ライフサイエンスコーパス: SDF-1alpha

1 SDF-1alpha (CXCL12) signaling via its receptor, CXCR4, s

2 SDF-1alpha acts as a chemoattractant for immune and hemo

3 SDF-1alpha also decreases monocyte adherence to brain mi

4 SDF-1alpha expression in cells was measured by enzyme-li

5 SDF-1alpha expression in nonstimulated Nur77(-/-) BMM is

6 SDF-1alpha expression is higher in lesions of Nur77(-/-)

7 SDF-1alpha in diabetic wounds were therapeutically incre

8 SDF-1alpha increased EC-EPC adhesion and specifically up

9 SDF-1alpha levels were determined by enzyme-linked immun

10 SDF-1alpha may be involved in the immune defense pathway

11 SDF-1alpha production by other cell types is regulated b

12 SDF-1alpha production increased significantly after 1 or

13 SDF-1alpha was increased in group 3 animal hearts (20-fo

14 SDF-1alpha-engineered cell-based therapy promotes diabet

15 SDF-1alpha-primed BMDSC significantly promote wound heal

16 SDF-1alpha/CXCR4 signaling plays a key role in leukemia/

17 genic factors stromal cell-derived factor 1 (SDF-1alpha), vascular endothelial growth factor (VEGF),

18 CXCR4 ligand stromal cell-derived factor 1 (SDF-1alpha, CXCL12) produced by stromal cells, and BTK-i

19 d its ligand, stromal cell-derived factor-1 (SDF-1alpha or CXC chemokine ligand 12) are involved in t

20 ligand, stromal cell-derived factor 1alpha (SDF-1alpha) / chemokine (C-X-C motif) ligand 12 (CXCL12)

21 hemokine stromal cell-derived factor 1alpha (SDF-1alpha) and elicits a number of biological effects,

22 MLP) and stromal cell-derived factor 1alpha (SDF-1alpha) as well as decreased alpha5beta1-integrin-me

23 expression of stromal-derived factor 1alpha (SDF-1alpha), a chemokine that promotes tissue retention

24 5 antagonized stromal-derived factor 1alpha (SDF-1alpha)-induced and stroma-induced chemotaxis and in

25 factors stromal cell-derived factor 1alpha (SDF-1alpha)/CXCL12, monocyte chemoattractant protein 1 (

26 Stromal cell-derived factor-1alpha (SDF-1alpha) and its chemokine receptor 4 (CXCR4) were re

27 expression of stromal-derived factor-1alpha (SDF-1alpha) and its mobilizing effects on BM.

28 f radioligand stromal-derived factor-1alpha (SDF-1alpha) binding to CXCR4, was also found to be highl

29 Stromal cell-derived factor-1alpha (SDF-1alpha) binding to its cognate receptor, CXCR4, regu

30 e marrow stromal cell-derived factor-1alpha (SDF-1alpha) expression (40% reduction, P < 0.01).

31 al release of stromal-derived factor-1alpha (SDF-1alpha) from an implant.

32 hemokine stromal cell-derived factor-1alpha (SDF-1alpha) has multiple effects on neuronal activity, s

33 Stromal cell-derived growth factor-1alpha (SDF-1alpha) is a member of the CXC chemokines and intera

34 Stromal cell-derived factor-1alpha (SDF-1alpha) is a natural ligand of CXCR4.

35 hemokine stromal cell-derived factor-1alpha (SDF-1alpha) is a pivotal player in angiogenesis.

36 own that stromal cell-derived factor-1alpha (SDF-1alpha) is downregulated within diabetic cutaneous w

37 describe that stromal-derived factor-1alpha (SDF-1alpha) ligation of CXCR4 on activated T cells promo

38 hemokine stromal cell-derived factor-1alpha (SDF-1alpha) on VLA-4-mediated lymphocyte adhesion, human

39 CXCL12/stromal cell-derived factor-1alpha (SDF-1alpha), a chemokine ligand for the G protein-couple

40 nd level stromal cell-derived factor-1alpha (SDF-1alpha), a chemokine that mediates EPC recruitment i

41 ligand, stromal cell-derived factor-1alpha (SDF-1alpha), correlate with increased fibrosis in these

42 protein stromal cell-derived factor-1alpha (SDF-1alpha), which activates the cell-survival factor pr

43 ncluding stromal cell-derived factor-1alpha (SDF-1alpha), which triggers mobilization and homing of b

44 able for stromal cell-derived factor-1alpha (SDF-1alpha)- or B-lymphocyte chemoattractant (BLC)-induc

45 to increased stromal-derived factor-1alpha (SDF-1alpha)-induced chemotaxis and chemokinesis (random

46 blocked stromal cell-derived factor-1alpha (SDF-1alpha)-stimulated LFA-1-ICAM-1 (intercellular adhes

47 hemokine stromal cell-derived factor-1alpha (SDF-1alpha).

48 emokine, stromal cell-derived factor-1alpha (SDF-1alpha).

49 elivered stromal cell-derived factor-1alpha (SDF-1alpha).

50 ted that stromal cell-derived factor-1alpha (SDF-1alpha, a homing signal for recruiting endothelial p

51 The chemokine stromal-derived factor-1alpha (SDF-1alpha, CXCL12) and its receptor CXCR4 are implicate

52 anti-CXCL12 [stromal derived factor-1alpha, (SDF-1alpha)] blocking serum resulted in a marked impairm

53 resulted in a significant increase in CXCR-4/SDF-1alpha expression and promoted CD133(+)/c-kit(+), CD

54 CXCR4-positive tumor cells migrated toward a SDF-1alpha gradient in vitro, whereas inhibition of CXCR

55 elial cells (EC) and circulating EPC achieve SDF-1alpha-mediated EPC homing.

56 Additionally, SDF-1alpha and SDF-1beta both inhibited activation of th

57 This study adds SDF-1alpha as a mediator within the neural-immune-hemopo

58 stromal cell-derived growth factor 1 alpha (SDF-1alpha) and interleukin 1 beta (IL-1beta) collaborat

59 ch increases stromal-derived factor 1 alpha (SDF-1alpha) expression in cancer and stromal cells and,

60 tment factor stromal-derived factor 1 alpha (SDF-1alpha) than control lung endothelial cells, and thu

61 ator of stromal cell-derived factor 1 alpha (SDF-1alpha)-induced Rap1 activation.

62 Inhibition of integrin-alpha4beta1, SDF-1alpha, or IL-1beta was sufficient to block tumor in

63 ogen and fibronectin and migration toward an SDF-1alpha gradient were reduced in Cib1(-/-) megakaryoc

64 ion via upregulation of heme oxygenase-1 and SDF-1alpha.

65 ol 3-kinase signaling blocked HIF-1alpha and SDF-1alpha upregulation induced by PTEN depletion.

66 Signals induced by IL-1beta and SDF-1alpha promoted the interaction of talin and paxilli

67 pha in an in vitro cell migration assay, and SDF-1alpha treatment triggered a robust induction of tyr

68 hepatic protein expression of both CXCR4 and SDF-1alpha is increased in hepatitis C cirrhotic livers

69 CD4 T cells are treated with both gp120 and SDF-1alpha, the SDF-1alpha-driven effects of Bim(EL) deg

70 t the effect of wounding on tumor growth and SDF-1alpha levels is host dependent and varies between m

71 expression of interleukin-12, IFNgamma, and SDF-1alpha and increased NO synthesis in (non)-stimulate

72 the diabetic defect in EPC mobilization, and SDF-1alpha reversed the diabetic defect in EPC homing.

73 ogenic growth factors (VEGF, HGF, PLGF), and SDF-1alpha receptor CXCR4.

74 CXCR4 activation with ubiquitin and SDF-1alpha lead to similar Galpha(i)-responses and to a

75 role in inducing the secretion of angiogenic SDF-1alpha/CXCL12, MCP-1/CCL2, and VEGF in RA ST fibrobl

76 ICAM-1 in the presence of uniformly applied SDF-1alpha were also found to migrate against the direct

77 We used CXCL12 (also known as SDF-1alpha) and epidermal growth factor (EGF), two well-

78 Chemokines such as SDF-1alpha play a crucial role in orchestrating T lympho

79 to the BM in response to chemokines, such as SDF-1alpha, the ligand for CXCR4.

80 tein-coupled receptor (GPCR) ligands such as SDF-1alpha, whereas p110delta is expressed at low level

81 s is consistent with the association between SDF-1alpha expression with fibrotic septa in cirrhotic l

82 results provide a novel causal link between SDF-1alpha-induced chemotaxis, degradation of Bim(EL), a

83 on factor Yin Yang 1 (YY1) as a link between SDF-1alpha/CXCR4 signaling and let-7a, as YY1 was upregu

84 rutinib and CXCR4-inhibitor plerixafor block SDF-1alpha-mediated CD20 upregulation.

85 Blocking SDF-1alpha activity with neutralizing antibodies abrogat

86 Blocking SDF-1alpha attenuated autocrine growth and blocked growt

87 Blocking SDF-1alpha/CXCR4 or Gr-1(+) myeloid cell infiltration ma

88 s G protein-associated signaling, and blocks SDF-1alpha-mediated chemotaxis.

89 Both SDF-1alpha and Tac1 peptides are relevant hemopoietic re

90 Blastema cells express both SDF-1alpha receptors, CXCR4 and CXCR7, although the migr

91 ent epitope of the beta(2) integrin LFA-1 by SDF-1alpha.

92 e activity of Nur77(-/-) BMM is abolished by SDF-1alpha inhibiting antibodies.

93 CXCR4 receptor activation by SDF-1alpha is profibrogenic through its effects on HSC a

94 In isolated myocytes, CXCR4 activation by SDF-1alpha resulted in increased phosphorylation of both

95 d that the miRNA let-7a was downregulated by SDF-1alpha-mediated CXCR4 activation and increased by CX

96 s in preventing HNSCC metastasis mediated by SDF-1alpha.

97 naling and let-7a, as YY1 was upregulated by SDF-1alpha and downregulated by treatment with a CXCR4 a

98 +)/c-kit(+), CD133(+)/CXCR-4(+) and CD133(+)/SDF-1alpha(+) cell recruitment into ischemic hearts.

99 n this study, we show that in human T cells, SDF-1alpha-mediated beta(2) integrin activation is drive

100 In these pathologies, the chemokine SDF-1alpha (CXCL12) is over-expressed and might attract

101 The chemokine SDF-1alpha was highly expressed in neurons, blood vessel

102 intained high-affinity binding of chemokines SDF-1alpha and RANTES to CXCR4 and CCR5, respectively.

103 CXCL12 (SDF-1alpha) and CXCR4 are critical for embryonic develop

104 , CCL5 (RANTES), CXCL11 (I-TAC), and CXCL12 (SDF-1alpha) bind the chemokines with high affinity (at n

105 ditions or when combined with apical CXCL12 (SDF-1alpha) under static conditions.

106 MIF internalized CXCR4, but unlike CXCL12 (SDF-1alpha), it did not phosphorylate Erk1/2 after CXCR4

107 nce the discovery that CXCR7 binds to CXCL12/SDF-1alpha, the role of CXCR7 in CXCL12-mediated biologi

108 ing the stromal-derived factor 1alpha/CXCR4 (SDF-1alpha/CXCR4) axis to overcome chemoresistance of AM

109 The CXCR4-SDF-1alpha axis has been postulated to increase melanoma

110 hat thymoglobulin effectively inhibits CXCR4/SDF-1alpha-driven T-cell chemotaxis.

111 ell migration is stimulated by the cytokine, SDF-1alpha, and that SDF-1alpha is expressed by the woun

112 ocytes using small interfering RNA decreases SDF-1alpha-mediated migration and prevents the inhibitio

113 as found to be dependent on platelet-derived SDF-1alpha.

114 ed that the CXCR4 peptide stabilizes dimeric SDF-1alpha, and that sulfotyrosine 21 binds a specific s

115 , decreased circulating EPCs, and diminished SDF-1alpha expression in cutaneous wounds.

116 imilar to that of mutant mice lacking either SDF-1alpha or CXCR4.

117 romoted tumor growth is mediated by elevated SDF-1alpha levels and indicate that the effect of acute

118 ri-infarct intramyocardial injection of ESA, SDF-1alpha, or saline.

119 kines, which bind CCR5 and CXCR4, especially SDF-1alpha/CXCL12, result in a transient opening (peak a

120 However, increased wound levels of exogenous SDF-1alpha results in elevated systemic levels of this p

121 dentified that PLCepsilon1 was necessary for SDF-1alpha-induced adhesion using shear stress, cell mor

122 enesis and provide a mechanistic pathway for SDF-1alpha-induced endothelial cell migration.

123 , several studies have implicated a role for SDF-1alpha in head and neck squamous cell carcinoma (HNS

124 rently there is little information about how SDF-1alpha promotes HNSCC metastasis.

125 However, SDF-1alpha expression was augmented in bile ducts and ov

126 , 30, and 55% of cell migration into Gtn-HPA/SDF-1alpha-PCN hydrogels involved MMP-2, 3, and 9, respe

127 (aNPCs) and their neuronal progeny, Gtn-HPA/SDF-1alpha-PCN hydrogels promoted chemotactic recruitmen

128 Overall, Gtn-HPA/SDF-1alpha-PCN hydrogels prove to be promising biomateri

129 n cross-linked with 0.85-0.95 mM HO, Gtn-HPA/SDF-1alpha-PCN hydrogels provided optimally permissive s

130 ty is responsive to stimulation by SCF, IL3, SDF-1alpha, and fibronectin.

131 Immobilized SDF-1alpha acted within the lifetime of a primary tether

132 plate flow chamber with surface-immobilized SDF-1alpha, a potent activator of firm adhesion.

133 As expected, the immobilized SDF-1alpha also increased the ratio of PBL firm adhesion

134 ogation of surface CXCR4 expression impaired SDF-1alpha directed migration and was mediated through t

135 kocyte-specific F-actin-bundling protein, in SDF-1alpha-stimulated human T lymphocyte polarization an

136 the N-terminus of SDF-1alpha play a role in SDF-1alpha signaling via CXCR4 and/or receptor internali

137 Thus, in SDF-1alpha-stimulated monocytes, Lyn acts as a positive

138 cell migration toward SMCs through increased SDF-1alpha production.

139 IL-18-induced SDF-1alpha/CXCL12 up-regulation was dependent on JNK, p3

140 and stroma-induced chemotaxis and inhibited SDF-1alpha-induced activation of prosurvival signaling p

141 uanine exchange factor CalDAG-GEFI inhibited SDF-1alpha- and phorbol 12-myristate 13-acetate (PMA)-in

142 selectin antagonists significantly inhibited SDF-1alpha-induced EC-EPC adhesion, EPC homing, wound ne

143 vascular E-selectin significantly inhibited SDF-1alpha-induced EPC homing, tumor angiogenesis, and d

144 key substrates including APOE, and inhibits SDF-1alpha/CXCR4-mediated chemotaxis, culminating in an

145 Inhibition of the iNOS/SDF-1alpha signaling pathway reduced vascular repair as

146 lts suggest that an increase in intratumoral SDF-1alpha triggered by LI recruits myelomonocytes/macro

147 describe the identification of an intricate SDF-1alpha-induced signaling cascade that involves endot

148 Two human SDF-1 isoforms, SDF-1alpha and SDF-1beta, have been reported to date.

149 After intravenous injection, 99mTc-labeled SDF-1alpha displays a blood half-life of 25.8 +/- 4.6 mi

150 We describe a 99mTc-labeled SDF-1alpha radiotracer that can be used as a sensitive a

151 to 45-fold relative to hydrogels that lacked SDF-1alpha or vehicles to sustain SDF-1alpha release.

152 orced overexpression of SDF-1alpha (by Lenti-SDF-1alpha) increased melanoma cell growth both in vitro

153 led switch mechanism in diabetic bone marrow SDF-1alpha expression (2.8% reduction) resulted in impai

154 ation is mediated by a switch in bone marrow SDF-1alpha levels.

155 Restoring the bone marrow SDF-1alpha switch (54% reduction, P < 0.01) with plerixa

156 ciated with diabetes by reducing bone marrow SDF-1alpha, restoring normal PC mobilization and tissue

157 han 5-fold, as quantified using [99mTc-MAS3]-SDF-1alpha and confirmed using confocal immunofluorescen

158 [99mTc-MAS3]-SDF-1alpha could be prepared in 2 h total with a specifi

159 [99mTc-MAS3]-SDF-1alpha exhibits high specificity for CXCR4 on the su

160 rance of intravenously injected [99mTc-MAS3]-SDF-1alpha were quantified in Sprague-Dawley rats before

161 d phosphoinositide 3-kinase pathways mediate SDF-1alpha-induced effects on HSC expression of collagen

162 out the actual signaling events that mediate SDF-1alpha-induced endothelial cell function.

163 minent role of the phosphatase is to mediate SDF-1alpha/CXCR4 signal in guiding cerebellar granule ce

164 ll recruitment through a HIF-1alpha-mediated SDF-1alpha/CXCR4 axis, thus identifying PTEN as a target

165 e ZAP-70 tyrosine kinase critically mediates SDF-1alpha-dependent migration and prolonged ERK mitogen

166 nsic signaling pathway of iNOS that mediates SDF-1alpha to promote GFP(+)-BMDC infiltration/targeting

167 he role of adhesion molecule(s) in mediating SDF-1alpha-induced EPC homing, and wound healing was fur

168 ting as stimulator, whereas 50 and 100 ng/ml SDF-1alpha acted as inhibitors.

169 -1alpha on luciferase activity with 20 ng/ml SDF-1alpha acting as stimulator, whereas 50 and 100 ng/m

170 n the repressive effects at 50 and 100 ng/ml SDF-1alpha.

171 Myocardial SDF-1alpha and CXCR4 mRNA and protein were found to be e

172 hich is associated with increased myocardial SDF-1alpha expression.

173 cted to ischemic preconditioning, myocardial SDF-1alpha mRNA was found to be increased 3 hours later

174 imary and immortalized keratinocytes show no SDF-1alpha-mediated NF-kappaB activity.

175 These results suggest that the ability of SDF-1alpha to activate CXCR4 signaling and internalizati

176 an digit regeneration involves activation of SDF-1alpha/CXCR4 signaling by endothelial cells to recru

177 In vivo, administration of SDF-1alpha before 30 minutes of coronary occlusion follo

178 Administration of SDF-1alpha into wounds reversed the EPC homing impairmen

179 alized with L-plastin at the leading edge of SDF-1alpha-stimulated lymphocytes.

180 ocalized with F-actin at the leading edge of SDF-1alpha-stimulated T lymphocytes and was also phospho

181 signals underlying the biological effect of SDF-1alpha on EPC homing and point to E-selectin as a ne

182 ell assays that showed an indirect effect of SDF-1alpha on hemopoiesis through substance P production

183 egion of Tac1 showed a bell-shaped effect of SDF-1alpha on luciferase activity with 20 ng/ml SDF-1alp

184 w paradigms for understanding the effects of SDF-1alpha and other chemokines on immunity.

185 The regulatory effects of SDF-1alpha on EC-EPC adhesion and EPC homing were specif

186 This study investigated the effects of SDF-1alpha on Tac1 expression in the major hemopoietic s

187 mediate prohealing/proangiogenic effects of SDF-1alpha-primed BMDSC was evaluated by polymerase chai

188 growth factor up-regulated the expression of SDF-1alpha.

189 rough a 3D ECM under artificial gradients of SDF-1alpha.

190 s significantly reduced by the inhibition of SDF-1alpha activity.

191 Conversely, systemic inhibition of SDF-1alpha signaling with the small molecule AMD 3100 ab

192 Conversely, treatment with an inhibitor of SDF-1alpha receptor CXCR4 (AMD3100) with LI significantl

193 re therapeutically increased by injection of SDF-1alpha-engineered bone marrow-derived fibroblasts ve

194 The low levels of SDF-1alpha in BCCs regulate interactions between BM stro

195 ith periodontal disease had higher levels of SDF-1alpha in their GCF compared to healthy subjects.

196 rly, inhibition of CXCR4 decreased levels of SDF-1alpha-induced phosphorylation of FAK, AKT, and ERK1

197 ells tested expressed undetectable levels of SDF-1alpha.

198 cal therapy demonstrated decreased levels of SDF-1alpha.

199 eukocyte extravasation but not the levels of SDF-1alpha.

200 Additional enforced overexpression of SDF-1alpha (by Lenti-SDF-1alpha) increased melanoma cell

201 centrations of EGF; however, the presence of SDF-1alpha and EGF together modulated tumor cell motilit

202 il migration was enhanced in the presence of SDF-1alpha, mimicking immune cell migration in periodont

203 stance P does not regulate the production of SDF-1alpha in stroma.

204 crine growth through increased production of SDF-1alpha.

205 crine stimulator to induce the production of SDF-1alpha.

206 While IL-18-induced production of SDF-1alpha/CXCL12 was also dependent on protein kinase C

207 -18 significantly enhanced the production of SDF-1alpha/CXCL12, MCP-1/CCL2, and VEGF in RA ST fibrobl

208 gen synthase kinase 3beta besides release of SDF-1alpha in parallel with IGF-1 expression in (IGF-1)M

209 main chain amide bonds in the N-terminus of SDF-1alpha play a role in SDF-1alpha signaling via CXCR4

210 main chain amide bonds in the N-terminus of SDF-1alpha.

211 ons suggest that adenoviral gene transfer of SDF-1alpha may be a useful strategy to accumulate dendri

212 Human melanoma cells overexpressing SDF-1alpha were xenografted on severe combined immunodef

213 ing a highly predicted ligand-receptor pair, SDF-1alpha - CXCR4, and both PPCs and RPCs exhibited sig

214 d in situ to induce chemokinesis, potentiate SDF-1alpha chemotactic recruitment, and increase prolife

215 However, prolonged SDF-1alpha treatment leads to CXCR4-mediated activation

216 he gradient) followed the ligand - receptor (SDF-1alpha - CXCR4) binding kinetics.

217 Recombinant SDF-1alpha was radiolabeled under aprotic conditions and

218 , and that direct application of recombinant SDF-1alpha increases wound closure rates, neovasculariza

219 Treatment of stellate cells with recombinant SDF-1alpha increases expression of alpha-smooth muscle a

220 h an IKKbeta inhibitor significantly reduces SDF-1alpha-mediated HNSCC invasion.

221 Furthermore, L-plastin also regulated SDF-1alpha-mediated lymphocyte migration on the integrin

222 Contrary to previous reports, SDF-1alpha-induced NF-kappaB activation is not mediated

223 has an anti-inflammatory function, represses SDF-1alpha expression and inhibits atherosclerosis.

224 diated downregulation of HIF-1alpha reversed SDF-1alpha induction by PTEN depletion and inhibition of

225 Serum SDF-1alpha levels were measured with enzyme-linked immun

226 ce, whereas AMPK-mediated elevation of serum SDF-1alpha levels and improvements of EPC function and r

227 e, we used this approach to design novel SMM-SDF-1alpha analogues containing unnatural N-methylated r

228 nstrate that after treatment with sorafenib, SDF-1alpha increased the survival of HSCs and their alph

229 Taken together, our data suggest SDF-1alpha/CXCR4 may promote HNSCC invasion and metastas

230 pancreatic, and breast tumors; surprisingly, SDF-1alpha was expressed only by tumor cells, whereas IL

231 hat lacked SDF-1alpha or vehicles to sustain SDF-1alpha release.

232 cells into wounds does not increase systemic SDF-1alpha levels.

233 el Kv2.1 in response to short- and long-term SDF-1alpha/CXCR4-mediated signaling as an underlying mec

234 ulated by the cytokine, SDF-1alpha, and that SDF-1alpha is expressed by the wound epidermis as well a

235 We conclude that SDF-1alpha and its receptor, CXCR4, constitute a paracri

236 In vitro studies confirmed that SDF-1alpha, acting through CXCR4, expressed on bone marr

237 We discovered that SDF-1alpha specifically upregulates E-selectin on endoth

238 We found that SDF-1alpha and IL-1beta are highly expressed in the micr

239 We found that SDF-1alpha-mediated NF-kappaB signaling is independent o

240 We demonstrate here that SDF-1alpha stimulates migration of monocytes through its

241 The studies indicate that SDF-1alpha levels above baseline production in bone marr

242 These findings indicate that SDF-1alpha/CXCR4 interactions contribute to the resistan

243 We observed that SDF-1alpha induces IkappaBalpha phosphorylation and degr

244 We previously reported that SDF-1alpha-induced EPC homing is mediated by a panel of

245 The results show that SDF-1alpha analogues with a modified N-methylated main c

246 from isolated primary hepatocytes show that SDF-1alpha and SDF-1beta inhibited glucose production vi

247 Here, we show that SDF-1alpha presented in wound tissue and released into c

248 Finally, we show that SDF-1alpha-expressing COS1 cells engrafted into a regene

249 Immunohistologic staining showed that SDF-1alpha and CXCR4 levels were elevated in samples obt

250 We have shown that SDF-1alpha-induced activation of Rap1 is transient in co

251 These studies suggest that SDF-1alpha may be a useful biomarker for the identificat

252 These findings suggest that SDF-1alpha may serve a tissue-protective and regenerativ

253 Inhibitor studies suggest that SDF-1alpha/CXCR4-dependent extracellular signal-regulate

254 -kappaB in HNSCC cell lines, suggesting that SDF-1alpha activates the classical NF-kappaB signaling p

255 The SDF-1alpha/C-X-C receptor type 4 (CXCR4) pathway directl

256 treated with both gp120 and SDF-1alpha, the SDF-1alpha-driven effects of Bim(EL) degradation and acq

257 In contrast, the SDF-1alpha receptor, CXCR4, was highly expressed in inva

258 s coexpressing SM-alpha-actin and CXCR4, the SDF-1alpha receptor, was detected in SMC PTEN-depleted m

259 cruitment of BM-derived cells expressing the SDF-1alpha receptor CXCR4; homing of FSP-1-positive cell

260 However, the role of the SDF-1alpha-CXCR4 axis in modulating myocardial ischemia/

261 a4)-mobilized cells is less dependent on the SDF-1alpha/CXCR4 axis.

262 Previous studies have demonstrated that the SDF-1alpha analog CTCE-0214 (CTCE) is beneficial in poly

263 We conclude that the SDF-1alpha dimer preferentially interacts with receptor

264 We demonstrate that the SDF-1alpha-induced activation of JNK3, critical for endo

265 Upon the development of diseased tissues, SDF-1alpha levels increase and may recruit host defensiv

266 etastatic mouse breast cancer cells (4T1) to SDF-1alpha, which is increased in wound fluid, results i

267 we found that the chemoinvasive behavior to SDF-1alpha gradients was abrogated or even reversed in t

268 Both, wounding and exposure of 4T1 cells to SDF-1alpha not only increased tumor growth, but also tum

269 h improved cardiac function, mice exposed to SDF-1alpha demonstrated significantly decreased scar for

270 cGMP production and migration to SDF-1alpha were also determined.

271 Acute exposure of neurons to SDF-1alpha led to dynamic dephosphorylation and altered

272 ignaling pathway is activated in response to SDF-1alpha in HNSCC while primary and immortalized kerat

273 actin assembly and chemotaxis in response to SDF-1alpha stimulation.

274 cycle and Akt phosphorylation in response to SDF-1alpha stimulation.

275 hout increasing eNOS activity in response to SDF-1alpha.

276 bioavailability and migration in response to SDF-1alpha.

277 in new blood vessel formation in response to SDF-1alpha.

278 reased Ca2+ rise and chemotactic response to SDF-1alpha.

279 luence changes in cAMP levels in response to SDF-1alpha.

280 When subjected to SDF-1alpha gradients alone, MDA-MB-231 cells migrated up

281 on VCAM-1 and the migration of cells toward SDF-1alpha.

282 cient granule cells failed to migrate toward SDF-1alpha in an in vitro cell migration assay, and SDF-

283 ore S1P3 than inflammatory monocytes, toward SDF-1alpha was also enhanced with FTY720 treatment, but

284 Unlike SDF-1alpha, gp120 ligation of CXCR4 has the opposite eff

285 Unlike SDF-1alpha, ubiquitin lacks interactions with an N-termi

286 ld stronger beta(2) integrin activation upon SDF-1alpha stimulation compared with CD28(+) T cells.

287 of multiple trophic factors including VEGF, SDF-1alpha, IGF-1, and Shh itself, for at least 48 hours

288 n induced massive stem cell mobilization via SDF-1alpha signaling and culminated in extensive angiomy

289 Our results reveal a signaling pathway where SDF-1alpha induces T-cell adhesion through activation of

290 rpose of this study was to determine whether SDF-1alpha secreted by host cells plays a role in recrui

291 is assays were also used to evaluate whether SDF-1alpha plays a role in the recruitment of host cells

292 R4 in vivo and in vitro and explored whether SDF-1alpha/CXCR4 receptor engagement promotes HSC activa

293 bone marrow-derived stem cells (BMDSC) with SDF-1alpha.

294 abrogated by receptor desensitization (with SDF-1alpha) or pretreatment with the specific antagonist

295 c Lepr mice were incubated for 20 hours with SDF-1alpha (100 ng/mL) or bovine serum albumin (control)

296 erapeutics devoid of major interference with SDF-1alpha function.

297 Cultured myocytes pretreated with SDF-1alpha were resistant to hypoxia/reoxygenation damag

298 The decrease in infarct size with SDF-1alpha administration also was blocked by AMD3100.

299 Activated primary CD4 T cells treated with SDF-1alpha therefore become resistant to the proapoptoti

300 Increasing wound SDF-1alpha via cell-based therapy promotes healing in di