

232 hesion molecules (CD49d, CD18, CD11a, CD11b, L-selectin) or of the chemokine receptor CCR3, but decre

233 n P-selectin glycoprotein ligand-1 (PSGL-1), L-selectin, or CD11b levels but caused PSGL-1 redistribu

234 uired trafficking molecules, including CCR9, L selectin, P selectin glycoprotein ligand-1, the integr

235 e 6-O-sulfation and is caused by blockade of L-selectin-, P-selectin-, and CXCL12-mediated leukocyte

236 The adhesion molecule L-selectin participated in MDP-induced vascular inflamma

237 ages of induced leukocyte apoptosis, soluble L-selectin production occurred independent of ADAM17, as

238 receptors involved in the adhesion cascade: L-selectin, PSGL-1, Mac-1, and LFA-1 for resting, spheri

239 In the case of L-selectin/PSGL-1 binding dynamics, the binding strength

240 whereas the velocities are due to increased L-selectin/PSGL-1 contacts.

241 es faster than rolling associated molecules (L-selectin; PSGL-1), but that the mobilities within each

242 rther subdivided into central memory (CCR7+, L-selectin+), recirculating through lymphoid tissues and

243 Proteins binding to the cytoplasmic tail of L-selectin regulate L-selectin functions.

244 L-selectin regulates leukocyte adhesion and rolling alon

245 L-selectin requires a threshold shear to enable leukocyt

246 responds to the entire cytoplasmic domain of L-selectin (residues Ala317-Tyr334 in the mature protein

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

248 both alpha(M)beta(2) integrin activation and L-selectin shedding after stimulation with 0.5 nM of fML

249 indicators of neutrophil activation, such as L-selectin shedding and alpha(M)beta(2) integrin activat

250 er neutrophil activation via FPR by reducing L-selectin shedding and alpha(M)beta(2) integrin activat

251 o the focus of infection, as well as induced l-selectin shedding and rise in CD11b of blood neutrophi

252 In addition, the mechanical L-selectin shedding causes an increase in cell rolling v

253 We conclude that L-selectin shedding directly regulates polarity in trans

254 AgC10 is likely due to its ability to induce L-selectin shedding from the monocyte membrane, since ph

255 nt of neutrophils with H(2)O(2) also induced L-selectin shedding in an ADAM17-dependent manner.

256 sing advanced imaging techniques, we observe L-selectin shedding occurring exclusively as primary hum

257 Pharmacological or genetic inhibition of L-selectin shedding significantly increased pseudopodial

258 AF-induced neutrophil activation in terms of L-selectin shedding, alphaMbeta2 integrin activation, an

259 tion ex vivo and in vitro, including reduced l-selectin shedding, oxidative burst, chemotaxis, neutro

260 RvE1 in the 10- to 100-nM range stimulated L-selectin shedding, while reducing CD18 expression in b

261 monstrated by increased CD11b expression and L-selectin shedding.

262 ed in human FUT4(-)7(-) dual knockdowns on P/L-selectin substrates.

263 embled the effect of a point mutation at the L-selectin surface (L-selectinA108H) predicted to contac

264 ion into the peritoneum in spite of elevated L-selectin surface levels, and their peritoneal influx w

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

266 of mu1A is required for interaction with the L-selectin tail and that L-selectin tail phosphorylation

267 identify the mu1A surface domain binding the L-selectin tail and to explain how phosphorylation of th

268 363)) in the membrane-proximal domain of the L-selectin tail as well as a doublet of aspartic acid re

269 reserve pool and that phosphorylation of the L-selectin tail blocks AP-1-dependent retrograde transpo

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

271 -length GST-mu1A did not bind to the phospho-L-selectin tail or phospho-mimetic S364D L-selectin tail

272 not the GST-mu1A N-terminal domain, bind to L-selectin tail peptide, and the intracellular pool of L

273 nteraction with the L-selectin tail and that L-selectin tail phosphorylation may regulate this intera

274 interaction in vivo Molecular docking of the L-selectin tail to mu1A was used to identify the mu1A su

275 Incubation of the L-selectin tail with cell extracts from phorbol 12-myris

276 tography/mass spectrometry to identify novel L-selectin tail-binding proteins.

277 pho-L-selectin tail or phospho-mimetic S364D L-selectin tail.

278 In contrast, L-selectin tether bond formation increased from 0.017 +/

279 L-selectin tether bond formation rates appeared to be en

280 t the shorter lifetimes of PSGL-1 bonds with L-selectin than P-selectin.

281 trate that the reduction in T cell levels of L-selectin that is commonly seen in individuals with can

282 lled the expression of the adhesion molecule L-selectin, the chemokine receptor CCR7 and the transcri

283 In contrast to P- and L-selectin, the E-selectin/PSGL-1 binding does not exhib

284 MDSC are likely to down-regulate L-selectin through their plasma membrane expression of A

285 ectin-dependent redistribution of PSGL-1 and L-selectin to a major pole on slowly rolling leukocytes

286 results distinguish molecular mechanisms for L-selectin to bind to PSGL-1 and peripheral node address

287 These N-glycans supported the binding of L-selectin to high endothelial venules in vitro and cont

288 rrelated with stronger binding of neutrophil L-selectin to mutant endothelial cells.

289 n, associates with the cytoplasmic domain of L-selectin to regulate ectodomain shedding of L-selectin

290 on of U937 monocytic cells stably expressing L-selectin (U937LAM) with AgC10 strongly reduced their a

291 ces pancreatic cancer cell binding to E- and L-selectin under flow.

292 this study, signaling induced by ligation of L-selectin using mAb or endothelial cell-expressed ligan

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

294 he PPV (P = .000) and PCV (P = .029) groups, L-selectin was expressed more frequently in the PPV grou

295 pneumoniae-specific plasmablasts expressing L-selectin was high, the proportion expressing alpha4bet

296 eg) cells expressed 30-40% more cell surface L-selectin when its endoproteolytic cleavage was blocked

297 The interactions of P- and L- selectins with their respective ligands exhibit catch

298 utrophils into TDLNs through interactions of l-selectin with HEV-expressed peripheral lymph node addr

299 ecede catch bonds for interactions of P- and L-selectin with their ligands.

300 ligands and expand the scope of function for L-selectin within circulatory systems to now include a n