ライフサイエンスコーパス: bFGF

1 bFGF and collagen type I synthesis was also increased in

2 bFGF and VEGF monotherapy significantly increased surviv

3 bFGF and VEGF reversed the antiangiogenic activity of As

4 bFGF expression was analyzed in the LH-betaTag transgeni

5 bFGF induced membrane receptor cooperation between integ

6 bFGF levels significantly increased during tumorigenesis

7 bFGF released by ECs induces ASCs differentiation toward

8 bFGF treatment could not rescue PGC proliferation in the

9 bFGF was localized to vascular and tumor cells and rarel

10 bFGF- and EGF-induced beta1-integrin up-regulation and p

11 bFGF-loaded NP (bFGF-NP) were prepared with Poloxamer 18

12 bFGF-NP/UTMD combined treatment significantly enhanced t

13 bFGF/HS promoted the downregulation of intracellular ker

14 Stat3 signaling and overexpression of MMP-2, bFGF, and VEGF, as well as enhanced invasion and angioge

15 Herein we have developed a bFGF release system with suitable release kinetics to si

16 Four factors - Bmp4, activin A, bFGF (Fgf2) and VEGF (VegfA) - are sufficient to drive t

17 on strength by 68-91% from week 2 after AAV2-bFGF treatment and by 82-210% from week 3 after AAV2-VEG

18 Wispostatin-1 completely abolished bFGF-induced neovascularization in the corneal micropock

19 s Raf-1/ASK1 complex formation but abolishes bFGF-mediated EC protection from genotoxic stress.

20 ls of both p38 and JNK were diminished after bFGF stimulation of MT1-MMP knockout cells compared with

21 h factor protein levels were increased after bFGF-stimulation of wild-type fibroblast cells compared

22 We find that both BMP-2 and bFGF are readily loaded onto NDs by physisorption, formi

23 Simultaneous delivery of BMP-2 and bFGF by ND induces differentiation and proliferation in

24 le alternative for the delivery of BMP-2 and bFGF to promote bone formation.

25 cantly induced in cultured ECs by VEGF-A and bFGF treatment.

26 tivity with an increase in MMP2 activity and bFGF levels, as well as accentuated CNV leakage when sub

27 l lines after stimulation with ephrin B1 and bFGF combinations.

28 factor receptor 1-expressing BaF3 cells and bFGF-induced axonal branching in hippocampal cultures.

29 bFGF), suggesting that PS1 dominates EFG and bFGF signaling pathways.

30 HGF and bFGF expression are increased posthepatectomy, and decre

31 e RFA group, there was a decrease in HGF and bFGF expression at 24 and 72 hours (P = 0.001 and P = 0.

32 There was an increase in HGF and bFGF expression at 24 hours (P = 0.005, and P = 0.001) i

33 HGF and bFGF expression was significantly higher at baseline in

34 rmosensitive, and fast gelation hydrogel and bFGF.

35 hesion-mediated desensitization of PDGF- and bFGF-mediated Erk and Akt signaling.

36 focal adhesion complexes on RGD- and RGD and bFGF-immobilized patterns as shown by immunostaining of

37 nti-carcinogenic effect by reducing VEGF and bFGF serum levels and by blocking flk-1 receptors, there

38 Reductions in plasma VEGF and bFGF were observed, and reductions in VEGF correlated wi

39 eline conditions and in response to VEGF and bFGF.

40 on of angiogenic factors, including VEGF and bFGF.

41 suggest that galectin-3 modulates VEGF- and bFGF-mediated angiogenesis by binding via its carbohydra

42 minant-negative galectin-3, reduce VEGF- and bFGF-mediated angiogenesis in vitro and that VEGF- and b

43 s on alphavbeta3 integrins and (b) VEGF- and bFGF-mediated angiogenesis.

44 ted angiogenesis in vitro and that VEGF- and bFGF-mediated angiogenic response is reduced in galectin

45 encoding the kinase PERK decreased VEGFA and bFGF expression, but neither gene was affected by the in

46 in solution were demonstrated using QD-anti-bFGF and QD-anti-PSA sensors.

47 genic response of specific cytokines such as bFGF and VEGF.

48 F can mobilize proangiogenic factors such as bFGF from their depot or storage sites on bovine corneal

49 and metastasis by targeting proteins such as bFGF.

50 potentiated the activity of amphotericin B. bFGF-containing regimens were associated with reduced ti

51 stic insights into the cooperativity between bFGF and alphavbeta3 integrin during angiogenic signalin

52 These were not achievable using free bFGF, bFGF-NP or UTMD treatment alone.

53 in addition to IGF1 and IGF2, IGFBP-3 binds bFGF, HGF, neuregulin, and PDGF AB with nanomolar affini

54 Bioactive bFGF was able to gradually release from the hydrogel for

55 Blocking bFGF in IL-mPFC before four extinction sessions resulted

56 Blocking bFGF-receptor or PI3K/AKT signaling in ASCs increased mi

57 icient to facilitate extinction, as blocking bFGF and returning rats to their home cage had no effect

58 ion of bFGF inhibits extinction, as blocking bFGF during extinction permits rapid extinction.

59 In contrast, blocking bFGF alone was not sufficient to facilitate extinction,

60 Thus, we determined whether blocking bFGF in IL-mPFC would facilitate extinction following co

61 In line with this, knockdown of CD9 blocks bFGF- but not VEGF-induced ERK1/2 activation.

62 In the presence of both bFGF and RGD, cell areas were larger.

63 al transcriptional activator of of MMP-13 by bFGF in human articular chondrocytes.

64 ate the enhancement in branching elicited by bFGF.

65 iferation were dose-dependently increased by bFGF but not by EGF.

66 processes, such as proliferation, induced by bFGF and EGF in NECs.

67 lar mechanism for chemoresistance induced by bFGF.

68 ion of multiple MAPKs (ERK, p38, and JNK) by bFGF, and more importantly, bFGF activation of protein k

69 icited by epidermal growth factor but not by bFGF or PDGF.

70 The stimulation of mesodermal precursors by bFGF and activin A switches on very rapidly the hematopo

71 In premalignant JB6 cells, bFGF stimulation (1) increases cellular phospho-ERK and

72 survival factor for neural precursor cells, bFGF was evaluated as a growth and chemoresistance facto

73 ls were cultured in growth medium containing bFGF (20 ng/ml), over-expression of CXCR4 significantly

74 Conversely, bFGF suppresses MYO18B mRNA irrespective of CEBPB, miR-5

75 echnique is an effective strategy to deliver bFGF to the heart, and the resulting growth factor thera

76 Upon in vivo delivery, bFGF induced re-cellularization and re-vascularization i

77 ation and shifted cells towards differential bFGF-responsive growth and motility, a known signal to b

78 -crystallin-positive lentoids by high-dosage bFGF treatment.

79 Low dosage bFGF promotes cell proliferation while high dosage induc

80 In contrast, low-dosage bFGF was unable to sustain those markers and, combined w

81 uced 3 weeks after implantation of high-dose bFGF resulted in a lymphatic vessel-dominant phenotype.

82 GFR-2 or VEGFR-3 RESULTS: Although high-dose bFGF stimulation induced a more potent angiogenic respon

83 F-NP showed good round morphology, efficient bFGF encapsulation and stable bioactivity of bFGF in vit

84 wild-type mouse corneas compared with either bFGF pellet implantation or naked MT1-MMP DNA-injected c

85 h induces EphB receptor activation, enhanced bFGF-induced tube formation in an in vitro aortic ring a

86 We also examined bFGF in intestinal tumor formation of APC(Min/+) mice wi

87 differentiation upon withdrawal of exogenous bFGF.

88 Following cocaine exposure, bFGF is increased in addiction-related brain regions, in

89 uman cell lines and primary tumors expressed bFGF.

90 d to migrate by migration stimulatory factor bFGF, active Rac1 and cdc42 small GTPase levels were dec

91 vations that basic fibroblast growth factor (bFGF or FGF-2) required binding to a cell-surface hepari

92 ors, such as basic fibroblast growth factor (bFGF or FGF2), are necessary for neuronal survival, grow

93 mulated with basic fibroblast growth factor (bFGF) and 12-O-tetradecanoyl phorbol-13-acetate (TPA).

94 cultured in basic fibroblast growth factor (bFGF) and activin A develop as epiblast-like cells (EpiL

95 r A (VEGFA), basic fibroblast growth factor (bFGF) and angiogenin (ANG) in human kidney epithelial ce

96 stem cells, basic fibroblast growth factor (bFGF) and epidermal growth factor (EGF) promote cell pro

97 roduction of basic fibroblast growth factor (bFGF) and matrix metalloproteinase-13 (MMP-13).

98 tion of both basic fibroblast growth factor (bFGF) and neuregulin-1 beta 1 (NRG1beta1).

99 or detecting basic fibroblast growth factor (bFGF) and prostate-specific antigen (PSA) in solution we

100 e effects of basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) on s

101 Binding of basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) to t

102 matrix-bound basic fibroblast growth factor (bFGF) as well as inhibited the mitogenic activity of bot

103 tain whether basic fibroblast growth factor (bFGF) enhances axonal branching through alterations in p

104 or (HGF) and basic fibroblast growth factor (bFGF) expression was measured at selected time intervals

105 antly, while basic fibroblast growth factor (bFGF) expression, a known inhibitor of transforming grow

106 ithdrawal of basic fibroblast growth factor (bFGF) from the culture induces neural differentiation of

107 tested, the basic fibroblast growth factor (bFGF) had the most significant effect in promoting the m

108 Basic fibroblast growth factor (bFGF) has shown promise as a molecular therapy for DCM,

109 (IGF-1) and basic fibroblast growth factor (bFGF) have been shown to protect against radiation-induc

110 s induced by basic fibroblast growth factor (bFGF) in a Matrigel plug assay (p<0.001).

111 s exposed to basic fibroblast growth factor (bFGF) in vitro generated four stereotypical clonal expan

112 Basic fibroblast growth factor (bFGF) is a protein that plays a crucial role in diverse

113 Since basic fibroblast growth factor (bFGF) is a survival factor for neural precursor cells, b

114 Basic fibroblast growth factor (bFGF) may protect stroke patients from cerebral ischemia

115 By basic fibroblast growth factor (bFGF) or vascular endothelial growth factor (VEGF) gene

116 imulation by basic fibroblast growth factor (bFGF) or vascular endothelial growth factor results in c

117 othesis that basic Fibroblast Growth Factor (bFGF) regulates SFD-related CNV.

118 oliferation, basic fibroblast growth factor (bFGF) release, collagen type I synthesis, and wound heal

119 Basic fibroblast growth factor (bFGF) released from a nanostructured mineral coating mai

120 or (EGF) and basic fibroblast growth factor (bFGF) to generate neuralized spheres containing primitiv

121 showed that basic fibroblast growth factor (bFGF) was downregulated in MDA-MB-231-injected tibiae fr

122 Basic fibroblast growth factor (bFGF) was immobilized by electrostatic interaction with

123 se (12.5 ng) basic fibroblast growth factor (bFGF) were placed in BALB/c corneas.

124 actor (LIF), basic fibroblast growth factor (bFGF), and nerve growth factor (NGF).

125 owth factor, basic fibroblast growth factor (bFGF), and platelet-derived growth factor (PDGF) in NIH-

126 e-2 (MMP-2), basic fibroblast growth factor (bFGF), and vascular endothelial growth factor (VEGF) and

127 ogether with basic fibroblast growth factor (bFGF), elicited subsequent neural lineage differentiatio

128 lpha (SDF1), basic fibroblast growth factor (bFGF), or bone morphogenetic protein-7 (BMP7).

129 or (EGF) and basic fibroblast growth factor (bFGF), suggesting that PS1 dominates EFG and bFGF signal

130 r (VEGF) and basic fibroblast growth factor (bFGF), which in turn, inhibits tumor growth and metastas

131 nhibitors on basic fibroblast growth factor (bFGF)- and vascular endothelial growth factor (VEGF)-med

132 (MT1-MMP) on basic fibroblast growth factor (bFGF)-induced corneal neovascularization in vivo and in

133 expressed in basic fibroblast growth factor (bFGF)-induced vascularized corneas.

134 (VEGF)- and basic fibroblast growth factor (bFGF)-mediated angiogenic response.

135 mplicated in basic fibroblast growth factor (bFGF)-regulated angiogenesis through incompletely unders

136 or BMP-2 and basic fibroblast growth factor (bFGF).

137 e blocked by basic fibroblast growth factor (bFGF).

138 e absence of basic fibroblast growth factor (bFGF).

139 or (NGF), or basic fibroblast growth factor (bFGF).

140 r absence of basic fibroblast growth factor (bFGF).

141 ; VEGF-A and basic fibroblast growth factor (bFGF)].

142 in 4 (BMP4), basic fibroblast growth factor (bFGF, also known as FGF2), vascular endothelial growth f

143 se in plasma basic fibroblast growth factor (bFGF; P = .04) and increase in plasma interleukin-18 (IL

144 roteins (eg, basic fibroblast growth factor [bFGF] but not vascular endothelial growth factor [VEGF]

145 rs (VEGF and basic fibroblast growth factor [bFGF]) play a role in promoting angiogenesis during SK a

146 eukin-8, and basic fibroblast growth factor [bFGF]) were determined before and during treatment.

147 aling pathways engaged by angiogenic factors bFGF and VEGF in tumor angiogenesis are not fully unders

148 Delivery of the growth factors bFGF and vascular endothelial growth factor using a mine

149 , including basic fibroblast growth factors (bFGF or FGF-2), transforming growth factor-beta (TGF-bet

150 blast growth factor (FGF) family, basic FGF (bFGF) and FGF-18, have been implicated in the regulation

151 Finally, we found that basic FGF (bFGF) exerts potent inhibitory effects on many TGFbeta-r

152 ted to be completely identical, however, for bFGF and EGF.

153 ction (UTMD) was reported the first time for bFGF delivery to the heart of diabetic rats.

154 These were not achievable using free bFGF, bFGF-NP or UTMD treatment alone.

155 Compared with free bFGF, nanoliposomal therapy was able to significantly im

156 Furthermore, bFGF protein expression increased in IL-mPFC following c

157 We identified bFGF (basic fibroblast growth factor) released by ECs as

158 p38, and JNK) by bFGF, and more importantly, bFGF activation of protein kinase C (PKC) delta played a

159 al therapy was able to significantly improve bFGF accumulation in brain tissues (p<0.05) including th

160 No significant changes in bFGF or IL-18 following treatment with bevacizumab were

161 cretion levels and a significant increase in bFGF were observed following light exposure, compared to

162 actor activity with significant increases in bFGF or VEGF from weeks 4 to 6 in the treated tendons (p

163 Involvement of beta1-integrin in bFGF- and EGF-induced proliferation was confirmed by the

164 morphology in the DCM rats were observed in bFGF-NP/UTMD group.

165 Therefore, targeted reductions in bFGF during therapeutic interventions could enhance trea

166 ling rate of PDLFs at 12 hours and increased bFGF and collagen type I release from GFs and PDLFs at 2

167 hMSC encapsulating matrix sharply increased bFGF expression in the patterned constructs.

168 via a FGFR-1-dependent pathway by increasing bFGF release and activity.

169 uced prostate tumorigenesis while increasing bFGF-p38 MAP kinase signaling, beta-catenin-HIF-1alpha e

170 wn of SUMO1, but not SUMO2/3, also inhibited bFGF action.

171 71, a c-Abl kinase inhibitor, only inhibited bFGF- but not VEGF-induced angiogenesis.

172 s by decreasing cell survival and inhibiting bFGF, HGF, and IGF1 growth factor rescue and also potent

173 molecular mechanisms by which EGCG inhibits bFGF expression in colorectal cancer.

174 After intranasal bFGF-nanoliposomal treatment for 3 consecutive days, fun

175 eling through paracrine mechanisms involving bFGF and TIMP-2.

176 Exogenous 18-kDa bFGF induced proliferation in two RB cell lines (WERI an

177 ies, exogenous low-molecular-weight (18 kDa) bFGF (1 ng) significantly enhanced carboplatin-induced a

178 y 42 by switching EGF-containing SHEM to LIF/bFGF-containing MESCM through transient activation of LI

179 myeloid-specific TGF-beta signaling-mediated bFGF in the bone promotes BCa bone metastasis.

180 Abl as a key factor differentially mediating bFGF- and VEGF-induced angiogenesis in microvascular end

181 c-Abl's differential functions in mediating bFGF- and VEGF-induced angiogenesis.

182 es the very efficient formation of mesoderm; bFGF and activin A induce the differentiation of these m

183 Results show TFP (1 ng/mL TGF-beta1, 5 ng/mL bFGF, 10 ng/mL PDGF) supplementation of serum-free chond

184 support the intranasal use of nanoliposomal bFGF as an efficient, non-invasive means to bypass the b

185 e and proteolytic degradation--unlike native bFGF.

186 mice 2 weeks after implantation of an 80-ng bFGF micropellet with VEGFR-3 blockade.

187 ained 3 weeks after implantation of an 80-ng bFGF micropellet without supplementary modulating agents

188 pression or function impairs VEGF-A- but not bFGF-dependent migration of endothelial cells.

189 3A selectively interferes with VEGF- but not bFGF-induced angiogenesis in vivo.

190 nt with this, Sema3A disrupted VEGF- but not bFGF-mediated endothelial cell signaling to FAK and Src,

191 bFGF-loaded NP (bFGF-NP) were prepared with Poloxamer 188-grafted hepari

192 In line with these observations, bFGF, but not VEGF, neutralizes the antiangiogenic effec

193 ogical role may be related to the ability of bFGF to decrease proteoglycan synthesis and to antagoniz

194 eview, we examined the biological actions of bFGF and FGF-18 in articular and IVD cartilage, the spec

195 ay interfere with the biological activity of bFGF and potentially of other heparin-binding growth fac

196 ndothelial cell growth-promoting activity of bFGF yet had remarkably increased stability (activity su

197 -catenin into the nucleus by the addition of bFGF after JW74 treatment.

198 AV2) vector to produce supernormal amount of bFGF or VEGF intrinsically in the tendon, we effectively

199 RB tumors produce significant amounts of bFGF, and the differential production and response to is

200 or obstacle to the widespread application of bFGF is its inherent instability during storage and deli

201 not interfere with high-affinity binding of bFGF to FGFR1 IIIc but can replace heparin as a required

202 bFGF encapsulation and stable bioactivity of bFGF in vitro.

203 encapsulation efficiency, and bioactivity of bFGF-NP were studied.

204 gnificantly increased after a combination of bFGF pellet implantation and naked MT1-MMP DNA injection

205 A combination of bFGF, forskolin, and the GSK3beta inhibitor BIO induced

206 The cellular uptake and cytotoxicity of bFGF-NP were evaluated with primary cultures of the left

207 ome, thereby resulting in the degradation of bFGF protein.

208 ovel nanoliposomes for the brain delivery of bFGF in a rat model of cerebral I/R.

209 These results demonstrate that delivery of bFGF with appropriate release kinetics alone may represe

210 nearly identical with high- and low-doses of bFGF.

211 enin acts on PGC proliferation downstream of bFGF.

212 confirmed in vivo, the inhibitory effects of bFGF have primarily been studied in culture.

213 Therapeutic effects of bFGF-NP/UTMD on the heart of DCM rats were studied by me

214 ent significantly enhanced the efficiency of bFGF cellular uptake (P<0.05) without obvious cytotoxici

215 s resulted in the differential inhibition of bFGF-induced (5%-57%) and VEGF-induced (3%-66%) corneal

216 ntial production and response to isoforms of bFGF may have implications for invasive tumor growth and

217 , but whether drug-induced overexpression of bFGF in this region affects extinction of drug seeking i

218 ggest that cocaine-induced overexpression of bFGF inhibits extinction, as blocking bFGF during extinc

219 the effect was suppressed in the presence of bFGF.

220 We examined posttranslational regulation of bFGF by EGCG in human colorectal cancer cells.

221 tributes significantly to down-regulation of bFGF expression by EGCG.

222 s, our findings revealed a neglected role of bFGF in sustaining self-renewal of human PS cells: preve

223 al (RPE) cells showed increased secretion of bFGF and conditioned medium from these cells induced inc

224 ht filters reduce light-induced secretion of bFGF and VEGF to near normal levels.

225 Here, we describe the stabilization of bFGF by covalent conjugation with a heparin-mimicking po

226 ealing process and increase the synthesis of bFGF and collagen type I from both GFs and PDLFs.

227 ression of colonic APN overlaps with that of bFGF and HB-EGF, which play a protective role in colitis

228 was also found to increase ubiquitination of bFGF and trypsin-like activity of the 20S proteasome, th

229 portant implications for the clinical use of bFGF and for the stabilization of heparin-binding growth

230 studies suggest the potential usefulness of bFGF and FGFR1 antagonists, as well as FGF-18 and FGFR3

231 Withdrawal of bFGF also promotes apoptosis and differentiation of the

232 27 also showed a strong inhibitory effect on bFGF, PDGF-BB, and serum-induced cell migration and prol

233 teroidal anti-inflammatory drugs (NSAIDs) on bFGF- and VEGF-induced angiogenesis.

234 Studies on bFGF from a variety of species have yielded contradictor

235 IGF-1 or bFGF impaired radiation-induced apoptosis and the expres

236 the lentivirus expressing chondroitinase or bFGF.

237 were recruited into collagen gel by SDF1 or bFGF than without cytokines in 7 days, whereas BMP7 had

238 Similar to other bFGF tumor studies, exogenous low-molecular-weight (18 k

239 ese results suggest that MT1-MMP potentiates bFGF-induced corneal neovascularization, likely by modul

240 Viability, proliferation, bFGF, and collagen type I synthesis from both cell types

241 n an in vitro aortic ring assay and promoted bFGF-induced corneal angiogenesis in vivo in a corneal p

242 DF also protects bFGF against digestion by trypsin and chymotrypsin and f

243 and intravenous injection of the recombinant bFGF to LysM(Cre)/Tgfbr2 KO mice rescued the inhibited m

244 le-treated mice, in association with reduced bFGF expression.

245 The released bFGF promoted cardiac fibroblast survival under ischemic

246 Furthermore, the released bFGF stimulated human umbilical endothelial cells to for

247 correlated with decreased levels of retinal bFGF, GDNF, and BDNF.

248 Cell membrane receptors for SDF1, bFGF, and BMP7 were up-regulated in treated DSCs.

249 ECs challenged with TGFbeta secrete bFGF, which blocks SMA expression in secondary cultures,

250 bited collagen contraction, while a specific bFGF inhibitor abolished this paracrine response.

251 Specifically, bFGF stimulation promotes the formation of a Raf-1/ASK1

252 owever, we found that IGF2 cannot substitute bFGF in the TeSR1-supported culture, although endogenous

253 effects of expansion medium supplementation (bFGF, TFP, FBS) and self-assembled construct seeding den

254 molecular mechanism by which EGCG suppresses bFGF expression is not known.

255 nhibitors were more effective at suppressing bFGF-induced angiogenesis than VEGF-induced angiogenesis

256 EGF rather than bFGF strongly induced the increase of beta1-integrin loc

257 Fluorescence microscopy confirmed that bFGF and VEGF were subsequently immobilized to the polym

258 Results demonstrated that bFGF-NP showed good round morphology, efficient bFGF enc

259 Collectively, these results indicate that bFGF enhances axonal branch formation by augmenting the

260 Our data suggest that bFGF regulates ERK oscillations in premalignant but not

261 Also, our findings suggest that bFGF stimulation of MMP-13 required the activation of mu

262 ly with monomeric JAM-A, which suggests that bFGF induces signaling by triggering JAM-A dimerization.

263 Evidence suggests that bFGF selectively activates FGF receptor 1 (FGFR1) to exe

264 The bFGF conjugate of this polymer retained bioactivity afte

265 The bFGF protein was quickly degraded in the presence of EGC

266 In addition, the bFGF release system significantly increased cardiac func

267 PKCdelta controls the bFGF response by regulating multiple MAPK pathways.

268 g shows that HKa significantly decreases the bFGF-transactivated phosphorylation of EGFR at Tyr 1173

269 s of implantation into infarcted hearts, the bFGF release system significantly increased blood vessel

270 In the bFGF- and EGF-responsive neural stem cells, beta1-integr

271 on is a principal rate-limiting event in the bFGF-dependent stimulation of MMP-13 in human adult arti

272 neovascularization, likely by modulating the bFGF signal transduction pathway.

273 On the other hand, all of the bFGF withdrawal effects observed here can be markedly pr

274 We further demonstrated that the bFGF-repressed anoikis is dependent on activation of ERK

275 llagen model mimicking the scenario when the bFGF release system was injected into hearts.

276 with alphavbeta3 integrin, which responds to bFGF stimulation by JAM-A release to regulate mitogen-ac

277 type c-Abl sensitized angiogenic response to bFGF, but kinase dead mutant c-Abl abolished this activi

278 e proliferation of chicken PGCs similarly to bFGF, whereas JW74 inhibited this proliferation.

279 in complex from which JAM-A is released upon bFGF stimulation.

280 ression of several angiogenic factors (VEGF, bFGF, IL-8, and ANGPTL-2), as well as ErbB (amphiregulin

281 signaling, p38 MAPK was important for VEGF, bFGF, EGF, IL-6, and other proangiogenic cytokine secret

282 Some angiogenic genes (VEGF, bFGF, TNF-alpha and PCNA) were up-regulated as well.

283 eration rate, as well as expression of VEGF, bFGF, and SDF-1, which was not seen when TGF-beta1 expre

284 ent causing a significant decrease in VEGF-, bFGF-, EGF-, and IL-6-induced endothelial cord formation

285 receptor whose expression is induced by VEGF/bFGF and repressed by DLL4 signaling.

286 the UPR is activated in parallel with VEGFA, bFGF, and ANG expression and independently of HIF-1alpha

287 io of high (34 kDa)- to low-molecular-weight bFGF isoforms, compared with the WERI line.

288 a two-pronged biological mechanism by which bFGF controls the production of catabolic enzymes that a

289 The mechanism by which bFGF rescued the bone lesion development was by promotio

290 rt a novel molecular mechanism through which bFGF or EGF promotes the proliferation of mouse neuroepi

291 t of malignant or transformed JB6 cells with bFGF is associated with a transient nuclear translocatio

292 wth: treatment of medulloblastoma cells with bFGF prevents them from forming tumors following transpl

293 anwhile, such treatments in combination with bFGF did not show a synergistic effect.

294 , and inoculation of tumor-bearing mice with bFGF markedly inhibits tumor growth in vivo.

295 eatment of cultured hippocampal neurons with bFGF heightens expression of both katanin and spastin, w

296 o cooperate during angiogenic signaling with bFGF and vascular endothelial growth factor (VEGF), resp

297 g experiments, axons of neurons treated with bFGF displayed greater numbers of dynamic free ends of m

298 In addition, treatment with bFGF enhances phosphorylation of tau at sites expected t

299 Treatment with bFGF plus amphotericin B was associated with neutrophil

300 growth of human embryonic stem cells without bFGF or TGFbeta/Activin/Nodal ligand supplementation.