ライフサイエンスコーパス: L-selectin

1 nteric adipose tissues is partly mediated by L-selectin.

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

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

4 ncreased expression of the adhesion molecule L-selectin.

5 molecules is constitutively associated with L-selectin.

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

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

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

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

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

11 -1 (PSGL-1), the leukocyte ligand for P- and L-selectin.

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

13 ire transmembrane and cytoplasmic domains of l-selectin.

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

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

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

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

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

19 -fold increase over T cells unable to cleave L-selectin.

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

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

22 this hypothesis for neutrophils adhering via L-selectin.

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

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

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

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

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

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

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

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

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

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

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

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

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

36 eutrophils enter the lymph node entirely via L-selectin and actively exit via efferent lymphatics via

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

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

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

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

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

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

43 cells expressing cleavable or non-cleavable L-selectin and determined the impact of L-selectin prote

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 have shown that activated T-cells re-express L-selectin before lymph node egress and use L-selectin t

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

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

82 L-selectin blockade also demonstrated significant hepato

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

99 tin in mouse and human T cells and show that L-selectin cleavage does not regulate T cell activation

100 L-selectin cleavage enhances integrin-mediated outside-i

101 Mechanistically, L-selectin cleavage from the neutrophil surface triggere

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

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

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

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

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

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

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

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

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

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

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

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

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

115 We demonstrate that L-selectin-deficient mice are prone to pulmonary infecti

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

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

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

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

120 L-selectin-dependent leukocyte rolling was completely ab

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

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

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

136 grin and metalloproteinase 17 (ADAM17) sheds L-selectin from the neutrophil surface in an IRhom2-depe

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

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

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

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

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

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

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

151 ole for ADAM17 in TCR-induced proteolysis of L-selectin in mouse and human T cells and show that L-se

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

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

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

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

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

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

158 egulation of monocyte recruitment genes (eg, L-selectin) in the macrophage compartment in wild-type m

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

160 L-selectin initiates lymphocyte interactions with high e

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

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

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

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

165 L-selectin is an adhesion molecule expressed by neutroph

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

167 L-selectin is constitutively expressed by neutrophils an

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

206 Thus, L-selectin mechanochemistry limits premature activation

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

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

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

210 L-selectin-mediated leukocyte rolling has been proposed

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

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

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

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

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

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

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

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

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

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

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

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

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

224 L-selectin on T-cells is best known as an adhesion molec

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

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

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

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

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

230 ement of NADPH oxidase activity, shedding of l-selectin, or mobilization of CD11b.

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

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

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

234 However, the molecular mechanism by which L-selectin participates in host defense against Klebsiel

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

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

237 able L-selectin and determined the impact of L-selectin proteolysis on T cell activation in virus-inf

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

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

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

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

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

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

244 L-selectin regulates leukocyte adhesion and rolling alon

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

246 othelial cell adhesion molecule (PECAM1) and L-selectin (SELL) were particularly significant in patie

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

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

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

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

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

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

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

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

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

261 propose that ADAM17-dependent proteolysis of L-selectin should be considered a regulator of T-cell ac

262 T cells unable to cleave L-selectin showed delayed proliferation in vitro which c

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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