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1 cellular pool of fibroblast growth factor 2 (FGF-2).
2 cell growth factors, such as neuregulin and FGF-2.
3 nce than cocultures completely deficient for FGF-2.
4 ifferentiation and survival factors CNTF and FGF-2.
5 -mediated Egr-1-dependent rapid induction of FGF-2.
6 y subcutaneous administration of recombinant FGF-2.
7 ned medium, which contains a large amount of FGF-2.
8 in the presence of provasculogenic VEGF and FGF-2.
9 RSK1, and the high-molecular-weight form of FGF-2.
10 n of Skp1 and Skp2 was temporally induced by FGF-2.
11 uman chondrocytes, and this was inhibited by FGF-2.
12 non-adherent culture conditions with EGF and FGF-2.
13 neoepitope, and this was also suppressed by FGF-2.
14 ndispensable for the pro-survival effects of FGF-2.
15 f target-derived FB and intrinsic VM-derived FGF-2.
16 n sensitive to the antidepressant actions of FGF-2.
17 and angiogenic tube formation in response to FGF-2.
18 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 e, nuclear FGFR1 or its 23-kDa FGF-2 ligand (FGF-2(23)) enhances Nurr1-dependent activation of the TH
21 ults indicate that FGF ligand genes, such as Fgf-2, -4, -8, and -18, displayed a differential and dyn
23 stimulated cell proliferation in hCECs; the FGF-2 action was completely blocked by pathway-specific
32 tion, downstream of DYRK1A, and mediates the FGF-2 and EZH2 effects on cell proliferation, migration,
33 ivo corneal tissue with IL-1beta upregulated FGF-2 and facilitated its nuclear location in corneal en
34 We used low molecular weight (LMW, 18 kDa) FGF-2 and high molecular weight (HMW) FGF-2 isoforms, wh
35 , respectively, inhibited the effects of LMW-FGF-2 and HMW-FGF-23 to stimulate FGF-23 promoter activi
39 ulation include IL-1, IL-6, TNF-alpha, PGE2, FGF-2 and PKCdelta, and pharmacologic inhibitors to thes
42 nvironment, the reciprocal interplay between FGF-2 and VEGF-C collaboratively stimulated tumor growth
44 factors such as fibroblast growth factor-2 (FGF-2) and bone morphogenetic protein-2 (BMP-2) work syn
46 heparanase, basic fibroblast growth factor (FGF-2), and angiopoietin-2 (Ang-2) increased in the peri
48 oteins including fibroblast growth factor 2 (FGF-2), and the chemokines CCL2, CCL5, CCL7, CCL13, CXCL
49 actor I (IGF-I), fibroblast growth factor-2 (FGF-2), and/or transforming growth factor-beta1 (TGF-bet
50 recombinant human FGF-2 (rh-FGF-2), 0.3% rh-FGF-2, and 0.4% rh-FGF-2 with beta-TCP-following scaling
51 ncrease in expression of ANT, PDGF-BB, VEGF, FGF-2, and IL-8 for the LCC group over the autograft gro
54 and measured the resulting changes in IGF-I, FGF-2, and TGF-beta1 gene expression and protein product
55 udies suggest that interactions among IGF-I, FGF-2, and TGF-beta1 substantially modulate their regula
57 ctor signaling pathways as IGFBP-4 inhibited FGF-2- and IGF-1-stimulated angiogenesis but failed to i
61 fied as an inhibitor of SOD1 that attenuates FGF-2- and VEGF-mediated phosphorylation of ERK1/2 in en
62 en corneal endothelium was stained with anti-FGF-2 antibody, the nuclear location of FGF-2 was observ
66 hat NF-kappaB is the transcription factor of FGF-2 as NF-kappaB binds the putative NF-kappaB binding
67 e in response to fibroblast growth factor-2 (FGF-2) as cancer cells isolated from wild-type mice, and
69 n detected a plateau in the 0.3% and 0.4% rh-FGF-2/beta-TCP groups with significant improvements over
76 terestingly, the number of LYVE-1(-) gaps in FGF-2, but not VEGF-A, implanted corneas was significant
77 hod for improving the biological activity of FGF-2 by codelivering the growth factor with a liposomal
80 ), combined with fibroblast growth factor-2 (FGF-2), can induce the dedifferentiation and proliferati
87 nts in mice, we examined the extent to which FGF-2 contributes to the cellular gene response to injur
88 ndividual VM and FB tissue from wildtype and FGF-2-deficient embryonic day (E)14.5 embryos, respectiv
89 unoprecipitated from the ventral midbrain of FGF-2-deficient embryonic mice, which previously showed
90 assays on osteoblast cell layers with (125)I-FGF-2 demonstrate a concentration-dependent inhibition o
92 ), and podoplanin (Pdpn), were significantly FGF-2 dependent following injury to cartilage in vitro a
93 9, unencumbered by TIMP-1, directly mediates FGF-2-dependent angiogenesis was also demonstrated in ou
96 lotting showed that MASH1 overexpression and FGF-2 deprivation additively increased beta-III-tubulin
97 osphodiesterase (CNPase) expression, whereas FGF-2 deprivation alone attenuated glial fibrillary acid
99 y the N-terminal portion of TIMP-3, although FGF-2 did not affect production of the inhibitors TIMP-1
103 we show that basic fibroblast growth factor (FGF-2) effectively blocks transforming growth factor-bet
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
116 ntly, although other pro-osteogenic factors [Fgf-2, Fgf-18, and bone morphogenic protein 2 (Bmp-2)] s
119 exogenous basic fibroblast growth factor 2 (FGF-2/Fgf-2) is commonly used to expand adult neural ste
120 ents survival of PECs in part by maintaining FGF-2/FGF-R1 signaling and through tonic Ser-473 phospho
122 bodies further indicated an involvement of a FGF-2/FGFR-2 pathway in neutrophil proMMP-9-induced angi
123 , thus implicating the novel TIMP-free MMP-9/FGF-2/FGFR-2 pathway in proMMP-9-induced angiogenesis in
127 inds of plasmid DNA encoding either BMP-2 or FGF-2 formulated into polyethylenimine (PEI) complexes.
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
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
139 tly lower (p < 0.05) in Groups 2 and 3: EGF, FGF-2, IFNalpha2, IL-1RA, HSA, keratin-6, and involucrin
140 f a number of proangiogenic mediators (VEGF, FGF-2, IL-6, etc.) and downregulation of several angioge
142 acute knockdown of Mbd1 or overexpression of Fgf-2 in adult NSPCs inhibited their neuronal differenti
144 is study to investigate the possible role of FGF-2 in aggrecan catabolism by aggrecanase in human art
146 nd in heterogeneous cocultures deficient for FGF-2 in FB and VM, respectively, similar phenotypes wit
147 Additionally, the loss of target-derived FGF-2 in FB explants resulted in decreased caudorostral
148 The current analysis addressed the role of FGF-2 in mDA axonal outgrowth, pathway formation, and in
150 y in the cornea after cryotreatment, whereas FGF-2 in normal corneal endothelium was localized at the
152 astrocytes in culture express high levels of FGF-2 in response to IL-1beta, and IGF-1 in response to
153 a (IL-1beta) and fibroblast growth factor 2 (FGF-2) in proteoglycan metabolism, catabolic protease ex
156 ation of ECs, stimulation with VEGF-A and/or FGF-2 induced expansion of E4ORF1(+) ECs in a contact-in
158 sing immunoblotting, the authors showed that FGF-2 induced phosphorylation of p27 at both serine 10 (
160 n overexpressed and is required not only for FGF-2-induced centriole overduplication but also for nor
162 d expression of alpha-SMA and TGF-beta1- and FGF-2-induced de novo expression of tenascin-C and the d
166 tern blot analyses show that LOX-PP inhibits FGF-2-induced ERK1/2 phosphorylation, signaling events t
172 inhibition downregulated both TGF-beta1- and FGF-2-induced tenascin-C expression, ROCK inhibition was
175 human kidney 2 (HK2) PTEC cultures, although FGF-2 induces EMT in the wild-type clone, it is ineffect
180 actor and inflammatory mediator, cleaves HMW FGF-2 into an LMW FGF-2-like form that stimulates endoth
184 wave of activation, triggered by the induced FGF-2, involves the promotion of cellular activities.
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
191 Furthermore, nuclear FGFR1 or its 23-kDa FGF-2 ligand (FGF-2(23)) enhances Nurr1-dependent activa
192 tory mediator, cleaves HMW FGF-2 into an LMW FGF-2-like form that stimulates endothelial cell migrati
193 , we show that Smad activity is repressed by FGF-2, likely an effect of the fact that FGF-2 treatment
195 nt study reveal a novel mechanism underlying FGF-2-mediated in vivo expansion of both HSPCs and their
203 the presence of fibroblast growth factor 2 (FGF-2), nerve growth factor (NGF), brain-derived neurotr
206 f subcutaneous administration of recombinant FGF-2 on OA progression was assessed in Fgf2(-/-) mice.
207 factor (VEGF) and fibroblast growth factor (FGF-2) on the revascularization of severed human dental
208 entivirus-transduced NPCs were maintained in FGF-2 or deprived of FGF-2 for varying lengths of time.
209 ts that had been stimulated with recombinant FGF-2 or FGF-18, or whole joints from either wild-type m
212 ed microenvironmental signaling cues such as FGF-2 overexpression and mitotic instability and provide
213 IL-1beta was measured, and the expression of FGF-2, p38, and Akt underwent Western blot analysis.
218 and the PI 3-kinase signaling to upregulate FGF-2 production through NF-kappaB, which plays a key ro
219 volves the inductive activity of IL-1beta on FGF-2 production; the second wave of activation, trigger
224 restingly, a drift in the ratio of different FGF-2 protein forms, with translation favoring the HMWFG
225 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
227 onstrated greater than 50-fold regulation of FGF-2 release as well as tunability, reversibility, and
228 that basic fibroblast growth factor (bFGF or FGF-2) required binding to a cell-surface heparin sulfat
230 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
233 e results suggest that chemically controlled FGF-2 secretion can significantly increase bone formatio
239 in LRs, and (3) Tat-mediated enhancement of FGF-2 signaling in human podocytes and HIV-transgenic mo
240 en with HIVAN, confirm Tat as a regulator of FGF-2 signaling in LRs, and identify the key domain of T
241 lpha interaction prevented proper VEGF-A and FGF-2 signaling, which are required for efficient angiog
242 vated autocrine fibroblast growth factors 2 (FGF-2) signaling promotes prostate cancer cell growth an
249 iRNA to KIS, which subsequently hampered the FGF-2-stimulated cell proliferation, while Thr187 of p27
253 -stimulated phosphorylation of FRS2alpha and FGF-2-stimulated DNA synthesis, even after inhibition of
258 ion of human CECs (hCECs) is also induced by FGF-2 stimulation through the p27 phosphorylation pathwa
260 um KIS expression was observed 4 hours after FGF-2 stimulation, while the maximum Cdc25A expression w
264 ed by PMNs into the aqueous humor stimulates FGF-2 synthesis in corneal endothelium via PI3-kinase an
265 fects of HC-HA/PTX3 on cell migration (EGF + FGF-2 + TGF-beta1) and collagen gel contraction (TGF-bet
270 In this report, we investigated if BMP-2 and FGF-2 together can synergistically promote bone repair i
272 beta (IL-1beta), fibroblast growth factor-2 (FGF-2), transforming growth factor beta-1 (TGFbeta-1), b
273 ing basic fibroblast growth factors (bFGF or FGF-2), transforming growth factor-beta (TGF-beta) and i
277 by FGF-2, likely an effect of the fact that FGF-2 treatment prevents the nuclear localization of Sma
278 ited abrogated HSPC expansion in response to FGF-2 treatment, which was accompanied by elevated react
283 anti-FGF-2 antibody, the nuclear location of FGF-2 was observed primarily in the cornea after cryotre
285 strated that basic fibroblast growth factor (FGF-2) was a major cytokine becoming bioavailable in the
289 No increases in specific antibody to rh-FGF-2 were detected, and no serious adverse events relat
292 ss of 3 doses of fibroblast growth factor 2 (FGF-2) when combined with a beta-tricalcium phosphate (b
293 of the elderly GAG capacities to potentiate FGF-2 whereas the potentiating effect on VEGF(165) was i
294 I 3-kinase for cell proliferation induced by FGF-2, whereas the ERK1/2 pathway in rCECs is parallel t
295 g growth factor, fibroblast growth factor 2 (FGF-2), which is bound to the pericellular matrix hepara
296 a (IL-1beta) and fibroblast growth factor-2 (FGF-2), which led to a marked increase in MMP-1 expressi
297 lls constitutively produce the growth factor FGF-2, which activates tumor-infiltrating B cells to pro
298 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
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