ライフサイエンスコーパス: SDF

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

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

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

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

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

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

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

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

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

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

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

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

13 evated inflammatory markers including: MCP-1 SDF-1a, IL-Ra, MIP-1b, IL-8, and VEGF in comparison to u

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

33 4 (CXCR4) and stromal cell-derived factor-1 (SDF-1, also known as CXCL12) is a natural regulatory pro

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

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

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

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

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

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

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

41 ized them for stromal-derived factor-1alpha (SDF)-induced migration.

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

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

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

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

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

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

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

49 One 1D SDF representation can be used to generate infinite sets

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

71 (CaCl2.2H2O + K2HPO4 in buffer solution) and SDF (Ag[NH3]2F in buffer solution).

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

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

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

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

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

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

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

79 Thus intermolecular interactions between SDF and BS depend on both SDF source and its molecular w

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

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

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

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

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

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

86 teractions between SDF and BS depend on both SDF source and its molecular weight and may occur alone

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

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

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

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

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

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

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

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

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

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

97 pacity to migrate toward the chemoattractant SDF-1.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

113 ogy to study evergreen (EF), semi-deciduous (SDF), dry forests (DF) and woody savanna (WS), we find t

114 Increasing PPCN concentration decreased SDF-1 release rate.

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

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

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

118 riment with calcium phosphate with different SDF concentrations (0.38, 1.52, 2.66, 3.80 mg/mL) to inv

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

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

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

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

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

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

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

126 Tet-Off-SDF-1beta BMSCs, which over-express SDF-1beta under tight doxycycline-control, thus providin

127 and its ligand stromal cell-derived factor (SDF)-1 are known to be involved in inflammation.

128 Stromal cell-derived factor (SDF)-1alpha facilitates EPC recruitment and is elevated

129 s ubiquitin and stromal cell-derived factor (SDF)-1alpha induced effects on cell signaling and functi

130 whereas plasma stromal cell-derived factor (SDF)-1alpha levels were significantly lower.

131 he secretion of stromal cell-derived factor (SDF)-1alpha were upregulated in EPCs derived from the tr

132 Soluble dietary fibre (SDF) is considered the most effective fraction of dietar

133 The soluble fibre (SDF) was composed of glucose, galacturonic acid and arab

134 interaction between soluble dietary fibres (SDFs), such as (1,3:1,4)-beta-D-glucan (betaG) and arabi

135 Silver diamine fluoride (SDF) is found to promote remineralization and harden the

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

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

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

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

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

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

142 -dimensional (1D) spectral density function (SDF) as the unique representation of non-deterministic q

143 terns by Fourier spectral density functions (SDFs) that could bridge the processing-structure and str

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

145 ad no effect on BMSC proliferation; however, SDF-1beta significantly protected genetically engineered

146 , 30, and 55% of cell migration into Gtn-HPA/SDF-1alpha-PCN hydrogels involved MMP-2, 3, and 9, respe

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

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

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

150 ing sublingual sidestream darkfield imaging (SDF) and endothelial function testing using peripheral a

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

152 ol polyphosphate 4-phosphatase show impaired SDF-induced PI(3,4)P2 responses and reduced migration in

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

154 n the a-direction but not the c-direction in SDF groups was revealed, which suggested that small loca

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

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

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

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

159 ut in common chemical file formats including SDF and SMILES and provides tools for visualizing the li

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

161 in resting CD4(+) T cells, and individually SDF-1beta, CCL14, and CCL27 suppressed R5 virus replicat

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

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

164 Initial SDF results showed a lower proportion of perfused vessel

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

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

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

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

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

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

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

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

173 trusion conditions, which produced a maximum SDF value of 30.36%, were as follows: barrel temperature

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

175 1c+ DCs dramatically reduced accumulation of SDF-1+CD11c+ DCs in regional LNs and LNM in LLC-injected

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

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

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

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

180 age of crystal size and the concentration of SDF.

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

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

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

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

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

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

187 ystem to investigate the isolated effects of SDF-1beta.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

203 ss in remineralization; however, the role of SDF in crystal formation is unknown.

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

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

206 scribed novel genetically engineered Tet-Off-SDF-1beta BMSCs, which over-express SDF-1beta under tigh

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

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

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

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

211 Compared with unextruded pomace, SDF fraction in extrudate had a higher level of uronic a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

236 We found that SDF-1beta had no effect on BMSC proliferation; however,

237 In this study we tested the hypothesis that SDF-1beta can mediate cell survival of BMSCs in vitro th

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

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

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

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

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

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

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

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

246 The results suggested that SDF reacted with calcium and phosphate ions and produced

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

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

249 field shift of the phosphate band in all the SDF groups and confirmed that the chemical environment o

250 e and silver chloride were formed in all the SDF groups.

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

252 -1/CXCR4 axis, specifically activated by the SDF-1beta isoform, plays a critical role in regulating B

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

254 rusion technology was applied to enhance the SDF obtained from orange pomace, a byproduct of juice ex

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

256 an with NPP (ii) total NPP is highest in the SDF site, then the EF followed by the DF and WS and that

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

258 oglucans made up approximately 40-60% of the SDF and arabinose-rich pectic polysaccharides represente

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

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

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

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

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

264 tive search of the optimal structure via the SDF representation enabled concurrent design of nanostru

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

266 rmed that all solids precipitated within the SDF groups were crystalline and that there was a positiv

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

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

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

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

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

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

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

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

275 on and migration of LSK cells in response to SDF or vascular endothelial growth factor.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

290 distinct carbon allocation patterns whereby SDF allocate in excess of 50% to canopy production and t

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

292 CCL27 suppressed R5 virus replication, while SDF-1beta, CCL21, and CCL14 suppressed X4 virus replicat

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

294 er MYD88 nor CXCR4 mutations correlated with SDF-1a (RS1801157) polymorphisms in 54 patients who were

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

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

299 rs for arrest of caries lesions treated with SDF.

300 -surface expression following treatment with SDF-1.