ライフサイエンスコーパス: PSGL-1

1 PSGL-1 also regulates T cell migration during homeostasi

2 PSGL-1 function was studied in our autoperfusion assay,

3 PSGL-1 interactions with endothelial selectins activate

4 PSGL-1 played a major role in the initial leukocyte capt

5 PSGL-1 was detected in venules of mesenteric lymph node

6 PSGL-1(lo) T cells from MRL(lpr) mice express CXCR4, loc

7 PSGL-1-deficient mice cleared the virus due to increased

8 PSGL-1/P-selectin interaction also is involved in the co

9 ans that decorate P selectin glycoprotein 1 (PSGL-1) and other glycoproteins is critical for infectio

10 in for its ligand P-selectin glycoprotein 1 (PSGL-1) and thereby the strength of P-selectin-mediated

11 SL-1), or in both P-selectin glycoprotein-1 (PSGL-1) and ESL-1, to explore and compare the contributi

12 lectin and P-selectin glycoprotein ligand 1 (PSGL-1) are critically involved in this process.

13 lectin and P-selectin glycoprotein ligand 1 (PSGL-1) are vascular adhesion molecules that play an imp

14 l usage of P-selectin glycoprotein ligand 1 (PSGL-1) as a receptor for adhesion and entry.

15 ing ligand P-selectin glycoprotein ligand 1 (PSGL-1) expression, as well as established cardiovascula

16 s, whereas P-selectin glycoprotein ligand 1 (PSGL-1) neutralization attenuated both the adoptively tr

17 tins, only P-selectin glycoprotein ligand 1 (PSGL-1), which also acts as an E-selectin ligand, has be

18 s CD45 and P-selectin glycoprotein ligand 1 (PSGL-1).

19 ulation of P-selectin glycoprotein ligand 1 (PSGL-1; also known as CD162).

20 electin or P-selectin glycoprotein ligand-1 (PSGL-1) alone inhibited platelet-neutrophil adhesion by

21 P-selectin glycoprotein ligand-1 (PSGL-1) and its glycostructural determinants facilitate

22 ression of P-selectin glycoprotein ligand-1 (PSGL-1) and of L-selectin.

23 gnition of P-selectin glycoprotein ligand-1 (PSGL-1) and the alpha2,3-sialylated- and alpha1,3-fucosy

24 , and that P-selectin glycoprotein ligand-1 (PSGL-1) and the integrins alphaLbeta2 (LFA-1) and alphaM

25 identified P-selectin glycoprotein ligand-1 (PSGL-1) as the essential E-selectin ligand and Fgr as th

26 pronounced P-selectin glycoprotein ligand-1 (PSGL-1) begin to increase only late in fetal life.

27 P-selectin glycoprotein ligand-1 (PSGL-1) binding to P-selectin controls early leukocyte r

28 -GSP-6) on P-selectin glycoprotein ligand-1 (PSGL-1) but not for a sulfated-glycan binding site (6-su

29 binding to P-selectin glycoprotein ligand-1 (PSGL-1) can activate the beta(2) integrin lymphocyte fun

30 icient for P-selectin glycoprotein ligand-1 (PSGL-1) develop a more severe form of experimental autoi

31 pressed in P-selectin glycoprotein ligand-1 (PSGL-1) from neutrophils at higher levels compared with

32 P-selectin glycoprotein ligand-1 (PSGL-1) has long been studied as an adhesion molecule in

33 leukocyte P-selectin glycoprotein ligand-1 (PSGL-1) in humans and mice.

34 e-anchored P-selectin glycoprotein ligand-1 (PSGL-1) inhibited integrin-dependent cell spreading.

35 er or anti-P-selectin glycoprotein ligand-1 (PSGL-1) inhibitory antibody but was not induced by plate

36 P-selectin glycoprotein ligand-1 (PSGL-1) is a homodimeric transmembrane mucin on leukocyt

37 P-selectin glycoprotein ligand-1 (PSGL-1) is constitutively expressed on leukocytes and wa

38 tro, where P-selectin-glycoprotein-ligand-1 (PSGL-1) is found in discrete sticky patches whereas LFA-

39 lectin and P-selectin glycoprotein ligand-1 (PSGL-1) loaded at a constant ramp rate to a constant hol

40 P-selectin glycoprotein ligand-1 (PSGL-1) mediates the capture (tethering) of free-flowing

41 P-selectin glycoprotein ligand-1 (PSGL-1) mediates the initial tethering of leukocytes to

42 subset of P-selectin glycoprotein ligand-1 (PSGL-1) molecules is constitutively associated with L-se

43 at involve P-selectin glycoprotein ligand-1 (PSGL-1) on MM cells and its interaction with selectins i

44 bonds with P-selectin glycoprotein ligand-1 (PSGL-1) on other leukocytes and with peripheral node add

45 involving P-selectin glycoprotein ligand-1 (PSGL-1) on the microvesicles and P-selectin on the plate

46 ocytes use P-selectin glycoprotein ligand-1 (PSGL-1) to roll on P-selectin and E-selectin and to acti

47 mon ligand P-selectin glycoprotein ligand-1 (PSGL-1) under shear flow.

48 lectin) to P-selectin glycoprotein ligand-1 (PSGL-1) via computational modeling (molecular dynamics)

49 P-selectin glycoprotein ligand-1 (PSGL-1) was identified as the major ligand facilitating

50 splayed by P-selectin glycoprotein ligand-1 (PSGL-1) with sialylated O-glycans expressed by CD43.

51 P-selectin glycoprotein ligand-1 (PSGL-1), a heavily glycosylated sialomucin expressed on

52 nophils of P-selectin glycoprotein ligand-1 (PSGL-1), a receptor for P-selectin that causes activatio

53 1 (ESL-1), P-selectin glycoprotein ligand-1 (PSGL-1), and CD44 encompassed all endothelial-selectin l

54 in, engage P-selectin glycoprotein ligand-1 (PSGL-1), and signal extension of integrin alpha(L)beta(2

55 al ligand, P-selectin glycoprotein ligand-1 (PSGL-1), both in cell lysates and in cell-free assays.

56 P-selectin glycoprotein ligand-1 (PSGL-1), CD43, and CD44 are O-glycosylated proteins on l

57 gests that P-selectin glycoprotein ligand-1 (PSGL-1), E-selectin ligand-1 (ESL-1), and CD44 encompass

58 effect on P-selectin glycoprotein ligand-1 (PSGL-1), L-selectin, or CD11b levels but caused PSGL-1 r

59 molecule, P-selectin glycoprotein ligand-1 (PSGL-1), that is upregulated on responding T cells.

60 esize that P-selectin glycoprotein ligand-1 (PSGL-1), the common ligand of P- and E-selectin on leuko

61 ce lacking P-selectin glycoprotein ligand-1 (PSGL-1), the leukocyte ligand for P- and L-selectin.

62 P-selectin/P-selectin glycoprotein ligand-1 (PSGL-1)-mediated binding, a primary interaction that all

63 apped with P-selectin glycoprotein ligand-1 (PSGL-1).

64 in-ligand, P-selectin glycoprotein ligand-1 (PSGL-1).

65 coprotein, P-selectin Glycoprotein Ligand-1 (PSGL-1).

66 ng through P-selectin glycoprotein ligand-1 (PSGL-1)/Akt/mTOR that resulted in synthesis of ROCK-1, b

67 e molecule P-selectin glycoprotein ligand-1 (PSGL-1, CD162) are important because they bind all selec

68 54), CD44, P-selectin glycoprotein ligand-1 (PSGL-1, CD162), cytokine receptors, Fc receptors, integr

69 r ovary cells transfected to express PSGL-1 (PSGL-1 CHO) were compared.

70 machinery (P-selectin glycoprotein ligand-1 [PSGL-1] and Sialyl-Lewis(x) [SLeX]) to rapidly target in

71 y DCs bound PSGL-1 CHO cells and did so in a PSGL-1-blocking antibody-inhibitable manner.

72 elium compared with Ly-6C(lo) monocytes in a PSGL-1-dependent manner.

73 n or Arg-337 and Lys-338 mutations abrogated PSGL-1-induced ERK activation, whereas they did not prev

74 In addition, PSGL-1(null) CD8(+) T cell proliferation was observed un

75 Although PSGL-1(null) T cells were less efficient at entering lym

76 villus tips in the case of LFA-1, Mac-1, and PSGL-1.

77 oE(-/-) mice, and mice lacking both ApoE and PSGL-1 genes (ApoE(-/-)/PSGL-1(-/-)).

78 s observed under steady-state conditions and PSGL-1(null) CD8(+) T cells were found to be hyperrespon

79 on (f), membrane tether growth dynamics, and PSGL-1/P-selectin binding lifetime.

80 for up-regulation of beta(2) -integrins and PSGL-1 on circulating eosinophils following segmental an

81 w demonstrated that PSGL-1 messenger RNA and PSGL-1 protein expression remained on endothelium, local

82 cathepsin G release requires L-selectin and PSGL-1 on neutrophils, P-selectin on platelets, and Src

83 ctin-like interaction between L-selectin and PSGL-1, the signaling output is dependent on this intera

84 -rich lipid rafts and found that both TF and PSGL-1, but not CD45, localize to lipid rafts in blood m

85 was impaired as compared with wild-type and PSGL-1(-/-), and similar to that observed for PSGL-1(-/-

86 c liver transplantation (OLT)) using an anti-PSGL-1 Ab with diminished Fc-mediated effector function.

87 sine kinases when plated on immobilized anti-PSGL-1 or anti-CD44 F(ab')2.

88 nd reperfusion model, pretreatment with anti-PSGL-1 Ab improved portal venous flow, increased bile pr

89 C1galt1(-/-) neutrophils incubated with anti-PSGL-1 F(ab')2 did not generate microparticles.

90 ApoE(-/-)/PSGL-1(-/-) mice also developed smaller neointima and at

91 acking both ApoE and PSGL-1 genes (ApoE(-/-)/PSGL-1(-/-)).

92 Moreover, ApoE(-/-)/PSGL-1(-/-) mice exhibited significantly reduced monocyt

93 ause they serve as adaptor molecules between PSGL-1 and Syk, we examined the role of PSGL-1 ERM-bindi

94 The temporal overlap between PSGL-1 and P-selectin up-regulation reveals an as yet un

95 These results demonstrate that both PSGL-1 and CD43 are major E-selectin ligands and are lik

96 Only DCs bound PSGL-1 CHO cells and did so in a PSGL-1-blocking antibod

97 conformation through signaling triggered by PSGL-1 engagement.

98 ocytes were released from the vasculature by PSGL-1 blockade, a large peripheral blood leukocyte (PBL

99 mitation, truncated forms of PSGL-1, called "PSGL-1 peptide probes," were developed.

100 L-1), L-selectin, or CD11b levels but caused PSGL-1 redistribution.

101 ns, including CD43, CD44, CD45, CD93, CD162 (PSGL-1; P-selectin glycoprotein ligand 1), and the surfa

102 follicular CD44(hi)CD62(lo)PSGL-1(lo)CD4(+) (PSGL-1(lo)CD4(+)) T cells.

103 Unlike chemokines, PSGL-1 did not signal cytoskeleton-dependent swing out o

104 te with a specific subset of UDMs containing PSGL-1, CD43, and CD44 but not ICAM-1, ICAM-3, or CD59.

105 In marked contrast, PSGL-1, CD43, and CD44 moved normally to the uropods of

106 de-resident CD4(+) ICOS(+) CXCR4(+) CXCR5(+) PSGL-1(lo) PD-1(hi) cells.

107 stigated mechanisms of P-selectin-dependent, PSGL-1-independent rolling using intravital microscopy.

108 Converting dimeric PSGL-1 to a monomer by replacing its transmembrane domai

109 all, of the uropod-directed proteins, i.e., PSGL-1, CD43, and CD44, in nonpolarized T cells.

110 We examined the effects of early PSGL-1 blockade in rat liver models of cold ischemia, fo

111 d leukocyte (PBL) population showed elevated PSGL-1, which could account for the reduced PSGL-1 in th

112 Endothelial PSGL-1 bound P-selectin-IgG and its blockade or genetic

113 ed through L-selectin N138G after it engages PSGL-1 or PNAd.

114 We generated "DeltaCD" mice that express PSGL-1 without the cytoplasmic domain.

115 e hamster ovary cells transfected to express PSGL-1 (PSGL-1 CHO) were compared.

116 Few PSGL-1(-/-)CD43(-/-) Th17 cells accumulated on E-selecti

117 BCR-ABL1-expressing cells deficient for PSGL-1 or the selectin ligand-synthesizing enzymes core-

118 SGL-1(-/-), and similar to that observed for PSGL-1(-/-)CD43(-/-) Th17 cells, indicating that CD43 al

119 ins did not activate platelets in blood from PSGL-1-deficient mice.

120 rate responsiveness of its dissociation from PSGL-1, the inverse mutation H108A in P-selectin acquire

121 as a T-cell E-selectin ligand distinct from PSGL-1 expands the role of CD43 in the regulation of T-c

122 Macrophages from PSGL-1-deficient mice recapitulated pharmacological inhi

123 -1 into bone marrow-derived macrophages from PSGL-1-deficient mice, we show that PSGL-1 required neit

124 ransferase 4 and 7 do not express functional PSGL-1, and do not home efficiently to the thymus.

125 s provide surprising evidence for functional PSGL-1 up-regulation in PBLs during acute inflammation.

126 dy, we examined the expression of functional PSGL-1 on bone marrow hematopoietic progenitors.

127 k shows the surprising finding of functional PSGL-1 up-regulation during acute inflammation.

128 We demonstrate that functional PSGL-1 is expressed at low levels on hematopoietic stem

129 Furthermore, PSGL-1 blockade was significantly more effective in redu

130 he matrix domain of Gag are required for Gag-PSGL-1 coclustering.

131 Furthermore, we have generated PSGL-1(-/-)/CD43(-/-) double-deficient mice (double knoc

132 te these disturbances in T cell homeostasis, PSGL-1(null) mice exhibited a normal acute response (day

133 Lipid microbubbles bearing recombinant human PSGL-1 (MB(YSPSL)) or P-selectin antibody (MB(Ab)) were

134 ted contrast agent bearing recombinant human PSGL-1 can detect myocardial ischemia hours after resolu

135 Ischemic memory imaging using human PSGL-1 as a targeting moiety may extend the time window

136 myosin tension in neutrophils did not impair PSGL-1- or chemokine-mediated integrin extension.

137 epitope and N-acetyl lactosamine content in PSGL-1 was also noted on 4F-GalNAc addition.

138 , EG increased with a concurrent decrease in PSGL-1.

139 rophils, but only the combined deficiency in PSGL-1 and ESL-1 completely abrogated leukocyte recruitm

140 isturbances in T cell homeostasis present in PSGL-1(null) mice.

141 mpanied by an approximately 20% reduction in PSGL-1 glycan content.

142 ets to five allows for greater resolution in PSGL-1 selection resulting in fractionation of a single

143 and LTNT patients' T cells showed increased PSGL-1-mediated rolling and residual adhesion, even unde

144 During inflammation, PSGL-1 dominated E-selectin binding, rolling, integrin a

145 Instead, PSGL-1-deficient Tregs lost the ability to modulate T ce

146 F-GalNAc was metabolically incorporated into PSGL-1, and this was accompanied by an approximately 20%

147 In vivo, ApoE(-/-) mice lacking PSGL-1 had impaired Ly-6C(hi) monocyte recruitment to at

148 ore severe than those of neutrophils lacking PSGL-1, CD44, and the mucin CD43.

149 We found that Tregs lacking PSGL-1 were unable to suppress experimental autoimmune e

150 A monomeric full-length PSGL-1 made by substituting the transmembrane domain wit

151 DeltaCD neutrophils expressed less PSGL-1 on their surfaces because of inefficient export f

152 Unexpectedly, they have 10-fold less PSGL-1 on their surfaces than WT leukocytes.

153 The selectin ligand PSGL-1 transduced signals emanating from these interacti

154 but continues to rely on the selectin ligand PSGL-1.

155 rin, radixin and moesin proteins (ERMs) link PSGL-1 to actin cytoskeleton and because they serve as a

156 pothesized that the cytoplasmic domain links PSGL-1 to the cytoskeleton.

157 expansion of extrafollicular CD44(hi)CD62(lo)PSGL-1(lo)CD4(+) (PSGL-1(lo)CD4(+)) T cells.

158 tedly, neutrophils from these mice localized PSGL-1 normally in microvilli, uropods, and lipid rafts.

159 ations of cells with high, moderate, and low PSGL-1 expression.

160 At matched PSGL-1 densities, both DeltaCD and wild-type neutrophils

161 ic precursor in the ER and decreasing mature PSGL-1 on the cell surface.

162 Mechanistically, PSGL-1 ligation on exhausted CD8(+) T cells inhibited T

163 tes share the ability to use sLe(x)-modified PSGL-1-dependent and -independent routes of entry into m

164 NCH-1 strain that utilize an sLe(x)-modified PSGL-1-independent means of entry can be enriched for by

165 NA expression of monocyte adhesion molecules PSGL-1, beta(1)-integrin, and beta(2)-integrin compared

166 by using the alternative adhesion molecules, PSGL-1 and MCAM, the latter representing an exclusive pa

167 sducing retroviruses expressing WT or mutant PSGL-1 into bone marrow-derived macrophages from PSGL-1-

168 Notably, PSGL-1 expression on myelin-specific effector T cells ha

169 a cancer in which T cell dysfunction occurs, PSGL-1 deficiency led to PD-1 downregulation, improved T

170 cular mechanism promoting the association of PSGL-1, CD43, and CD44 with assembling HIV-1 which relie

171 In the eye, systemic blockade of PSGL-1 with a monoclonal antibody or recombinant soluble

172 drb1 in haematopoietic cells, or blockade of PSGL-1, the receptor involved in neutrophil-platelet int

173 mmation and malignancy inhibited cleavage of PSGL-1 by Pic.

174 data highlight the critical contribution of PSGL-1 to the regulation of growth, dissemination, and d

175 domains cooperate to promote dimerization of PSGL-1.

176 The transmembrane domain of PSGL-1 is required for dimerization, and the cytoplasmic

177 n the initial signaling events downstream of PSGL-1 that are required to initiate neutrophil slow rol

178 rast, we found that E-selectin engagement of PSGL-1 or CD44 triggered slow rolling through a common,

179 ng pathways linking E-selectin engagement of PSGL-1 to Syk activation are unknown.

180 E-selectin engagement of PSGL-1 was dependent on its cytoplasmic domain to activa

181 tive and 4.4-fold and 3.2-fold enrichment of PSGL-1 negative Jurkat and HL60 cells, respectively.

182 monstrate 26-fold and 3.8-fold enrichment of PSGL-1 positive and 4.4-fold and 3.2-fold enrichment of

183 Expansion of PSGL-1(lo)CD4(+) T cells is also prevented by BCL6 or St

184 impaired dimerization and delayed export of PSGL-1 from the endoplasmic reticulum (ER), markedly inc

185 Endothelial expression of PSGL-1 adds a new dimension to the various cellular inte

186 es based on their differential expression of PSGL-1 ligand by using a ridged channel coated with P se

187 selectin substrate enabled by the failure of PSGL-1 patches under hydrodynamic forces.

188 overcome this limitation, truncated forms of PSGL-1, called "PSGL-1 peptide probes," were developed.

189 , we examined the expression and function of PSGL-1 on Ly-6C(hi) and Ly-6C(lo) monocytes from wild-ty

190 2016) report homing-independent functions of PSGL-1 in immune checkpoint regulation and T cell effect

191 LTNT led to an increase of PSGL-1 expression on peripheral T cells.

192 The cytoskeletal independence of PSGL-1-initiated, alpha(L)beta(2)-mediated slow rolling

193 in Th17 cells that functions independent of PSGL-1, and they suggest that CD43 may hold promise as a

194 demonstrate a novel pleiotropic influence of PSGL-1 deficiency on several aspects of T cell homeostas

195 ing inflammation, reversible interactions of PSGL-1 with selectins mediate leukocyte rolling on vascu

196 6C(hi) monocytes expressed a higher level of PSGL-1 and had enhanced binding to fluid-phase P- and E-

197 home to the thymus expressed high levels of PSGL-1 transcripts compared with hematopoietic stem cell

198 and explain in part the shorter lifetimes of PSGL-1 bonds with L-selectin than P-selectin.

199 The lateral mobility of PSGL-1 similarly increased by depolymerizing actin filam

200 ar-normal cellularity seen in lymph nodes of PSGL-1(null) mice.

201 n anticipated based on the mild phenotype of PSGL-1(null) mice.

202 rovides a key signal to export precursors of PSGL-1 from the ER to the Golgi apparatus en route to th

203 iated E-selectin-dependent redistribution of PSGL-1 and L-selectin to a major pole on slowly rolling

204 d cells documented cytoskeletal restraint of PSGL-1.

205 ween PSGL-1 and Syk, we examined the role of PSGL-1 ERM-binding sequence (EBS) on cell capture, rolli

206 Thus, the multiple roles of PSGL-1 may explain why targeting this single adhesion mo

207 toplasmic tails with the cytoplasmic tail of PSGL-1 significantly enhanced their coclustering with Ga

208 1(-/-) neutrophils blocked raft targeting of PSGL-1, CD43, and CD44, but not of other glycosylated pr

209 P-Selectin binds to the amino-terminus of PSGL-1 through recognition of a sialyl Lewis(x) (SLe(x))

210 sulfopeptide modeled after the N terminus of PSGL-1.

211 ce of antibody that blocks the N terminus of PSGL-1.

212 yl Lewis X and CHO-131 antigen expression on PSGL-1, whereas sialylated O-glycans on CD43 were minima

213 N-glycans on ESL-1 and CD44 and O-glycans on PSGL-1 constitute all E-selectin ligands, with neither g

214 ot detected with L-selectin beads rolling on PSGL-1.

215 ether bond formation rates for P-selectin on PSGL-1 decreased with increasing wall shear stress, from

216 with antibodies to L-selectin (DREG-200) or PSGL-1 (PL-1) significantly (P < 0.001) inhibited this e

217 t of this, antagonists against P-selectin or PSGL-1 caused dissociation of previously formed platelet

218 rease in microparticle surface L-selectin or PSGL-1 expression.

219 Antibodies to L-selectin or PSGL-1 had no effect on IL-8-induced migration but preve

220 In addition, but through a distinct pathway, PSGL-1 engagement activates ERK.

221 p of uropod-directed transmembrane proteins, PSGL-1, CD43, and CD44, at the plasma membrane of T cell

222 tion; however, flow cytometry showed reduced PSGL-1.

223 PSGL-1, which could account for the reduced PSGL-1 in the remaining unbound population.

224 We summarize what is known regarding PSGL-1 structure and function and highlight how it may a

225 scale the magnitude of the immune response, PSGL-1 has emerged as an important checkpoint during thi

226 The resulting PSGL-1 oligosaccharide is properly protected for glycope

227 Blockade of P-selectin (P-sel)/PSGL-1 interactions holds significant potential for trea

228 GSnP-6 potently blocks P-sel/PSGL-1 interactions in vitro and in vivo and represents

229 ere varied, a shear threshold for P-selectin PSGL-1 binding was also noted at shear rates <100/s when

230 sion and weak shear threshold for P-selectin PSGL-1 interactions that may be physiologically relevant

231 al receptor-ligand interactions, P-selectin &PSGL-1 and Notch &DLL1.

232 s expressed at all CNS barriers, P-selectin (PSGL-1-receptor) was mainly detected at the choroid plex

233 nvolved in the adhesion cascade: L-selectin, PSGL-1, Mac-1, and LFA-1 for resting, spherical, and hum

234 We show that E-selectin-PSGL-1 interaction during neutrophil rolling triggers Mr

235 Because of the importance of P-selectin-PSGL-1 binding in the interaction between platelets and

236 than previously thought, and that P-selectin-PSGL-1 bonds were relaxed at the leading edge of the rol

237 P-selectin-PSGL-1 interaction causes rolling of leukocytes on the e

238 regulatory role via inhibition of P-selectin-PSGL-1-dependent formation of platelet-leukocyte complex

239 ontrast to P- and L-selectin, the E-selectin/PSGL-1 binding does not exhibit significant changes at a

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

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

242 are illustrated with two systems, P-selectin/PSGL-1 and FimH/mannose, subjected to both constant and

243 The P-selectin/PSGL-1 binding is strengthened at acidic pH, as evidence

244 to roll in the absence of optimal P-selectin/PSGL-1 interaction using an alternative mechanism that i

245 y usually one precipitous step of P-selectin:PSGL-1 dissociation.

246 an rolling associated molecules (L-selectin; PSGL-1), but that the mobilities within each of these gr

247 a monoclonal antibody or recombinant soluble PSGL-1 drastically reduced the severe manifestations of

248 In other autoimmune strains, PSGL-1(lo) T cells are also abundant but may exhibit eit

249 d leukocyte rolling velocity, which suggests PSGL-1 up-regulation; however, flow cytometry showed red

250 m and exhibit marked polarization of surface PSGL-1, but not LFA-1, to the trailing edge.

251 Thus, targeting PSGL-1 with a blocking Ab that has diminished Fc-mediate

252 ating glycosulfopeptide mimics of N-terminal PSGL-1 through development of a stereoselective route fo

253 hey also remained in lymph nodes longer than PSGL-1(+/+) T cells, suggesting that PSGL-1 supports T c

254 these O-glycans are on protein(s) other than PSGL-1, CD44, and CD43; and that PSGL-1, CD44, and ESL-1

255 other than PSGL-1, CD44, and CD43; and that PSGL-1, CD44, and ESL-1 do not constitute all glycoprote

256 These studies demonstrate that PSGL-1 EBS plays a critical role in recruiting leukocyte

257 Blood, Azab and colleagues demonstrate that PSGL-1 expressed on myeloma cells is involved with regul

258 th PSGL-1(-/-) bone marrow demonstrated that PSGL-1 messenger RNA and PSGL-1 protein expression remai

259 microscopy in the lymph node, we found that PSGL-1 expression on Tregs had no role in the suppressio

260 However, recent findings indicate that PSGL-1 can also negatively regulate T cell function.

261 These data indicate that PSGL-1 is a new marker for Ly-6C(hi) monocytes and a maj

262 These results indicate that PSGL-1-conjugated fluorescent microspheres allow specifi

263 We show that PSGL-1 is highly expressed on MM cells and regulates the

264 an-selectin inhibitor GMI-1070, we show that PSGL-1 regulates the activation of integrins and downstr

265 Our data show that PSGL-1 represents a previously unknown, phase-specific m

266 ges from PSGL-1-deficient mice, we show that PSGL-1 required neither dimerization nor cytoskeletal an

267 utes, the nucleopod had dissipated such that PSGL-1 was localized in a crescent or ring away from the

268 Studies in cell lines have suggested that PSGL-1 requires its cytoplasmic domain to localize in me

269 s than wild type animals do, suggesting that PSGL-1 has a role in the negative regulation of autoimmu

270 er than PSGL-1(+/+) T cells, suggesting that PSGL-1 supports T cell egress.

271 The PSGL-1-L-selectin complex signals through Src family kin

272 The PSGL-1-L-selectin complex-induced signaling effects on n

273 escribe the glycan microheterogeneity at the PSGL-1 N-terminus.

274 ha2,3Galbeta1,3(NeuAcalpha2,6)GalNAc) at the PSGL-1 N-terminus.

275 the presence of a polybasic sequence in the PSGL-1 cytoplasmic domain significantly enhanced this co

276 sialyl-Lewis x (sLe(x)), which modifies the PSGL-1 N terminus, is important for adhesion to and inva

277 veloped a highly convergent synthesis of the PSGL-1 oligosaccharide linked to threonine based on the

278 protein endopeptidase was used to reduce the PSGL-1 density to that on DeltaCD neutrophils.

279 These data demonstrate that the PSGL-1 cytoplasmic domain is dispensable for leukocyte r

280 dergo biphasic development and hint that the PSGL-1-targeting adhesin(s) may be upregulated or optima

281 recruiting phosphoinositide-3-kinase to the PSGL-1 cytoplasmic domain was reported to activate integ

282 to polarize or to transduce signals through PSGL-1 displayed aberrant crawling, and blockade of this

283 Thus, PSGL-1 plays a fundamental role in balancing viral contr

284 th an approximately 9-fold lower affinity to PSGL-1, a physiological ligand, due to faster dissociati

285 nts to both alpha(M)beta(2)/GPIbalpha and to PSGL-1/P-selectin completely abrogates MP-induced platel

286 lecular mechanisms for L-selectin to bind to PSGL-1 and peripheral node addressin and explain in part

287 tin, cellular or soluble, through binding to PSGL-1, promotes NETosis, suggesting that this pathway i

288 ical effects that: 1) reduced capture due to PSGL-1 redistribution, 2) reduced rolling velocity due t

289 e compartment, and a functional shift toward PSGL-1 dependence in mature neutrophils.

290 Indeed, triple-transfected PSGL-1/SLeX/IL-10 MSCs transiently increased levels of I

291 knock-in "DeltaCD" mice express a truncated PSGL-1 that lacks the cytoplasmic domain.

292 selectin binding as compared with wild-type, PSGL-1(-/-), or CD43(-/-) Th1 cells.

293 IL-15 also upregulates PSGL-1 and CXCR3, molecules associated with CNS traffick

294 bition of monocyte-platelet interactions via PSGL-1 or P-selectin is not sufficient to prevent platel

295 We asked whether PSGL-1 must interact with the cytoskeleton to initiate s

296 of P-selectin and that L-selectin bonds with PSGL-1 may be tuned for the compressive forces character

297 cific because CD43 requires cooperation with PSGL-1 in Th1 cells for binding to E-selectin.

298 ition, reconstitution of wild-type mice with PSGL-1(-/-) bone marrow demonstrated that PSGL-1 messeng

299 -5, adherent eosinophils were polarized with PSGL-1 at the nucleopod tip and F-actin distributed diff

300 t detect interactions of P-selectinE88D with PSGL-1.