ライフサイエンスコーパス: FGF-2

1 cellular pool of fibroblast growth factor 2 (FGF-2).

2 then cultured and stimulated with VEGF A and FGF 2.

3 and angiogenic tube formation in response to FGF-2.

4 cell growth factors, such as neuregulin and FGF-2.

5 nce than cocultures completely deficient for FGF-2.

6 -mediated Egr-1-dependent rapid induction of FGF-2.

7 y subcutaneous administration of recombinant FGF-2.

8 ned medium, which contains a large amount of FGF-2.

9 in the presence of provasculogenic VEGF and FGF-2.

10 RSK1, and the high-molecular-weight form of FGF-2.

11 n of Skp1 and Skp2 was temporally induced by FGF-2.

12 uman chondrocytes, and this was inhibited by FGF-2.

13 non-adherent culture conditions with EGF and FGF-2.

14 neoepitope, and this was also suppressed by FGF-2.

15 ifferentiation and survival factors CNTF and FGF-2.

16 ndispensable for the pro-survival effects of FGF-2.

17 f target-derived FB and intrinsic VM-derived FGF-2.

18 n sensitive to the antidepressant actions of FGF-2.

19 ontrol) and 0.1% recombinant human FGF-2 (rh-FGF-2), 0.3% rh-FGF-2, and 0.4% rh-FGF-2 with beta-TCP-f

20 This was inhibited by FGF-2 (1-100 ng/ml).

21 e, nuclear FGFR1 or its 23-kDa FGF-2 ligand (FGF-2(23)) enhances Nurr1-dependent activation of the TH

22 ults indicate that FGF ligand genes, such as Fgf-2, -4, -8, and -18, displayed a differential and dyn

23 Injection of FGF-2 (6 pmoles) induced synovial angiogenesis without s

24 stimulated cell proliferation in hCECs; the FGF-2 action was completely blocked by pathway-specific

25 FGF-2 activated Rac1 through Akt, and Rac1 inhibitor gre

26 ed in their downregulation in TGF-beta1- and FGF-2-activated keratocytes.

27 This pool of FGF-2 activates chondrocytes upon tissue loading and is

28 FGF-2 activation of both membrane FGFRs and INFS-depende

29 t a deranged HS/syndecans regulation impairs FGF-2 activity.

30 and nuclear localization in comparison with FGF-2 alone.

31 ls were cultured and treated with VEGF A and FGF 2 and the mRNA expression pattern of EGR family memb

32 Especially after combined FGF-2 and 8-OH-DPAT treatment, a marked and significant

33 Intracellular location of FGF-2 and actin cytoskeleton was determined by immunoflu

34 tion, downstream of DYRK1A, and mediates the FGF-2 and EZH2 effects on cell proliferation, migration,

35 ivo corneal tissue with IL-1beta upregulated FGF-2 and facilitated its nuclear location in corneal en

36 Additionally, intraarticular treatment with FGF-2 and FGF-8 was found to suppress joint inflammation

37 We used low molecular weight (LMW, 18 kDa) FGF-2 and high molecular weight (HMW) FGF-2 isoforms, wh

38 , respectively, inhibited the effects of LMW-FGF-2 and HMW-FGF-23 to stimulate FGF-23 promoter activi

39 FGF-2 and IGF-1 are known to be important for myelinatio

40 Because the interaction between FGF-2 and its receptor is mediated by heparan sulfate (H

41 ulation include IL-1, IL-6, TNF-alpha, PGE2, FGF-2 and PKCdelta, and pharmacologic inhibitors to thes

42 The combined treatment with FGF-2 and the 5-HT1A agonist also synergistically increa

43 tion of some vascular growth factors such as FGF-2 and VEGF-A.

44 nvironment, the reciprocal interplay between FGF-2 and VEGF-C collaboratively stimulated tumor growth

45 Here we show that FGF-2 and VEGF-C, two lymphangiogenic factors, collabora

46 factors such as fibroblast growth factor-2 (FGF-2) and bone morphogenetic protein-2 (BMP-2) work syn

47 ability (cytotoxicity), proliferation (EGF + FGF-2) and EMT (TGF-beta1).

48 heparanase, basic fibroblast growth factor (FGF-2), and angiopoietin-2 (Ang-2) increased in the peri

49 rophin-3 (NT-3), fibroblast growth factor-2 (FGF-2), and insulin-like growth factor-1 (IGF-1).

50 oteins including fibroblast growth factor 2 (FGF-2), and the chemokines CCL2, CCL5, CCL7, CCL13, CXCL

51 actor I (IGF-I), fibroblast growth factor-2 (FGF-2), and/or transforming growth factor-beta1 (TGF-bet

52 recombinant human FGF-2 (rh-FGF-2), 0.3% rh-FGF-2, and 0.4% rh-FGF-2 with beta-TCP-following scaling

53 oncentrate (BMAC) and growth factors (BMP-2, FGF-2, and FGF-8) and 2) increase matrix strength retent

54 ncrease in expression of ANT, PDGF-BB, VEGF, FGF-2, and IL-8 for the LCC group over the autograft gro

55 The effects of IGF-I, TGF-beta1, FGF-2, and PDGF on proliferation and ECM production by p

56 and measured the resulting changes in IGF-I, FGF-2, and TGF-beta1 gene expression and protein product

57 udies suggest that interactions among IGF-I, FGF-2, and TGF-beta1 substantially modulate their regula

58 s of the aged myocardial GAGs to bind FGF-1, FGF-2, and VEGF but not HB EGF.

59 ctor signaling pathways as IGFBP-4 inhibited FGF-2- and IGF-1-stimulated angiogenesis but failed to i

60 Extrapolating from the present study, FGF-2- and TGF-beta1-activation of JNK signaling pathway

61 Thus, intervention and targeting of the FGF-2- and VEGF-C-induced angiogenic and lymphangiogenic

62 for the lymphatic tip cell formation in both FGF-2- and VEGF-C-induced lymphangiogenesis.

63 fied as an inhibitor of SOD1 that attenuates FGF-2- and VEGF-mediated phosphorylation of ERK1/2 in en

64 en corneal endothelium was stained with anti-FGF-2 antibody, the nuclear location of FGF-2 was observ

65 rly; and 2) if the antidepressant actions of FGF-2 are mediated specifically by the PFC.

66 Thus, both CNTF and FGF-2 are present in regions of elevated OPC proliferati

67 These data identify FGF-2 as a novel endogenous chondroprotective agent in a

68 data identify CREB activation via PGE(2) and FGF-2 as a previously unrecognized molecular controller

69 hat NF-kappaB is the transcription factor of FGF-2 as NF-kappaB binds the putative NF-kappaB binding

70 e in response to fibroblast growth factor-2 (FGF-2) as cancer cells isolated from wild-type mice, and

71 Stimulation of angiogenesis with FGF-2 at the time of carrageenan injection was followed

72 n detected a plateau in the 0.3% and 0.4% rh-FGF-2/beta-TCP groups with significant improvements over

73 ficant improvements over control and 0.1% rh-FGF-2/beta-TCP groups.

74 ects can be enhanced with the addition of rh-FGF-2/beta-TCP.

75 ceptor protein revealed that LOX-PP inhibits FGF-2 binding in an uncompetitive manner.

76 ontrol cells without changes in HS-dependent FGF-2 binding or FGF-2.FR1c complex formation.

77 rate a concentration-dependent inhibition of FGF-2 binding to osteoblasts by LOX-PP.

78 cancer cells through CEP57, an intracellular FGF-2-binding and trafficking factor.

79 terestingly, the number of LYVE-1(-) gaps in FGF-2, but not VEGF-A, implanted corneas was significant

80 hod for improving the biological activity of FGF-2 by codelivering the growth factor with a liposomal

81 These data suggest that CECs produce FGF-2 by IL-1beta stimulation through PI 3-kinase and p3

82 The induction of FGF-2 by IL-1beta was completely blocked by inhibitors t

83 ), combined with fibroblast growth factor-2 (FGF-2), can induce the dedifferentiation and proliferati

84 signaling and up-regulates the expression of FGF-2, CD44, and Oct-4 enriching tumorigenesis.

85 Significantly more FGF-2+ cells were noted along lesion borders at 7 and 28

86 expression, we examined the distribution of FGF-2+ cells.

87 This technique was shown to increase FGF-2 cellular signaling, uptake, and nuclear localizati

88 Interestingly, PC-3 cells did not respond to FGF-2, consistent with previous reports.

89 FGF-2 contributes to MAPK/IKK activation but not to Src-

90 nts in mice, we examined the extent to which FGF-2 contributes to the cellular gene response to injur

91 ndividual VM and FB tissue from wildtype and FGF-2-deficient embryonic day (E)14.5 embryos, respectiv

92 unoprecipitated from the ventral midbrain of FGF-2-deficient embryonic mice, which previously showed

93 assays on osteoblast cell layers with (125)I-FGF-2 demonstrate a concentration-dependent inhibition o

94 sing rat lens epithelial explants undergoing FGF-2 dependent differentiation in vitro.

95 ), and podoplanin (Pdpn), were significantly FGF-2 dependent following injury to cartilage in vitro a

96 9, unencumbered by TIMP-1, directly mediates FGF-2-dependent angiogenesis was also demonstrated in ou

97 ubular-interstitial compartment favoring the FGF-2-dependent EMT of tubular cells.

98 FGF-2-dependent gene expression occurs in vitro and in v

99 lotting showed that MASH1 overexpression and FGF-2 deprivation additively increased beta-III-tubulin

100 osphodiesterase (CNPase) expression, whereas FGF-2 deprivation alone attenuated glial fibrillary acid

101 However, FGF-2 deprivation resulted in a small, but significantly

102 Similarly, VEGF-A and FGF-2 did not enhance the migration of hepatic endotheli

103 FGF-2 did not prevent IL-1alpha suppression of proteogly

104 ype cocultures, proving a regulatory role of FGF-2 during nigrostriatal wiring.

105 we show that basic fibroblast growth factor (FGF-2) effectively blocks transforming growth factor-bet

106 FGF-2 enables phosphorylation of p27 at both the Thr-187

107 The IL-1beta-induced FGF-2 exerted cellular activities using distinct pathway

108 In addition to increased TGF-beta1 and FGF-2 expression levels, cross-sectional studies of the

109 Malignant tumors with deregulated FGF-2 expression such as prostate cancer are also freque

110 Similarly, FGF-2 expression was increased in a time-dependent manne

111 Because CNTF can potentiate FGF-2 expression, we examined the distribution of FGF-2+

112 tart site is required for 15(S)-HETE-induced FGF-2 expression.

113 (S)-HETE induced fibroblast growth factor-2 (FGF-2) expression rapidly via Src-mediated production of

114 actor (CNTF) and fibroblast growth factor-2 (FGF-2) expression, because both factors alter progenitor

115 The IL-1beta-induced FGF-2 facilitates cell migration via PI 3-kinase and p38

116 ntly, although other pro-osteogenic factors [Fgf-2, Fgf-18, and bone morphogenic protein 2 (Bmp-2)] s

117 The canonical HBS in FGF-1, FGF-2, FGF-7, FGF-9, and FGF-18 differs in its size, and

118 Here, we use a panel of FGFs (FGF-1, FGF-2, FGF-7, FGF-9, FGF-18, and FGF-21) spanning five F

119 ents survival of PECs in part by maintaining FGF-2/FGF-R1 signaling and through tonic Ser-473 phospho

120 These findings demonstrate that FGF-2/FGFR signaling is sufficient and necessary for the

121 bodies further indicated an involvement of a FGF-2/FGFR-2 pathway in neutrophil proMMP-9-induced angi

122 , thus implicating the novel TIMP-free MMP-9/FGF-2/FGFR-2 pathway in proMMP-9-induced angiogenesis in

123 tionale for the therapeutic targeting of the FGF-2/FGFR1/CEP57 axis in prostate cancer.

124 Here, we aim to determine if 1) FGF-2/fibroblast growth factor receptor (FGFR) signaling

125 NPCs were maintained in FGF-2 or deprived of FGF-2 for varying lengths of time.

126 inds of plasmid DNA encoding either BMP-2 or FGF-2 formulated into polyethylenimine (PEI) complexes.

127 Interestingly, PCNs utilized FGF-2 found in situ to induce chemokinesis, potentiate S

128 out changes in HS-dependent FGF-2 binding or FGF-2.FR1c complex formation.

129 ere TIMPs negatively regulate the release of FGF-2 from chondrocytes to allow IHH expression.

130 of pericellular fibroblast growth factor 2 (FGF-2) from the articular cartilage.

131 eutralizing antibody-mediated suppression of FGF-2 function also attenuated the effects of 15(S)-HETE

132 nding of NF-kappaB to the promoter region of FGF-2 gene was determined by chromatin immunoprecipitati

133 lays a key role as a transcription factor of FGF-2 gene.

134 ted in a serum-free medium were treated with FGF-2/heparin or TGF-beta1 in the presence or absence of

135 NK inhibitor (SP600125), were activated with FGF-2/heparin sulfate (HS) or TGF-beta1 in the presence

136 giogenic factors fibroblast growth factor-2 (FGF-2), hepatocyte growth factor (HGF), vascular endothe

137 The FGF-2/HS- or TGF-beta-induced activation of corneal stro

138 DsiRNA) and then activated with TGF-beta1 or FGF-2/HS.

139 tly lower (p < 0.05) in Groups 2 and 3: EGF, FGF-2, IFNalpha2, IL-1RA, HSA, keratin-6, and involucrin

140 We identify TIMP/FGF-2/IHH as a novel nexus underlying bone lengthening w

141 f a number of proangiogenic mediators (VEGF, FGF-2, IL-6, etc.) and downregulation of several angioge

142 nin (ANG), angiostatin (ANT), PDGF-BB, VEGF, FGF-2, IL-8, TIMP-1, TIMP-2, GM-CSF, and IP-10.

143 egulated the expression of stem cell mitogen Fgf-2 in adult NSPCs.

144 In fact, we show that loss of FGF-2 in both FB and VM results in significantly increas

145 nd in heterogeneous cocultures deficient for FGF-2 in FB and VM, respectively, similar phenotypes wit

146 Additionally, the loss of target-derived FGF-2 in FB explants resulted in decreased caudorostral

147 The current analysis addressed the role of FGF-2 in mDA axonal outgrowth, pathway formation, and in

148 his study to investigate the in vivo role of FGF-2 in murine cartilage.

149 y in the cornea after cryotreatment, whereas FGF-2 in normal corneal endothelium was localized at the

150 epithelial-mesenchymal transition induced by FGF-2 in renal tubular cells.

151 astrocytes in culture express high levels of FGF-2 in response to IL-1beta, and IGF-1 in response to

152 ds to VEGF-A and fibroblast growth factor-2 (FGF-2) in human plasma and colocalizes with VEGF-A in EC

153 a (IL-1beta) and fibroblast growth factor 2 (FGF-2) in proteoglycan metabolism, catabolic protease ex

154 It was observed that VEGF A and FGF 2 induced angiogenesis, cell proliferation and stero

155 FGF-2 induced both KIS and Cdc25A during the G1 phase; t

156 The FGF-2 induced EMT is through a stable activation of PI3K

157 ation of ECs, stimulation with VEGF-A and/or FGF-2 induced expansion of E4ORF1(+) ECs in a contact-in

158 We found that LMW-FGF-2 induced NFAT and Ets1 binding to conserved cis-ele

159 sing immunoblotting, the authors showed that FGF-2 induced phosphorylation of p27 at both serine 10 (

160 c loop for handling syndecan-1, facilitating FGF-2 induced-EMT.

161 n overexpressed and is required not only for FGF-2-induced centriole overduplication but also for nor

162 wth in a dose-dependent fashion and prevents FGF-2-induced chemoresistance.

163 d expression of alpha-SMA and TGF-beta1- and FGF-2-induced de novo expression of tenascin-C and the d

164 TGF-beta1- and FGF-2-induced decreases in cell-associated and secreted

165 However, FGF-2-induced decreases in keratocan mRNA levels were pr

166 TGF-beta1- or FGF-2-induced downregulation of the expression of alpha3

167 tern blot analyses show that LOX-PP inhibits FGF-2-induced ERK1/2 phosphorylation, signaling events t

168 NA reduced Smad phosphorylation but enhanced FGF-2-induced Erk1/2 signaling.

169 ells is a crucial receptor that mediates the FGF-2-induced lymphangiogenesis.

170 fic neutralizing antibody markedly inhibited FGF-2-induced lymphangiogenesis.

171 orylation, signaling events that mediate the FGF-2-induced proliferative response.

172 Persistence of carrageenan/FGF-2-induced synovitis was prevented by systemic admini

173 inhibition downregulated both TGF-beta1- and FGF-2-induced tenascin-C expression, ROCK inhibition was

174 In PTECs, FGF-2 induces an autocrine loop which sustains its signa

175 FGF-2 induces EMT in PTECs.

176 human kidney 2 (HK2) PTEC cultures, although FGF-2 induces EMT in the wild-type clone, it is ineffect

177 Chronic FGF-2 infusions (intracerebroventricular) blocked the de

178 Although FGF-2 inhibited collagen production, it could be restore

179 Fibroblast growth factor 2 (FGF-2) inhibited ADAMTS-5 expression in isolated aortic

180 The authors suggest that FGF-2 initiates the hypercellular phase of corneal wound

181 Lastly, subchronic infusions of FGF-2 into the PFC but not into the dorsal striatum prod

182 d/or 6 pmoles of fibroblast growth factor 2 (FGF-2) into rat knees.

183 FGF-2 to produce EMT in PTECs and to sustain FGF-2 intracellular signaling.

184 wave of activation, triggered by the induced FGF-2, involves the promotion of cellular activities.

185 The inductive activity of IL-1beta on FGF-2 is further evidenced by the conditioned medium, wh

186 Fibroblast growth factor 2 (FGF-2) is an important neurotrophic factor that promotes

187 he expression of fibroblast growth factor-2 (FGF-2) is decreased in the prefrontal cortex (PFC) of de

188 8 kDa) FGF-2 and high molecular weight (HMW) FGF-2 isoforms, which, respectively, activate cell surfa

189 is normal in basic fibroblast growth factor (FGF-2)-knockout mice, parathyroid hormone stimulation an

190 These inhibitors also reduced FGF-2 levels and partially blocked morphologic changes a

191 Furthermore, nuclear FGFR1 or its 23-kDa FGF-2 ligand (FGF-2(23)) enhances Nurr1-dependent activa

192 , we show that Smad activity is repressed by FGF-2, likely an effect of the fact that FGF-2 treatment

193 Our findings suggest that FGF-2 may play a chondroprotective role in human articul

194 nt study reveal a novel mechanism underlying FGF-2-mediated in vivo expansion of both HSPCs and their

195 leads to the inhibition of EGF-, IGF-1-, and FGF-2-mediated phosphorylation of ERK1/2.

196 rgeted mice demonstrated reduced VEGF-C- and FGF-2-mediated sprouting in collagen matrix.

197 (2) (PGE(2)) and fibroblast growth factor 2 (FGF-2) -mediators known to influence fibroblast activati

198 FGF-2(-/-) mice showed significantly less preexisting ly

199 r whole joints from either wild-type mice or FGF-2(-/-) mice.

200 factor (EGF) and fibroblast growth factor-2 (FGF-2) mitogens.

201 FGF-2 mRNA expression, detected in neurons and astrocyte

202 The FGF-2-NDY1/EZH2-miR-101-EZH2 axis described here was fou

203 the presence of fibroblast growth factor 2 (FGF-2), nerve growth factor (NGF), brain-derived neurotr

204 treatment effect on the expression of BDNF, FGF-2, NT-3 and IGF-1 [p<0.01], but not NGF.

205 f subcutaneous administration of recombinant FGF-2 on OA progression was assessed in Fgf2(-/-) mice.

206 factor (VEGF) and fibroblast growth factor (FGF-2) on the revascularization of severed human dental

207 entivirus-transduced NPCs were maintained in FGF-2 or deprived of FGF-2 for varying lengths of time.

208 ts that had been stimulated with recombinant FGF-2 or FGF-18, or whole joints from either wild-type m

209 factors, such as fibroblast growth factor-2 (FGF-2) or VEGF-A, may also contribute.

210 However, a link between FGF-2 overexpression and chromosome missegregation has s

211 ed microenvironmental signaling cues such as FGF-2 overexpression and mitotic instability and provide

212 IL-1beta was measured, and the expression of FGF-2, p38, and Akt underwent Western blot analysis.

213 Expression and/or activation of FGF-2, p38, ERK1/2, and Akt was analyzed by immunoblot a

214 FGF-2 predominantly expanded a heterogeneous population

215 FGF-2 prevents the induction of alpha-smooth muscle acti

216 and the PI 3-kinase signaling to upregulate FGF-2 production through NF-kappaB, which plays a key ro

217 volves the inductive activity of IL-1beta on FGF-2 production; the second wave of activation, trigger

218 Cloning and mutational analysis of FGF-2 promoter revealed that Egr-1 binding site proximal

219 s the putative NF-kappaB binding site of the FGF-2 promoter.

220 restingly, a drift in the ratio of different FGF-2 protein forms, with translation favoring the HMWFG

221 al lymphangiogenesis (VEGF-A: r=0.7, P=0.01; FGF-2: r=0.96, P=10(-5)) in BALB/c but not in C57BL/6 mi

222 Here, we show that FGF-2 rapidly uncouples centrosome duplication from the

223 onstrated greater than 50-fold regulation of FGF-2 release as well as tunability, reversibility, and

224 that basic fibroblast growth factor (bFGF or FGF-2) required binding to a cell-surface heparin sulfat

225 e, SK-N-MC, with fibroblast growth factor-2 (FGF-2) results in induction of BAG3 expression.

226 P alone (control) and 0.1% recombinant human FGF-2 (rh-FGF-2), 0.3% rh-FGF-2, and 0.4% rh-FGF-2 with

227 lopmental gene regulator in cooperation with FGF-2, RSK1, and CREB-binding protein (CBP).

228 sses, hindering the pro-survival activity of FGF-2/S6K2 signalling.

229 e results suggest that chemically controlled FGF-2 secretion can significantly increase bone formatio

230 role in OPC migration through regulation of FGF-2 secretion during neuronal development.

231 We then applied conditional control of FGF-2 secretion to a cell-based, skeletal tissue enginee

232 ole of EGR mediated regulation of VEGF A and FGF 2 signaling in buffalo luteal cells.

233 owever, their role in controlling VEGF A and FGF 2 signaling in the CL of water buffalo is not known.

234 These results suggest that low FGF-2 signaling and MASH1 activity can operate in concer

235 The role of FGF-2 signaling in behavioral models of depression and a

236 ol and did not associate with LRs or enhance FGF-2 signaling in cultured podocytes.

237 in LRs, and (3) Tat-mediated enhancement of FGF-2 signaling in human podocytes and HIV-transgenic mo

238 en with HIVAN, confirm Tat as a regulator of FGF-2 signaling in LRs, and identify the key domain of T

239 lpha interaction prevented proper VEGF-A and FGF-2 signaling, which are required for efficient angiog

240 vated autocrine fibroblast growth factors 2 (FGF-2) signaling promotes prostate cancer cell growth an

241 Fibroblast growth factor 2 (FGF-2) signalling-induced S6 kinase 2 (S6K2) activation

242 FGF-2 stimulated cell proliferation in hCECs; the FGF-2

243 In contrast, HMW-FGF-2 stimulated FGF-23 promoter activity in osteoblasts

244 FGF-2 stimulated the highest level of proliferation and

245 ERK1/2 was also involved in FGF-2-stimulated CEC proliferation and phosphorylation o

246 erum- and FGF-2-stimulated DNA synthesis and FGF-2-stimulated cell growth.

247 ased activation of the MAP kinases ERK1/2 in FGF-2-stimulated cell lines of affected individuals that

248 iRNA to KIS, which subsequently hampered the FGF-2-stimulated cell proliferation, while Thr187 of p27

249 kt, and Rac1 inhibitor greatly inhibited the FGF-2-stimulated cell proliferation.

250 LOX-PP was found to inhibit serum- and FGF-2-stimulated DNA synthesis and FGF-2-stimulated cell

251 FGF-2-stimulated DNA synthesis, ERK1/2, AKT and FRS2alph

252 -stimulated phosphorylation of FRS2alpha and FGF-2-stimulated DNA synthesis, even after inhibition of

253 Focal adhesions in FGF-2-stimulated fibroblasts of affected individuals con

254 ell tip cell formation is a prerequisite for FGF-2-stimulated lymphangiogenesis.

255 LOX-PP inhibits FGF-2-stimulated phosphorylation of FRS2alpha and FGF-2-

256 FGF-2 stimulates cell proliferation of rabbit corneal en

257 CONCLUSIONS; FGF-2 stimulates proliferation of hCECs through PI 3-kin

258 ion of human CECs (hCECs) is also induced by FGF-2 stimulation through the p27 phosphorylation pathwa

259 Decreased ERK activation after FGF-2 stimulation was observed in TGF-beta1-treated NHLF

260 um KIS expression was observed 4 hours after FGF-2 stimulation, while the maximum Cdc25A expression w

261 elial cells in vitro required either VEGF or FGF-2 stimulation.

262 In vitro, FGF-2 suppresses interleukin-1-driven aggrecanase activi

263 ed by PMNs into the aqueous humor stimulates FGF-2 synthesis in corneal endothelium via PI3-kinase an

264 fects of HC-HA/PTX3 on cell migration (EGF + FGF-2 + TGF-beta1) and collagen gel contraction (TGF-bet

265 e-lining cells, and increased mRNA levels of FGF-2, TGFbeta-1, BMP-2, and BMP-6.

266 LOX-PP reduced specific binding of FGF-2 to DU 145 cells, suggesting that LOX-PP targets FG

267 o induce fibrosis and blocked the ability of FGF-2 to inhibit TGF-beta1 signaling.

268 Thus, heparanase is necessary for FGF-2 to produce EMT in PTECs and to sustain FGF-2 intra

269 In this report, we investigated if BMP-2 and FGF-2 together can synergistically promote bone repair i

270 Fgf-2 transcript was down-regulated, while Fgf-18 transc

271 beta (IL-1beta), fibroblast growth factor-2 (FGF-2), transforming growth factor beta-1 (TGFbeta-1), b

272 ing basic fibroblast growth factors (bFGF or FGF-2), transforming growth factor-beta (TGF-beta) and i

273 In vivo FGF-2 treatment expanded stromal cells, including periva

274 e downstream nuclear effectors of TGF-beta1, FGF-2 treatment inhibits fibrosis in VICs.

275 Furthermore, FGF-2 treatment of VICs blocks the development of pathol

276 by FGF-2, likely an effect of the fact that FGF-2 treatment prevents the nuclear localization of Sma

277 ited abrogated HSPC expansion in response to FGF-2 treatment, which was accompanied by elevated react

278 We placed fibroblast growth factor 2 (FGF-2) under conditional control of a small molecule and

279 cers, of which the vast majority also showed FGF-2 upregulation.

280 Results suggest that FGF-2 uses both PI 3-kinase/Rac1 and ERK pathways for ce

281 NDY1 is induced by FGF-2 via CREB phosphorylation and activation, downstrea

282 hough both PGE(2) (via protein kinase A) and FGF-2 (via protein kinase B, also known as AKT) depended

283 anti-FGF-2 antibody, the nuclear location of FGF-2 was observed primarily in the cornea after cryotre

284 However, when FGF-2 was removed in order for differentiation to be com

285 strated that basic fibroblast growth factor (FGF-2) was a major cytokine becoming bioavailable in the

286 Fibroblast growth factor-2 (FGF-2) was one of the first growth factors to be tested

287 up-regulated by CNTF and to a lesser extent FGF-2, was also detected.

288 kappaB kinase (IKK), IkappaB, NF-kappaB, and FGF-2 were analyzed by immunoblot analysis.

289 No increases in specific antibody to rh-FGF-2 were detected, and no serious adverse events relat

290 ray, and their bindings with a growth factor FGF-2 were examined.

291 a, and scratch-assay responses to VEGF-C and FGF-2 were reduced in Ndst1-deficient cells.

292 te growth factor, FGF-13, and IGF-1, but not FGF-2, were significantly higher by up to 7-fold than in

293 ss of 3 doses of fibroblast growth factor 2 (FGF-2) when combined with a beta-tricalcium phosphate (b

294 of the elderly GAG capacities to potentiate FGF-2 whereas the potentiating effect on VEGF(165) was i

295 I 3-kinase for cell proliferation induced by FGF-2, whereas the ERK1/2 pathway in rCECs is parallel t

296 g growth factor, fibroblast growth factor 2 (FGF-2), which is bound to the pericellular matrix hepara

297 a (IL-1beta) and fibroblast growth factor-2 (FGF-2), which led to a marked increase in MMP-1 expressi

298 lls constitutively produce the growth factor FGF-2, which activates tumor-infiltrating B cells to pro

299 FGF-2 (rh-FGF-2), 0.3% rh-FGF-2, and 0.4% rh-FGF-2 with beta-TCP-following scaling and root planing o

300 an oncogenic pathway that functionally links FGF-2 with EZH2 via NDY1 and miR-101.

301 We hypothesized that CNTF and FGF-2 would increase after SCI, especially in regions of