ライフサイエンスコーパス: SDF-1

1 SDF-1 and HGF were significantly increased in reduced si

2 SDF-1 and its receptor CXCR4 mRNAs were upregulated in t

3 SDF-1 engineered to be resistant to dipeptidylpeptidase

4 SDF-1 signaling via the CXCR4-TCR heterodimer uses PLC-b

5 SDF-1 treatment caused rapid down-modulation of CXCR4 in

6 SDF-1 treatment caused RasGRP1 to localize to the plasma

7 SDF-1 was entrapped via gelation of the PPCN+SDF-1 solut

8 SDF-1 was observed in identical locations but was not se

9 SDF-1 was significantly increased in the pancreas after

10 SDF-1 was upregulated in ischemic brain.

11 SDF-1, antibodies, pepducins and bioluminescence have al

12 SDF-1, in turn, induced migration of EOL-1 cells in a do

13 SDF-1, VEGF, and beta-actin up-regulation was detected a

14 SDF-1-dependent localization of RasGRP1 did not require

15 SDF-1-induced apoptosis was inhibited by dominant negati

16 SDF-1-induced c-kit phosphorylation also required the ac

17 SDF-1-induced cell migration and activation of extracell

18 SDF-1-mediated EC migration in hypoxic and/or radiation-

19 SDF-1-mediated inactivation of ERM proteins is blocked b

20 SDF-1/CXCR4 increases phosphorylation in 60 cell migrati

21 cle actin and stromal cell-derived factor 1 (SDF-1) and are tumorigenic when injected into mice.

22 e the role of stromal cell-derived factor 1 (SDF-1) and regulated on activation, normal T-cell expres

23 heir ligands, stromal cell-derived factor 1 (SDF-1) and VCAM-1, which could be selectively blocked us

24 pporting an active stromal-derived factor 1 (SDF-1) gradient near endosteum after irradiation.

25 nd, chemokine stromal cell-derived factor 1 (SDF-1) is expressed in the bone marrow adjacent to hyper

26 okine CXCL12 (stromal cell-derived factor 1 (SDF-1)), abundantly produced by stromal cells, promotes

27 he cytokine stromal derived growth factor 1 (SDF-1), CXCR-4, was assessed by flow cytometry.

28 ted basal and stromal cell-derived factor 1 (SDF-1)-induced BMC migration.

29 and impaired stromal cell-derived factor 1 (SDF-1)-induced chemotaxis of GPI(neg) NK cells.

30 However, stromal cell-derived factor 1 (SDF-1)/CXCR4-mediated signaling pathways in breast CSCs

31 Stromal cell derived factor-1 (SDF-1 or CXCL12) and its receptor CXCR4 are involved in

32 ype 4 (CXCR4)/stromal cell derived factor-1 (SDF-1 or CXCL12) interaction and the resulting cell sign

33 F-1-dependent stromal cell-derived factor-1 (SDF-1) and its receptor, CXCR4.

34 The CXCR4/stromal cell-derived factor-1 (SDF-1) axis is essential for cell trafficking and has be

35 ority of EPCs, and stromal-derived factor-1 (SDF-1) induced EPC migration, which was blocked by pretr

36 Stromal cell-derived factor-1 (SDF-1) is a chemokine that attracts endothelial progenit

37 Stromal cell-derived factor-1 (SDF-1) is the most prominent BMC homing factor known to

38 ition, median stromal cell-derived factor-1 (SDF-1) levels were 43% higher in ECs than in NCs.

39 A library and stromal cell-derived factor-1 (SDF-1) migration screening assay, we identified the hist

40 In mammals, stromal cell-derived factor-1 (SDF-1) promotes hematopoietic cell mobilization and migr

41 he binding of stromal cell-derived factor-1 (SDF-1) to its receptor CXC motif receptor-4 (CXCR4) with

42 TH-stimulated stromal cell-derived factor-1 (SDF-1) was decreased in mutant mice, suggesting SDF-1 as

43 Stromal cell-derived factor-1 (SDF-1) was elevated in DCs before LLC cell infiltration

44 he chemokine, stromal cell-derived factor-1 (SDF-1), and factors that may attenuate the angiogenic re

45 regulation of stromal cell-derived factor-1 (SDF-1), as well as endothelial migration, all of which a

46 detection of stromal cell-derived factor-1 (SDF-1), beta-actin, vascular endothelial growth factor (

47 receptor for stromal cell-derived factor-1 (SDF-1), is involved in bone morphogenic protein 2 (BMP2)

48 The chemokine stromal cell-derived factor-1 (SDF-1), signaling through CXCR4, is implicated in the ma

49 n response to stromal cell-derived factor-1 (SDF-1), the sole chemokine ligand of CXCR4.

50 adhesion was CXCR4/stromal-derived factor-1 (SDF-1)-dependent.

51 the chemokine stromal cell-derived factor-1 (SDF-1).

52 and the chemokine stromal-derived factor-1 (SDF-1).

53 ther with the stromal cell-derived factor-1 (SDF-1)/C-X-C chemokine receptor 4 axis, in the developme

54 The stromal cell-derived factor-1 (SDF-1)/CXC chemokine receptor 4 (CXCR4) signaling axis a

55 production of stromal cell-derived factor-1 (SDF-1)/CXCL12 in human fibroblasts.

56 emoattractant stromal cell-derived factor-1 (SDF-1)/CXCL12 in the injured cord and matrix metalloprot

57 4 (CXCR4) and stromal cell-derived factor-1 (SDF-1, also known as CXCL12) is a natural regulatory pro

58 eptor for the stromal cell-derived factor-1 (SDF-1/CXCL12) chemokine is one of the key stimuli involv

59 (IL)-6, IL-8, and stromal derived factor-1 (SDF-1/CXCL12) in both human gingival fibroblasts (HGF) a

60 ding the chemokine stromal derived factor-1 (SDF-1; also called CXCL 12).

61 or that binds stromal cell-derived factor-1 (SDF-1; also known as CXCL12).

62 okine ligand (stromal cell-derived factor-1 [SDF-1]) in Stx-mediated pathophysiology.

63 s receptor ligand (stromal-derived factor-1 [SDF-1], also known as CXCL12) in th hallmark of WHIM-exc

64 ated with vascular cell adhesion molecule 1, SDF-1 and stem cell factor increased phospho-c-kit level

65 d 17days for wounds treated with PPCN+SDF-1, SDF-1 only, PPCN only, and PBS, respectively.

66 CNS (known as stromal cell-derived factor 1; SDF-1), regulates cleavage of fractalkine from neurons.

67 0), a small molecule inhibitor of the CXCR-4/SDF-1 axis, was combined with BIO5192.

68 ition, CXCR7 induction was associated with a SDF-1 signaling switch from the pro-survival ERK and AKT

69 ith 20 U/mL heparin for 30 minutes abrogated SDF-1-induced BMC invasion (16+/-8% of control; P<0.01),

70 In addition, SDF-1 also up-regulates expression of the fractalkine ge

71 In addition, SDF-1/CXCR4 upregulates the phosphorylation of 44 previo

72 ation as well as SDF-1/CXCR4 signaling after SDF-1 stimulation.

73 Stabilization of altered SDF-1 gradients directly affects MK location.

74 The alternative SDF-1/CXCL12 receptor, CXCR7, is frequently and specific

75 omote directional migration of B cells in an SDF-1 gradient was dependent on its PI(3,4)P2-binding PH

76 o the lymph nodes, and a COX-2 inhibitor, an SDF-1 antagonist, and a CXCR4 neutralizing antibody all

77 shed a bifunctional protein consisting of an SDF-1 domain and a glycoprotein VI (GPVI) domain with hi

78 5 Gray IR-induced EC HIF-1alpha and SDF-1 expression was greater when combined with hypoxia

79 a synergistic partnership between MMP-9 and SDF-1 in facilitating transmigration of monocytes into t

80 lishment of the self-sustaining TGF-beta and SDF-1 autocrine signaling gives rise to tumor-promoting

81 ne signaling loops, mediated by TGF-beta and SDF-1 cytokines, which both act in autostimulatory and c

82 te, as well as expression of VEGF, bFGF, and SDF-1, which was not seen when TGF-beta1 expression was

83 oietic progenitors and BM stromal cells, and SDF-1 release.

84 asma and tissue content of CXCR4, CXCR7, and SDF-1 after Stx exposure.

85 f CXCR4 was determined through leukocyte and SDF-1 actin polymerization blood biomarker assays.

86 stem cell chemoattractants, substance P and SDF-1, in both the injured cornea and blood.

87 The role of RANTES and SDF-1 in the therapeutic effect of exogenous BMSCs was e

88 The dynamic cross-talk between S1P and SDF-1 integrates BM stromal cells and hematopoeitic prog

89 acrophage-derived factors TGF-beta, VEGF and SDF-1 abolished VEGFR1(+) myeloid cell migration and fib

90 can be inhibited by antagonists of VEGF and SDF-1.

91 njections of normal saline, AMD3100, or anti-SDF-1 antibody from postnatal day 1 to 7 (preventive str

92 erve-derived chemokine Cxcl12 (also known as SDF-1), acting through its receptor Cxcr4, initiates blo

93 the secretion of paracrine factors, such as SDF-1, and the migration of MPCs into ischemic myocardiu

94 ), blocking CXCR4 internalization as well as SDF-1/CXCR4 signaling after SDF-1 stimulation.

95 Because SDF-1 satisfied model predictions for an invasion-promot

96 Blocking SDF-1/CXCR4 interaction suppresses the expression of Run

97 Conversely, blocking SDF-1 activity with neutralizing antibodies diminished s

98 To study the effects of blocking SDF-1, rats with monocrotaline-induced pulmonary hyperte

99 Heparin blocks SDF-1/CXCR4 signaling by binding to the ligand as well a

100 findings on the neuroprotective role of both SDF-1 and fractalkine, suggest that this novel interacti

101 The CD69 and CXCR4 effects were driven by SDF-1, while CCL21 downregulated CCR7.

102 e in breast cancer patients may be driven by SDF-1-CXCR4 signaling.

103 of stimulation of chondrocyte hypertrophy by SDF-1/CXCR4, which is mediated by Runx2.

104 examined protein phosphorylation induced by SDF-1/CXCR4 signaling in breast CSCs.

105 d to low dosages of chemotactic induction by SDF-1, whereas that of naive cells cannot, despite a sim

106 promoted by the small grafts and mediated by SDF-1 resulting in stem cell influx.

107 mbined modulation of these family members by SDF-1 coordinates their interplay to produce apoptosis.

108 so significantly higher for ASCs and SSCs by SDF-1 and TGF-beta3 codelivery.

109 that the regulation of BM PC trafficking by SDF-1 and CXCR4 is dependent on Src-mediated c-kit phosp

110 owever, both the network events triggered by SDF-1 alpha in this microcircuit and the cellular target

111 sforming growth factor beta, chemokine CCL2, SDF-1, and complements C3, C4, and factor B (CFB), were

112 Immunohistochemical analysis for CD31, SDF-1, and CXCR4 was performed on mouse eyes 2 weeks aft

113 , heparin binds to both, the chemoattractant SDF-1 and its receptor, chemokine receptor 4 (CXCR4), bl

114 nd CXCR4, a receptor for the chemoattractant SDF-1, in response to bone marrow damage only in control

115 pacity to migrate toward the chemoattractant SDF-1.

116 pha controls chemotaxis toward the chemokine SDF-1 by regulating expression of its receptor Cxcr4.

117 esponded in a graded manner to the chemokine SDF-1, demonstrating that the system output of the MAPK

118 stimulating factor (M-CSF) ] and chemokines (SDF-1, MCP-1).

119 disrupting the SDF-1-CXCR4-axis by cleaving SDF-1, a chemotaxin recruiting CXCR4(+) SC.

120 ata revealed the requirement for cooperative SDF-1 expression, a prediction supported biologically by

121 In organ culture SDF-1 infiltrates cartilage and accelerates growth plate

122 binds chemokines CXCL11 (I-TAC) and CXCL12 (SDF-1) but does not act as a classical chemoattractant r

123 appeared to be mediated, in part, by CXCL12 (SDF-1)/CXCR4 signaling.

124 The chemokine CXCL12 (SDF-1) and its cognate receptor CXCR4 are involved in a

125 and migration toward the chemokines CXCL12 (SDF-1) and CCL25 in vitro.

126 sion also results in potentiation of CXCL12 (SDF-1)-mediated downstream beta-arrestin-dependent cell

127 pon stromal cell-derived factor-1 or CXCL12 (SDF-1) stimulation in human T cells to prolong ERK activ

128 ssion of IL-1beta, IL-6, CCL2(MCP-1), CXCL12(SDF-1), CCL5(RANTES), CCR7, CXCR4, GM-CSF, CD40, CD40L,

129 /stromal cell-derived factor-1 alpha (CXCL12/SDF-1 alpha) is highly expressed in the postnatal CA1 st

130 /stromal cell-derived factor-1 alpha (CXCL12/SDF-1) via the CXC chemokine receptor 4 (CXCR4).

131 support for osteoblasts and decreased Cxcl12/SDF-1 production by mesenchymal progenitors.

132 MIP-1beta, and CCL5/RANTES but not of CXCL12/SDF-1.

133 pan3 deficiency disabled responses to CXCL12/SDF-1 and led to defects in AML localization within the

134 Similar changes of CXCR4, SDF-1, and AT1 receptor expression were found in Munich

135 These data demonstrate a) CXCR4/SDF-1-dependent adhesion increases in ischemia; b) CXCR4

136 ent adhesion increases in ischemia; b) CXCR4/SDF-1 activation is dependent on MSC surface caveolin-1;

137 The CXCR4/SDF-1 axis is a potential therapeutic target in AML to r

138 Because the CXCR4/SDF-1 axis is an important mechanism of leukemic stem ce

139 ools to study diseases mediated by the CXCR4/SDF-1 axis, including myocardial infarction, ischemic st

140 Furthermore, inhibition of the CXCR4/SDF-1 interaction decreased endothelial activation and o

141 tively, these data implicate the CXCR4/CXCR7/SDF-1 pathway in Stx-mediated pathogenesis and suggest n

142 Increasing PPCN concentration decreased SDF-1 release rate.

143 It decreased SDF-1-induced migration of MM cells, and down-regulated

144 tumorogenic role of microenvironment-derived SDF-1 in regulating adult pre-B LIC activity that may pr

145 r for SDF-1 places many previously described SDF-1 functions attributed to CXCR4 in question, though

146 e number of blood leukocytes, and diminished SDF-1 induced actin polymerization in whole blood.

147 antagonism, most probably by downregulating SDF-1 and the second receptor of the chemokine (CXCR4) e

148 ion of SDF-1 and stabilization of endogenous SDF-1 acutely increase MK-vasculature association and th

149 nts showing that inhibition of DPP4 enhances SDF-1-mediated progenitor cell survival, ex vivo cytokin

150 we performed system-based analyses examining SDF-1/CXCR4-mediated phosphoproteome, including construc

151 ogen independence in vivo, whereas exogenous SDF-1 treatment negated the inhibitory effects of treatm

152 ed in these cells by stromal-derived factor (SDF-1), an agonist known to regulate tumor cell metastas

153 ival in the absence of added growth factors, SDF-1-induced migration, NO release, and in vivo retinal

154 mRNA levels for SDF-1, VEGF, and IGF-1 and their receptors were increase

155 me PCR was used to determine mRNA levels for SDF-1, VEGF, IGF-1, and their cognate receptors in the r

156 lls, we evaluated the expression of mRNA for SDF-1 in damaged pancreatic tissue.

157 The discovery of CXCR7 as a new receptor for SDF-1 places many previously described SDF-1 functions a

158 A second chemokine receptor for SDF-1, CXCR7 was discovered recently and found on activa

159 phage differentiation, which is required for SDF-1 and I-TAC signaling to JNK and p38 pathways, leadi

160 emonstrate that PLC activity is required for SDF-1 to induce ERK activation, migration, and CXCR4 end

161 ts delineated two CXCR4 regions required for SDF-1 treatment to decrease cell-surface CXCR4 in neurob

162 C-gamma1, but not PLC-beta3, is required for SDF-1-mediated migration via a mechanism independent of

163 bility to protect co-cultured AML cells from SDF-1-induced apoptosis.

164 Furthermore, SDF-1-induced migration of WT EPCs was inhibited by AMD3

165 In lymphocytes, chemokine (e.g., SDF-1) stimulation inactivates ERM proteins, causing the

166 igh systemic TIMP-1 led to increased hepatic SDF-1 levels, which in turn promoted recruitment of neut

167 Immunohistochemically, SDF-1 expression was greatest at the 12-hour time point

168 Depletion of RasGRP1 impaired SDF-1-stimulated human T cell migration, expression of t

169 knockdown in zebrafish significantly impairs SDF-1/CXCR4-dependent migration of primordial germ cells

170 f the TMJ displays a synchronous increase in SDF-1 and RANTES expression and a higher capability of a

171 screened a peptide library for mutations in SDF-1 that provide resistance to matrix metalloproteinas

172 EK, ERK1/2, delta-catenin, and PPP1Calpha in SDF-1/CXCR4 signaling in breast CSCs.

173 f cultured DCs with an EP3 agonist increased SDF-1 production.

174 Importantly, we found that S1P induced SDF-1 secretion from BM stromal cells including Nestin(+

175 After myocardial infarction, SDF-1 expression is rapidly upregulated and promotes myo

176 In addition, they inhibit SDF-1-dependent signal transduction and cell migration i

177 Instead, SDF-1 treatment led via a CXCR4-dependent mechanism to a

178 Interestingly, SDF-1 administration reversed mobilization defect in KO

179 Intriguingly, SDF-1 treatment of T cells induced the formation of a no

180 ory activity in response to the CXCR4 ligand SDF-1/CXCL12, effects mediated by P-Rex1, a Rac-guanine

181 Nevertheless, CXCR4 and its ligand SDF-1 have been implicated in skin wound healing, system

182 ic seeding of organs that express its ligand SDF-1.

183 mpathetic ganglia, and (2) the CXCR4 ligand, SDF-1, is a chemoattractant for NCCs in vivo and is expr

184 suppression of CXCR4 as well as its ligand, SDF-1 (CXCL12), decreased THP-1 cell numbers due to redu

185 ccompanied by high expression of its ligand, SDF-1, in podocytes.

186 on of the three major myofibroblast markers, SDF-1, alpha-smooth muscle actin (alpha-SMA), and TGF-be

187 jury, we find dynamic fluctuations in marrow SDF-1 distribution that spatially and temporally correla

188 ing of the molecular mechanisms that mediate SDF-1 effects on T cells and reveal a novel mechanism of

189 PK pathway, indicating that RasGRP1 mediates SDF-1 functions.

190 Moreover, SDF-1-mediated signaling by both Gi proteins and ZAP-70

191 1c+ DCs dramatically reduced accumulation of SDF-1+CD11c+ DCs in regional LNs and LNM in LLC-injected

192 es and cancer stemness through activation of SDF-1/CXCR4 and AP-1 pathways.

193 e demonstrate that both IV administration of SDF-1 and stabilization of endogenous SDF-1 acutely incr

194 ysiological effects caused by application of SDF-1 alpha on either cell type.

195 N (PPCN+SDF-1) versus a bolus application of SDF-1 in phosphate buffered saline (PBS) on wound healin

196 y, we tested the hypothesis that blockade of SDF-1 (stromal cell-derived factor 1), a key stem cell m

197 view of phosphorylation events downstream of SDF-1/CXCR4 signaling in breast CSCs, providing a resour

198 and feedback regulation loops downstream of SDF-1/CXCR4 signaling in breast CSCs.

199 l CXCR7 inhibition potentiated the effect of SDF-1 antagonism, most probably by downregulating SDF-1

200 The effect of SDF-1 is blocked by an inhibitor of both ADAM10 and -17,

201 The angiogenic effect of SDF-1, alone or in combination with IGF-1 and VEGF, was

202 condary to the short transient expression of SDF-1 and the delayed expression of CM-CXCR4 following A

203 migration directly through the expression of SDF-1 independent of HIF-1alpha induction.

204 In LSCs, p38alpha induces the expression of SDF-1, which activates the stroma.

205 ing LNM via COX-2/EP3-dependent induction of SDF-1 and suggest that inhibition of this signaling axis

206 Furthermore, a continuous infusion of SDF-1 into the rabbit proximal tibial physis results in

207 -Kit(+)/Lin(-) (SKL) cells via inhibition of SDF-1 release.

208 Both inhibition of SDF-1-mediated neutrophil recruitment and systemic deple

209 drug AMD3100, a small molecule inhibitor of SDF-1/CXCR4 interactions.

210 Thus, interaction of SDF-1 and CXCR4 is required for Runx2 expression.

211 pathological alterations of local levels of SDF-1 alpha or CXCR4 expression may affect the functions

212 Finally, we demonstrate that manipulation of SDF-1 gradients can improve radiation-induced thrombocyt

213 dose tacrolimus also increased the number of SDF-1-bearing macrophages in the wound sites amplifying

214 cause of the mismatch in timings of peaks of SDF-1 and CXCR4, has no major role in ventricular remode

215 or type 1 (CCR1), which are the receptors of SDF-1 and RANTES, respectively.

216 increased markedly, and the up-regulation of SDF-1, and its receptor C-X-C chemokine receptor 7, was

217 The effect of sustained release of SDF-1 from PPCN (PPCN+SDF-1) versus a bolus application

218 In conclusion, sustained release of SDF-1 from PPCN is a promising and easy to use therapeut

219 h was to assess whether sustained release of SDF-1, a chemokine that promotes endothelial progenitor

220 etic cell transplantation (HCT), the role of SDF-1 in the adult zebrafish has yet to be determined.

221 Therapeutic use of SDF-1 in hindlimb ischemia may be challenged by proteoly

222 thesized that protease-resistant variants of SDF-1 can increase blood flow in an experimental model o

223 on by hypoxia alone, it had little effect on SDF-1 induction by IR, demonstrating an independent path

224 and VEGF demonstrated an additive effect on SDF-1-induced in vitro angiogenesis.

225 lirudin did not interfere with BMC homing or SDF-1/CXCR4 signaling.

226 e of ligand, activation by formyl peptide or SDF-1 did not result in a significant exposure of HUTS-2

227 ors (CD26, FGF, HGF, MMP-8, MMP-9, OPN, PF4, SDF-1) and cytokines (IL-1ra, IL-16) in BM Soup.

228 ildren infected with E. coli O157:H7, plasma SDF-1 levels were elevated in individuals who progressed

229 ting the role of ang II in inducing podocyte SDF-1 production, which ultimately activates PECs.

230 f sustained release of SDF-1 from PPCN (PPCN+SDF-1) versus a bolus application of SDF-1 in phosphate

231 SDF-1 was entrapped via gelation of the PPCN+SDF-1 solution above its lower critical solution tempera

232 Wounds treated with PPCN+SDF-1 had the shortest time for complete healing (24days

233 ays, and 17days for wounds treated with PPCN+SDF-1, SDF-1 only, PPCN only, and PBS, respectively.

234 treatment of human CB HSCs and HPCs promoted SDF-1-CXCR4-axis-mediated chemotaxis, homing, and long-t

235 Recombinant SDF-1 proteins carrying the mutations were designed, exp

236 onocyte responses and stem-cell recruitment (SDF-1) prevailed.

237 HIF-1alpha protein induction down-regulated SDF-1 induction by hypoxia alone, it had little effect o

238 Simulations replicating SDF-1 expression data revealed the requirement for coope

239 We identified the granulosa cell-secreted SDF-1 as a main chemoattractant that recruits malignant

240 ogenic factors IGF-1 and VEGF both stimulate SDF-1-induced angiogenesis.

241 ation-treated media showed IR induced strong SDF-1-dependent migration of ECs, augmented by hypoxia.

242 Here, we have studied SDF-1 alpha-mediated neuromodulation of the stratum lacu

243 -1) was decreased in mutant mice, suggesting SDF-1 as a candidate regulator of proteoglycan 4 actions

244 kit levels, and AMD3100 treatment suppressed SDF-1-induced, but not SCF-induced, c-kit phosphorylatio

245 Thus, rather than mediating survival, SDF-1 may be a means to induce apoptosis of CXCR4-expres

246 together, our data support the concept that SDF-1 regulates the spatial distribution of MKs in the m

247 We demonstrate that SDF-1 alpha dramatically reduces spontaneous firing in C

248 DF-1 inhibits gluconeogenesis, we found that SDF-1 promoted phosphorylation of Akt, FoxO1, and c-Src,

249 Exploring the mechanism, we found that SDF-1 treatment induced IQGAP1 binding to alpha-tubulin

250 Our data indicated that SDF-1/CXCR4 and RANTES/CCR1 signals are pivotal and func

251 ts, taken together with our observation that SDF-1 alpha reduces evoked field responses at the entorh

252 We show that SDF-1, the sole ligand for CXCR4, induces the expected m

253 We previously showed that SDF-1, a chemokine abundant in the bone marrow, induces

254 Our data suggest that SDF-1-mediated signaling plays a critical role in EPC-me

255 resulted in a 45% reduction, suggesting that SDF-1 and MMP-9 function independently to promote the tr

256 t volume 3 days after tMCAO, suggesting that SDF-1-mediated signaling was involved in EPC-mediated ne

257 AUF1 binds the SDF-1, alpha-SMA, TGF-beta1, and IL-6 mRNAs and reduces

258 s identified as target enzyme disrupting the SDF-1-CXCR4-axis by cleaving SDF-1, a chemotaxin recruit

259 Ischemic injury disrupts the SDF-1-CXCR4 interaction and releases BM PCs into the per

260 f CXCR4-expressing AML cells directly in the SDF-1-rich bone marrow microenvironment if the survival

261 Surprisingly, this was independent of the SDF-1-CXCR4 axis implicated in stem-cell migration.

262 ist AMD3100, but the other components of the SDF-1-CXCR4 signaling pathway are largely unknown.

263 ta offer novel insights into the role of the SDF-1/CXCR4 axis in the pathogenesis of neonatal hypoxia

264 compared to normal saline, inhibition of the SDF-1/CXCR4 axis significantly improved lung alveolariza

265 Pharmacologic inhibition of HIF-1 or of the SDF-1/CXCR4 interaction prevented the influx of BMDCs, p

266 rthermore, we demonstrate that targeting the SDF-1/CXCR4 pathway in the context of KLF10 deletion sub

267 We therefore conclude that the SDF-1/CXCR4 axis both prevents and reverses hypoxia-indu

268 together, we provide novel evidence that the SDF-1/CXCR4 axis, specifically activated by the SDF-1bet

269 ociated with chemokine signaling through the SDF-1-CXCR4 axis.

270 neovascularization by signaling through the SDF-1/CXCR4 axis.

271 VI) domain with high binding affinity to the SDF-1 receptor CXCR4 and extracellular matrix proteins t

272 e recruited toward endothelial cells via the SDF-1/CXCR4 axis and are induced to become pericytes pre

273 Importantly, these SDF-1-mediated changes have functional consequences for

274 This SDF-1-induced death pathway was partially inhibited by h

275 e medium of rat neuronal cultures exposed to SDF-1.

276 +) cells, resulting in enhanced migration to SDF-1 (P < 0.0001).

277 face expression, enhances their migration to SDF-1 in vitro and homing to bone marrow in vivo, and st

278 igrate through restrictive membrane pores to SDF-1 or Scf in vitro.

279 -null HSC/Ps fail to polarize in response to SDF-1 and cannot migrate through restrictive membrane po

280 ding Runx2, Col X, and MMP-13 in response to SDF-1 treatment.

281 1 mobilization and activation in response to SDF-1 was dependent on TCR expression, suggesting that C

282 ion and activation of RasGRP1 in response to SDF-1, a chemokine that signals via the G protein-couple

283 stem/progenitor cells (HSPC) in response to SDF-1.

284 ssociated signaling molecules in response to SDF-1.

285 stream transcriptional events in response to SDF-1.

286 an intracellular compartment in response to SDF-1.

287 ically unchanged in abundance in response to SDF-1/CXCR4 stimulation.

288 iting normal proximal signaling responses to SDF-1, but reduced adhesiveness, F-actin assembly, and r

289 e also defective in chemotactic responses to SDF-1.

290 lts in increased migratory responsiveness to SDF-1 and soluble VCAM-1, which are among the chemokines

291 We identified a previously unidentified SDF-1/CXCR4-PKA-MAP2K2-ERK signaling pathway and demonst

292 Upon SDF-1 stimulation, CXCR4 localizes to Rab11(+) vesicles,

293 These results indicated that, upon SDF-1 treatment, Galpha13 and Rho mediate the actin poly

294 was subsequently used to investigate whether SDF-1 was the invasion signal.

295 In examining the mechanism by which SDF-1 inhibits gluconeogenesis, we found that SDF-1 prom

296 lated positively with LDL cholesterol, while SDF-1 levels were not significantly affected.

297 of CXCR4 overexpression were correlated with SDF-1-mediated activation of downstream signaling via ER

298 ver, treatment of the neuronal cultures with SDF-1 stimulates expression of the inducible metalloprot

299 eptor pathway may participate, together with SDF-1/CXCR4 axis, to the dysregulated response of renal

300 -surface expression following treatment with SDF-1.