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 significantly increased in the pancreas after

9 SDF-1 was upregulated in ischemic brain.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

54 4 (CXCR4) and stromal cell-derived factor-1 (SDF-1, also known as CXCL12) is a natural regulatory pro

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

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

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

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

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

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

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

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

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

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

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

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

67 a and AKT kinase were associated with active SDF-1/CXCL12-stimulated P-REX1.

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

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

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

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

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

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

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

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

76 5 Gray IR-induced EC HIF-1alpha and SDF-1 expression was greater when combined with hypoxia

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

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

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

80 The levels of CTACK, IP-10, SCGF-beta, and SDF-1 alpha were significantly higher in patients with d

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

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

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

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

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

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

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

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

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

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

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

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

93 Autocrine SDF-1/CXCR4 signaling induces L-CSC proliferation and su

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

114 pacity to migrate toward the chemoattractant SDF-1.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

140 Increasing PPCN concentration decreased SDF-1 release rate.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

172 we found AF treatment dramatically increased SDF-1 expressing cells, HGF expressing Ym1+ M2 macrophag

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

174 PDGFRalpha signaling induces SDF-1 expression and secretion, and the autocrine activa

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

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

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

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

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

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

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

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

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

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

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

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

208 regulates SDF-1 expression and inhibition of SDF-1/CXCR4 and PDGFR pathways blocks distant metastasis

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 ) express CXCR4 and CXCR7, both receptors of SDF-1.

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

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

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

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

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

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

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

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

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

226 ab4-positive vesicles following either AM or SDF-1/CXCL12 binding, thereby enabling formation of dyna

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

228 cate that functional crosstalk between PDGFR/SDF-1 signaling regulates tumor cell invasion and metast

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

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

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

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

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

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

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

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

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

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

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

240 Furthermore, PDGFR regulates SDF-1 expression and inhibition of SDF-1/CXCR4 and PDGFR

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 which increases their recruitment to tumors, SDF-1 secretion, and metastasis-promoting phenotype.See

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

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

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

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

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.