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1                                              S1P can bind to several G-protein-coupled receptors (GPC
2                                              S1P deficiency aggravated vasoplegia in this model, argu
3                                              S1P deficiency impaired aggregation and spreading of was
4                                              S1P did not increase production of this pro-inflammatory
5                                              S1P exerts its effects in S1P receptor-independent manne
6                                              S1P induced SynI relocation to extrasynaptic regions of
7                                              S1P is a ligand for five G-protein-coupled receptors, S1
8                                              S1P levels within the mammalian host are tightly regulat
9                                              S1P production was selectively impaired in mouse platele
10                                              S1P promotes cell growth, survival, and migration and is
11                                              S1P serum level in humans was correlated with endothelia
12                                              S1P signalling maintains the mitochondrial content of na
13                                              S1P-induced SynI relocation occurred in a Ca(2+)-indepen
14                                              S1P-R1 and Kruppel-like factor 2 expression were monitor
15                                              S1P-R1 was the prevalent S1P receptor on mature human th
16  resulted in a fully mature and active SKI-1/S1P chimera.
17  GPC-derived target sequences by human SKI-1/S1P in a quantitative manner.
18     Our study suggests that primordial SKI-1/S1P likely contained a simpler prodomain consisting of t
19                               Notably, SKI-1/S1P of arthropods, like the fruit fly Drosophila melanog
20 cover a modular structure of the human SKI-1/S1P prodomain and define its function in folding and act
21                  Zymogen activation of SKI-1/S1P requires removal of an N-terminal prodomain, by a mu
22 eloped cell-based molecular sensor for SKI-1/S1P to characterize the processing of arenavirus GPC-der
23 ver, little is known about the role of the 2 S1P-specific phosphohydrolase isoforms, SGPP1 and SGPP2,
24 und that Th17 cells egress from the gut in a S1P-receptor-1-dependent fashion and subsequently migrat
25 were abolished following administration of a S1P receptor 2 (S1P2) antagonist or a PI3K inhibitor.
26  Knockdown of either MRTF-A or YAP abrogates S1P-stimulated CCN1 expression, demonstrating that both
27 ike factor 2 expression were monitored after S1P exposure by using flow cytometry and quantitative PC
28 s QSG-7701's proliferation, in which AKR1B10-S1P signaling plays a pivotal role.
29                 Pretreatment with FTY720, an S1P-R1 nonselective modulator significantly reduced migr
30  which was partially rescued by VPC23109, an S1P receptor antagonist.
31 ockdown (TRPC1-KD) ML-1 cells, the basal and S1P-evoked invasion and migration was attenuated.
32 ic process and suggest that p120 catenin and S1P/S1pr2 signaling enhance cancer progression by regula
33                           We describe MC and S1P as novel pathogenic effectors that initiate remodeli
34         There are 5 known S1P receptors, and S1P induces adherens junction formation between endothel
35 transporter, spinster homolog 2 (Spns2), and S1P receptor, S1P1, in lamellipodia formation and perhap
36  We used a highly specific neutralizing anti-S1P antibody (mAb) and the sphingosine-1-phosphate recep
37                Reconstitution of plasma ApoM/S1P or treatment with an S1P1 receptor agonist (SEW2871)
38 ical inhibitors of the Hippo pathway such as S1P recover the ER instability and necrosis in HD model
39 ted that inhibition of SphK2 increases blood S1P levels.
40        Phosphate moiety of the surface bound S1P engages in a highly positive region close to alpha1-
41 naive T cells were readily chemoattracted by S1P in an FTY720-sensitive, S1PR1-dependent manner.
42 er, we show that early activation of RhoA by S1P inactivates Rac1 but not Cdc42, and vice versa.
43 lowed by proteolytic activation of SREBPs by S1P and S2P in the Golgi.
44                              In these cells, S1P, but not TNF, promotes IkappaB kinase (IKK) and p65
45 MI HF progression in mice as much as chronic S1P treatment.
46 R knockout mice does not elevate circulating S1P levels, nor does it ameliorate post-MI dysfunction,
47 eta1AR-blockers display elevated circulating S1P levels, confirming that Meto promotes S1P secretion/
48                                  Circulatory S1P has critical roles in maturation and homeostasis of
49                            Thus, circulatory S1P confinement could be a primordial strategy of verteb
50                                 Constitutive S1P-R expression was quantified by means of real-time PC
51 te (S1P) signaling via the G protein-coupled S1P receptor 1 in these progenitors.
52         These compounds effectively decrease S1P levels in vitro.
53 ypes, including a delay in epiboly, depleted S1P levels, elevated levels of sphingosine, and resistan
54 dered both platelet- and erythrocyte-derived S1P essential for survival, with a contribution from blo
55 urkholderia-infected macrophages with either S1P or a selective agonist of S1P receptor 1 enhanced ba
56 inase-2 deficient mice had higher endogenous S1P levels and the LPS/PepG-induced impaired systolic co
57 ect SynI distribution and whether endogenous S1P could be involved in the process.
58 lly manipulating the S1P-metabolizing enzyme S1P lyase (SPL).
59   Here, we report that increased erythrocyte S1P binds to deoxygenated sickle Hb (deoxyHbS), facilita
60 abolomic profiling, we show that erythrocyte S1P levels rapidly increase in 21 healthy lowland volunt
61 source redundancy normally secures essential S1P signaling in developing and mature blood vessels, pr
62 ocyte population or populations that express S1P-Rs and respond to S1P by migrating across a concentr
63 egulated genes in various cell types and for S1P-stimulated glioblastoma cell proliferation.
64 egia in this model, arguing a vital role for S1P in maintaining vascular resistance during recovery f
65 ion and reveal a previously unknown role for S1P in positioning cells within the medulla.
66            These results indicate a role for S1P signaling in B. pertussis-mediated pathology and hig
67 y reduced migration and suggested a role for S1P-R2 in retaining thymocytes in the tissue.
68 YAP associate in coimmunoprecipitations from S1P-stimulated cells.
69 ates thymic exit via a process distinct from S1P-mediated migration.
70 ociated with reduced survival signaling from S1P receptor 2, resulting in selective downregulation of
71 y inhibiting SPHK1 activity, which generates S1P.
72 liver tissue from mice and patients, hepatic S1P levels increased owing to increased hepatic sphingos
73 ed with WT ECs, resulting in a 2-fold higher S1P level.
74 nhibitors of sphingolipid cascade identified S1P as the sphingolipid mediating SynI redistribution.
75                      Recently, we identified S1P as an acute ERM activator (via phosphorylation) thro
76 s tumour aggressiveness in OSCC and identify S1P signalling as a potential therapeutic target.
77                      These findings identify S1P metabolism as a novel player in modulating synaptic
78                    S1P exerts its effects in S1P receptor-independent manner.
79 est that Galphaq activity is not involved in S1P-mediated regulation of barrier integrity.
80 f inflammation and associated with increased S1P generation.
81  Mechanistically, we found that Meto-induced S1P secretion is beta3AR-dependent because Meto infusion
82 show that elevated erythrocyte Sphk1-induced S1P protects against tissue hypoxia by inducing O2 relea
83  attractive chemotypes capable of inhibiting S1P formation in cells.
84 a SphK1, which was mediated by intracellular S1P, independent of S1P receptors.
85 1 phosphorylation and enhanced intracellular S1P levels in HLMVECs, which was blocked by inhibition o
86 activation of SphK1, increased intracellular S1P, and up-regulated expression of SphK1, Col alpha1(I)
87 e, we investigated the role of intracellular S1P in insulin-secreting INS1E cells by genetically mani
88  Mechanistically, we show that intracellular S1P promotes deoxygenated Hb anchoring to the membrane,
89                                 Intriguingly S1P completely stops the decline of motor function of HD
90 PL), the enzyme responsible for irreversible S1P cleavage was inactivated.
91 lbumin-sized particles in ApoM deficiency is S1P- and S1P1-dependent and this dependency exacerbates
92                            There are 5 known S1P receptors, and S1P induces adherens junction formati
93 eversible degradation of the bioactive lipid S1P.
94 he use of a reporter for the signaling lipid S1P (sphingosine 1-phosphate), we found that cells sense
95 , which contributed to a reduced liver:lymph S1P gradient and limited HSC egress from the liver.
96  a subset of tumours, which in part mediates S1P-induced migration of OSCC cells.
97 cantly reduces expression of genes mediating S1P/S1pr2 signaling in vivo and in vitro, and this effec
98       We have shown previously that neuronal S1P accumulation is toxic leading to ER-stress and an in
99 of fingolimod was found to be a nonselective S1P receptor agonist, agonism specifically of S1P1 is re
100 L(fl/fl/CaMK)) caused marked accumulation of S1P.
101 re completely abrogated by the activation of S1P/S1pr2 signaling.
102 y regulated, in part through the activity of S1P lyase (S1PL) which catalyses its irreversible degrad
103 es with either S1P or a selective agonist of S1P receptor 1 enhanced bacterial colocalisation with LA
104    Fourteen fluorine-containing analogues of S1P ligands were synthesized and their in vitro binding
105 tor mediated most of the survival benefit of S1P, whereas the endothelial S1P1 receptor was dispensab
106                         The concentration of S1P is higher in circulatory fluids than in lymphoid org
107 d that cells sensed higher concentrations of S1P in the medullary cords than in the T cell zone and t
108 dy, we have investigated the contribution of S1P signalling to the pathogenesis of OSCC.
109 -013 to study the signaling contributions of S1P and S1PR2 to MC- and IgE-dependent airway allergic r
110 ases in ceramide and consequent decreases of S1P reduce proliferation of various cancers, AC might of
111 d SGPP2, which catalyze dephosphorylation of S1P to sphingosine.
112  lung epithelial cells in a manner devoid of S1P agonism.
113          To clarify the neuronal function of S1P, we generated brain-specific knockout mouse models i
114                   Physiological functions of S1P are tightly linked to shear stress, the key biophysi
115  is dependent on intracellular generation of S1P via activation and localization of SphK1 to cell per
116                   The relative importance of S1P sources sustaining these processes remains unclear.
117                                Incubation of S1P with airway smooth muscle cells significantly increa
118 ediated by intracellular S1P, independent of S1P receptors.
119 hat SPL's pro-IFN function is independent of S1P.
120                                Inhibition of S1P signaling has been proposed as a strategy for treatm
121                Pharmacological inhibition of S1P synthesis reduced vasoconstriction of mesenteric art
122                           The interaction of S1P with the S1P receptors plays a fundamental physiolog
123   Herein, we investigated the involvement of S1P in human liver fibrosis.
124 Cohort (n = 6099), suggesting involvement of S1P signalling in human hearing loss.
125                  Interestingly, the level of S1P was also higher in PHC tissues than in peri-tumor ti
126 t it is caused by decreased plasma levels of S1P and reduced S1P1 stimulation.
127                                    Levels of S1P in liver, bone marrow, and lymph fluid were measured
128    In this work, we dissect the mechanism of S1P generation downstream of epidermal growth factor (EG
129 ro-survival actions seen after modulation of S1P-metabolizing enzymes allows this axis to emerge as a
130            We demonstrate a novel outcome of S1P-mediated regulation of lymphocyte trafficking, where
131 is, further highlighting the pivotal role of S1P in host-pathogen interactions.
132 lso challenge previous models of the role of S1P in lymphocyte recirculation and suggest that S1P pro
133 s, neither platelets nor any other source of S1P was essential for vascular development, vascular int
134     As the key mediators in the synthesis of S1P, sphingosine kinase (SphK) isoforms 1 and 2 have att
135 esicles for exocytosis, as the key target of S1P action.
136 study was to identify presynaptic targets of S1P action controlling exocytosis.
137 ns2-mediated extracellular transportation of S1P and its inside-out signaling via S1P1.
138              Mature human thymocytes rely on S1P-R1 to migrate toward S1P.
139 apeutically antagonizing TNF (etanercept) or S1P (JTE013) signaling corrects this defect.
140 BH3 mimetics with either SPHK1 inhibition or S1P receptor 2 antagonism triggered synergistic AML cell
141 equired for transcriptional control of other S1P-regulated genes in various cell types and for S1P-st
142 vity on S1P1 while sparing activity on other S1P receptors could offer equivalent efficacy with reduc
143 mation, suggesting a key role for inside-out S1P signaling.
144 ingosine and its metabolite sphingosine-1-P (S1P) stimulate excitatory transmission.
145 ing evidence indicates that sphingosine-1-P (S1P) upregulates glutamate secretion in hippocampal neur
146 1P egress signal, whereas thymic parenchymal S1P levels are kept low through S1P lyase (SPL)-mediated
147 at deficiency of the sphingosine-1-phoshate (S1P) transporter gene Spns2 in endothelium increased imm
148         The role of sphingosine-1 phosphate (S1P) in leukocyte trafficking has been well deciphered i
149 ations of SphK1 and sphingosine 1 phosphate (S1P).
150 the bioactive lipid sphingosine 1-phosphate (S1P) and has established roles in tumor initiation, prog
151 active sphingolipid sphingosine-1-phosphate (S1P) and the kinase that produces it have been implicate
152  the lipid mediator sphingosine-1-phosphate (S1P) are reduced in septic patients and are inversely as
153 ctivation and local sphingosine-1-phosphate (S1P) are significantly augmented after OVA treatment in
154 duced intracellular sphingosine-1-phosphate (S1P) generation catalyzed by sphingosine kinase 1 (SphK1
155  chemotaxis along a sphingosine-1-phosphate (S1P) gradient.
156 The chemoattractant sphingosine 1-phosphate (S1P) guides T cell circulation among secondary lymphoid
157  phospholipids like sphingosine-1-phosphate (S1P) in AKR1B10's oncogenic function.
158 M (ApoM) transports sphingosine-1-phosphate (S1P) in plasma, and ApoM-deficient mice (Apom(-/-)) have
159             Chronic sphingosine-1-phosphate (S1P) infusion resulted in a development of significantly
160                     Sphingosine 1-phosphate (S1P) is a bioactive lipid that interacts with cell-surfa
161                     Sphingosine-1-phosphate (S1P) is a bioactive signalling lipid highly enriched in
162                     Sphingosine-1-phosphate (S1P) is a bioactive sphingolipid metabolite that regulat
163 The bioactive lipid sphingosine 1-phosphate (S1P) is a degradation product of sphingolipids that are
164                     Sphingosine 1-phosphate (S1P) is a multifunctional bioactive sphingolipid involve
165                     Sphingosine 1-phosphate (S1P) is a pleiotropic signaling molecule that interacts
166                     Sphingosine 1-phosphate (S1P) is a sphingolipid and the natural ligand for five G
167            Elevated sphingosine 1-phosphate (S1P) is detrimental in Sickle Cell Disease (SCD), but th
168                     Sphingosine-1-phosphate (S1P) is generated through phosphorylation of sphingosine
169                     Sphingosine 1-phosphate (S1P) is the endogenous ligand for the sphingosine 1-phos
170  Here, we show that sphingosine 1-phosphate (S1P) levels are not only increased in palmitate-stimulat
171                     Sphingosine 1-phosphate (S1P) lyase (SPL) is an intracellular enzyme that mediate
172 GPL1, which encodes sphingosine-1-phosphate (S1P) lyase.
173  the lipid mediator sphingosine 1-phosphate (S1P) may be one such mechanism.
174                     Sphingosine-1-phosphate (S1P) mediates egress of immune cells from the lymphoid o
175 rray data indicated sphingosine 1-phosphate (S1P) metabolism and signalling was deregulated in OSCC.
176 Rs for thrombin and sphingosine-1-phosphate (S1P) on human glioblastoma cells robustly couple to RhoA
177 ndependently of the sphingosine 1-phosphate (S1P) pathway was unknown.
178                     Sphingosine 1-phosphate (S1P) produces significant endothelial barrier enhancemen
179 phingosine used for sphingosine-1-phosphate (S1P) production.
180 ed the potential of sphingosine 1-phosphate (S1P) receptor (S1PR) agonism in the treatment of infecti
181 ng mutations in the sphingosine-1-phosphate (S1P) receptor 2 (S1PR2) promoter have been associated wi
182 he cardioprotective sphingosine-1-phosphate (S1P) receptor-1 (S1PR1).
183 role of endothelial sphingosine 1-phosphate (S1P) receptor-1, a G protein-coupled receptor known to p
184       Modulation of sphingosine 1-phosphate (S1P) receptors in a non-selective manner decreases disea
185 ion and function of sphingosine-1-phosphate (S1P) receptors in human thymocyte egress.
186                     Sphingosine-1-phosphate (S1P) signaling is essential for vascular development and
187 drug FTY720 affects sphingosine-1-phosphate (S1P) signaling on targeted cells that bear the S1P recep
188 velopment, required sphingosine 1-phosphate (S1P) signaling via the G protein-coupled S1P receptor 1
189 c tone via enhanced sphingosine-1-phosphate (S1P) signaling.
190    The sphingolipid sphingosine-1-phosphate (S1P) signals through five G-protein-coupled receptors (S
191             Because sphingosine-1-phosphate (S1P) strengthens AJs, we determined if TRPC1 functioned
192 sis was observed in sphingosine-1-phosphate (S1P) transporter spinster homologue 2 (Spns2)-deficient
193  However, levels of sphingosine-1-phosphate (S1P) were significantly increased in Ormdl3(Delta2-3/Del
194  2 (SK2) synthesize sphingosine-1-phosphate (S1P), a bioactive lipid messenger critically involved in
195                     Sphingosine-1-phosphate (S1P), a bioactive sphingolipid metabolite, plays a criti
196 ve bioactive lipid, sphingosine-1-phosphate (S1P), could ameliorate the microvascular leakage followi
197 n be metabolized to sphingosine-1-phosphate (S1P), linked to inflammation and tumorigenesis.
198 d the metabolism of Sphingosine-1-phosphate (S1P), one of the most important bioactive lipids, in bot
199 h cl-CD95L produced sphingosine-1-phosphate (S1P), which promoted endothelial transmigration by activ
200 nced sensitivity to sphingosine 1-phosphate (S1P).
201 ed receptor agonist sphingosine-1-phosphate (S1P).
202 -signaling molecule sphingosine-1-phosphate (S1P).
203 de (-50 +/- 3%) and sphingosine 1-phosphate (S1P, -40 +/- 4%), which ended up to reduction in cell mo
204  bioactive sphingosine-1-phosphatephosphate (S1P) is present in plasma, bound to carrier proteins, an
205 necessary for recovery and high basal plasma S1P levels protective during anaphylactic shock.
206   Yet rapid and profound depletion of plasma S1P during systemic anaphylaxis rendered both platelet-
207  blood vessels, profound depletion of plasma S1P renders both erythrocyte and platelet S1P pools nece
208 (-/-)) have approximately 50% reduced plasma S1P levels.
209 ma S1P renders both erythrocyte and platelet S1P pools necessary for recovery and high basal plasma S
210 spirin in mice with but not without platelet S1P, suggesting that platelet activation and stimulus-re
211                 We show that LpSpl possesses S1P lyase activity that was abrogated by mutation of the
212                     S1P-R1 was the prevalent S1P receptor on mature human thymocytes (CD3(hi)CD27(+)C
213 ng S1P levels, confirming that Meto promotes S1P secretion/signaling.
214 report that the Arabidopsis SITE-1 PROTEASE (S1P) cleaves endogenous RAPID ALKALINIZATION FACTOR (RAL
215 sin kexin isozyme-1 (SKI-1)/site-1 protease (S1P) is implicated in lipid homeostasis, the unfolded pr
216 sin kexin isozyme 1 (SKI-1)/site 1 protease (S1P).
217       Together, our data show that the rapid S1P-induced increase in endothelial integrity is mediate
218 We aimed to determine whether S1P receptors (S1P-Rs) play a role in mature human thymocyte egress and
219 ssion of the two major enzymes that regulate S1P levels were altered in OSCC: SPHK1 was significantly
220 t, FTY720 and FTY720-P significantly repress S1P-induced IL-6 and IL-8 production.
221                        Altogether, we reveal S1P as an intracellular hypoxia-responsive biolipid prom
222 support the survival of T cells by secreting S1P via the transporter SPNS2, that this S1P signals thr
223 he safety and efficacy of the oral selective S1P receptor modulator ozanimod in patients with relapsi
224 gical or genetic approaches that alter serum S1P may attenuate cardiac dysfunction and whether S1P si
225 e that activation of S1P2 by increased serum S1P and the subsequent activation of the PI3K-Akt surviv
226 f the immunomodulator FTY720 increased serum S1P, improved impaired systolic contractility and activa
227 red systolic contractility and reduced serum S1P.
228                           We show that serum S1P is reduced in human sepsis and in murine models of s
229 mphatic circulation, thus comprising a sharp S1P gradient across the endothelial barrier.
230 uffice to activate local MC and elevate skin S1P.
231                            Furthermore, skin S1P levels remain unchanged in MC-deficient mice exposed
232 n catalyzed by sphingosine kinase 1 (SphK1), S1P transporter, spinster homolog 2 (Spns2), and S1P rec
233                         In in vitro studies, S1P enhanced the migration/invasion of OSCC cells and at
234                              Lastly, surface S1P-R1 expression, as well S1PR1 and Kruppel-like factor
235                                Surprisingly, S1P had the opposite effect on effector memory T cells,
236 tructure at 1.9 A resolution deciphered that S1P binds to the surface of 2,3-BPG-deoxyHbA and causes
237                     We also demonstrate that S1P receptor expression is deregulated in primary OSCCs
238  of the CCN1 gene promoter demonstrated that S1P increases coactivator binding at the canonical trans
239                   Here, we demonstrated that S1P metabolism is significantly disrupted in HD even at
240 he context of murine work demonstrating that S1P is required for thymocyte egress to the periphery, o
241  data represent the first demonstration that S1P induces SynI mobilization from synapses, thereby ind
242        In addition, we provide evidence that S1P can be produced at mature axon terminals as well as
243                           We next found that S1P effectively could reverse alcohol-induced endothelia
244                     Lastly, we observed that S1P administration ameliorated hypotension and microvasc
245             Functional studies revealed that S1P and 2,3-BPG work synergistically to decrease both Hb
246                            Here we show that S1P is essential not only for the circulation of naive T
247                                 We show that S1P promotes cell spreading and endothelial barrier func
248           Taken together, our data show that S1P signalling promotes tumour aggressiveness in OSCC an
249 lysis of rat hippocampal neurons showed that S1P applied at nanomolar concentration alters the distri
250 , vascular transcriptome analysis shows that S1P pathway is critical in the regulation of vascular fu
251                 The present study shows that S1P stimulation of human, primary pDCs substantially dec
252           In addition, our data suggest that S1P pathway modulators have potential for the treatment
253 in lymphocyte recirculation and suggest that S1P promotes retention of memory T cell subsets in secon
254                                          The S1P signalling pathway is being targeted therapeutically
255 eficiency in sphingosine kinase (SphK)1, the S1P-producing enzyme, or in MC, remarkably mitigates all
256 endothelial transmigration by activating the S1P receptor 3.
257 P) signaling on targeted cells that bear the S1P receptors S1P1, S1P3, S1P4, and S1P5.
258 an TECs or other stromal cells, disrupts the S1P gradient, preventing egress.
259                               Mice given the S1P antagonist (FTY720) with HSCs had increased hepatic
260                                 However, the S1P degradation-incompetent form of SPL also enhanced IF
261  INS1E cells by genetically manipulating the S1P-metabolizing enzyme S1P lyase (SPL).
262 sses the cellular and molecular basis of the S1P gradients and aims to interpret its physiological si
263 essels) and underscore the importance of the S1P pathway in vascular development.
264        We found that genetic deletion of the S1P receptor 1 (S1pr1) alone in CD11b(hi) CD206(+) TAMs
265  that expression of SPNS2, expression of the S1P receptor S1PR5 on NK cells, and expression of the ch
266 In an attempt to investigate the role of the S1P/S1P2 axis in vivo, the New Zealand obese (NZO) diabe
267 at the corticomedullary junction produce the S1P egress signal, whereas thymic parenchymal S1P levels
268 y cords than in the T cell zone and that the S1P transporter SPNS2 on lymphatic endothelial cells gen
269              The interaction of S1P with the S1P receptors plays a fundamental physiological role in
270  cells from C57BL6 mice, with or without the S1P antagonist FTY720; we then studied HSC mobilization
271 ovel role for Abl kinases in mediating these S1P effects.
272 ing S1P via the transporter SPNS2, that this S1P signals through S1P1R on T cells, and that the requi
273  parenchymal S1P levels are kept low through S1P lyase (SPL)-mediated metabolism.
274 sion is NF-kappaB-dependent, and unlike TNF, S1P did not activate NF-kappaB.
275 herapies for humans with hearing loss due to S1P signalling defects need to target strial function.
276             Human thymocytes were exposed to S1P in Transwell plate migration assays coupled to flow
277 ecreased in mature thymocytes on exposure to S1P.
278 t as ceramides, but cannot be metabolized to S1P.
279 pulations that express S1P-Rs and respond to S1P by migrating across a concentration gradient.
280 t also demonstrated the greatest response to S1P in migration assays.
281 s study, we assessed the ex vivo response to S1P of primary human T cell subsets.
282 o flow cytometry to evaluate the response to S1P of thymocytes at different stages of maturation.
283  but not blood leukocytes were responsive to S1P gradients, suggesting that T cell responsiveness is
284  thymocytes rely on S1P-R1 to migrate toward S1P.
285 ) expression and diminished migration toward S1P in the Pparg(C/-) splenocytes, which impeded lymphoc
286 e functional and structural bases underlying S1P-mediated pathogenic metabolic reprogramming in SCD a
287                                Unexpectedly, S1P also enhances MRTF-A binding at TEA sites.
288 0 and FTY720-P with S1P, we show that unlike S1P, the sphingosine analogs do not induce cytokine prod
289                              In vertebrates, S1P is spatially compartmentalized in the blood and lymp
290  FTY720 triggers MDSCs to release GM-CSF via S1P receptor 3 (S1pr3) through Rho kinase and extracellu
291                        We found that whereas S1P promotes IL-1-induced expression of IL-6, it inhibit
292 ay attenuate cardiac dysfunction and whether S1P signaling might serve as a novel theragnostic tool i
293                We aimed to determine whether S1P receptors (S1P-Rs) play a role in mature human thymo
294                           To examine whether S1P contributes to the morphologic changes of islets via
295  complexes, the molecular mechanism by which S1P promotes neurotransmission remained largely undefine
296 rain-specific knockout mouse models in which S1P-lyase (SPL), the enzyme responsible for irreversible
297 osphoprotein as a novel target through which S1P controls exocytosis.
298 ever, the molecular mechanisms through which S1P enhances excitatory activity remain largely undefine
299 ultiple cytoskeletal changes associated with S1P-mediated endothelial barrier enhancement and suggest
300           Comparing FTY720 and FTY720-P with S1P, we show that unlike S1P, the sphingosine analogs do

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