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1 FGF receptor substrate 2alpha (FRS2alpha) is an FGF rece
2 FGF receptors 1 and 2 (Fgfr1 and Fgfr2) are both express
3 FGF signaling abnormalities have been associated with sk
4 FGF signaling has emerged as a significant "late-stage"
5 FGF signaling promotes epicardium formation in vivo, and
6 FGF signaling represses the NMP markers brachyury (ntla)
7 FGF signaling through receptors Fgfr3 and Fgfr4 is cruci
8 FGF signaling, an important component of intercellular c
9 FGF-1 applied to rat spinal astrocytes in culture initia
10 FGF-1-induced dye uptake by astrocytes is prevented by B
11 FGF-10 can prevent or reduce lung specific inflammation
12 FGF-23 demonstrated an increased discriminatory power fo
13 FGF-23 is independently associated with an increased ris
14 FGF-mediated PM induction in NMPs functions in tight coo
15 Importantly, fibroblast growth factor-10 (FGF-10) was markedly suppressed in IPF subjects with pro
16 ss of 3 doses of fibroblast growth factor 2 (FGF-2) when combined with a beta-tricalcium phosphate (b
17 oteins including fibroblast growth factor 2 (FGF-2), and the chemokines CCL2, CCL5, CCL7, CCL13, CXCL
18 factors such as fibroblast growth factor-2 (FGF-2) and bone morphogenetic protein-2 (BMP-2) work syn
19 y downregulated fibroblast growth factor-21 (FGF-21) and TubA significantly reversed this downregulat
20 derived hormone fibroblast growth factor-23 (FGF-23) activates complexes composed of FGF receptors (F
23 tereoisomers, with only one able to act as a FGF trap molecule and to inhibit FGF-dependent receptor
25 ed chaperone that mobilizes paracrine-acting FGFs, stored in the extracellular matrix, and presents t
29 receptor substrate 2alpha (FRS2alpha) is an FGF receptor-associated protein required for activation
33 In this report, we investigated if BMP-2 and FGF-2 together can synergistically promote bone repair i
34 that displays distinct responses to BMP and FGF signaling from the traditional neural border genes.
35 of the delicate temporal effects of BMP and FGF signaling, and find that NC development is separable
40 role of fibroblast growth factors (FGFs) and FGF receptors (FGFRs) in establishing and maintaining co
42 arily conserved between mice and humans, and FGF signaling, although required for thyroid specificati
43 developmental gene re-activation in IPF, and FGF-10 deficiency as a potentially critical factor in di
44 vestigate the regulation of renal Klotho and FGF receptor (FEFR)-1 in healthy and uremic rats induced
45 s Previous studies have implicated Nodal and FGF signals in the specification of lateral and ventral
46 ome of these genes are in the HOX, NOTCH and FGF signalling pathways, which regulate both skeletal an
47 duces elevation of both plasma phosphate and FGF-23 concentrations, potentially contributing to cardi
48 nd link tissue subdivision (Wnt receptor and FGF receptor activity domains) to receptor-ligand parame
50 inhibitors of YAP (such as verteporfin) and FGF receptors (such as BGJ398) can provide a novel thera
51 ycolysis in the tail bud coordinates Wnt and FGF signaling to promote elongation of the embryonic axi
53 , we have previously identified an autocrine FGF signaling induced by loss of Pten in keratinocytes.
55 te that there is signaling crosstalk between FGF and Wnt, and that beta-catenin acts on PGC prolifera
56 was a strong competitive interaction between FGF-23 and ADMA in the risk of renal events (P<0.01 in a
59 nimal signaling pathways (Wnt+BMP versus BMP+FGF) that regulate distinct lung- versus thyroid-lineage
61 Spatiotemporally regulated domains of BMP, FGF, and other signaling molecules in late gastrula-earl
62 sional culture system, we modulate TGF, BMP, FGF, and WNT signaling to generate multiple otic-vesicle
63 portant in organogenesis (Wnt, TGFbeta/ BMP, FGF, Notch, SHH, Erbb) were differentially expressed bet
64 ted changes in genes regulating TGF-beta/BMP/FGF signaling, as well as in genes controlling ECM struc
65 to induce diabetes remission and that brain FGF receptors are potential pharmacological targets for
69 nscription factor, ETV4, which is induced by FGF signalling and acts as a repressor of ZRS activity,
70 but inactive state of the ZRS is induced by FGF signalling and in combination with balanced histone
71 se in Etd(+) uptake by astrocytes induced by FGF-1, although they are activated by FGF-1 treatment.
74 a prototypical SH2 containing substrate, by FGF receptors (FGFR) entails formation of an allosteric
76 several angiogenesis-related factors (CD26, FGF, HGF, MMP-8, MMP-9, OPN, PF4, SDF-1) and cytokines (
77 ents redirecting a signal-peptide-containing FGF family member from the endoplasmic reticulum/Golgi-d
78 m(2)), serum 25-hydroxyvitamin D (25(OH)D), FGF-23, and Klotho levels were measured at baseline and
79 l expression of Lhx2 and neuroretina-derived FGF factors are crucial for lens fiber development in vi
80 ally layer and required Dally (but not Dlp), FGF-receiving ASP cytonemes navigated in the Dlp layer,
81 fects of HC-HA/PTX3 on cell migration (EGF + FGF-2 + TGF-beta1) and collagen gel contraction (TGF-bet
83 ouble-negative" PCs are notable for elevated FGF and MAPK pathway activity, which can bypass AR depen
84 factor 21 (FGF21), a member of the endocrine FGF subfamily, is expressed in thymic stromal cells alon
86 ement membrane proteins, and members of ERK, FGF and PDGF signaling pathways, which play key roles in
87 enuated LVH in the Hyp mouse model of excess FGF-23, but did not induce a response in FGFR1(DT-cKO) m
89 expression of multiple neuroretina-expressed FGFs and canonical FGF-regulated genes in neuroretina.
91 lls constitutively produce the growth factor FGF-2, which activates tumor-infiltrating B cells to pro
92 -activity study of fibroblast growth factor (FGF) 1 and FGF2 signaling through FGF receptor (FGFR) 1c
95 a co-receptor for Fibroblast Growth Factor (FGF) 23, a known pro-inflammatory, prognostic marker in
96 applying Wnt, BMP, fibroblast growth factor (FGF) and retinoic acid (RA) signaling to obtain lung and
97 ave implicated the fibroblast growth factor (FGF) family in affect regulation and suggest a potential
98 Members of the fibroblast growth factor (FGF) family play essential and important roles in primar
101 n concert with the fibroblast growth factor (FGF) pathway to promote branch morphogenesis, while corr
102 protein (BMP), and fibroblast growth factor (FGF) pathways are activated at the transition from pre-i
103 taplegic (Dpp) and Fibroblast growth factor (FGF) proteins produced by the wing imaginal disc and tra
104 ating mutations in fibroblast growth factor (FGF) receptor 3 and inactivating mutations in the NPR2 g
105 activation of the fibroblast growth factor (FGF) receptor, phospholipase C (PLC), protein kinase C (
106 ctivation of brain fibroblast growth factor (FGF) receptors, we explored the antidiabetic efficacy of
108 Although restoring Fibroblast growth factor (FGF) signaling can partially rescue SHF addition in Cyp2
112 Hippo/YAP and the fibroblast growth factor (FGF) signaling pathways formed an autocrine/paracrine-po
113 beta (TGFbeta) and fibroblast growth factor (FGF) signaling pathways play important roles in the prol
118 rain and show that fibroblast growth factor (FGF) signalling regulates FBM neuron migration in an HS2
119 f an intracellular fibroblast growth factor (FGF), FGF13, in the mouse DRG neurons selectively abolis
120 fying a network of fibroblast growth factor (FGF), wingless-related integration site (WNT), and bone
122 omeostasis include fibroblast growth factor (FGF)-23, a bone-derived hormone that inhibits 1,25-dihyd
124 st studied are the fibroblast growth factor (FGF)-ERK1/2 pathway, PI3K-AKT, the leukemia inhibitory f
129 iological role of fibroblast growth factors (FGFs) and FGF receptors (FGFRs) in establishing and main
134 These phenotypes reflect important roles for FGF signaling in promoting ventricular traits, both in e
135 decreased downstream forkhead box P1 (FOXP1)/FGF and NOTCH1/EPHB2 signaling, indicating that SHP2 is
136 egulated loci that receive direct input from FGF signaling to balance self-renewal and cell fate dete
137 ial for mng survival mediated by gliotrophic FGF signaling.How glial cells, such as astrocytes, acqui
139 imposing this prepattern's condition of high FGF and low BMP activity across the entire skin reveals
140 and contributes to our understanding of how FGF signaling plays diverse developmental roles.SIGNIFIC
141 FRs could therefore in principle explain how FGFs play several distinct roles in other developing tis
142 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
143 sue of Nature, Nacu et al. (2016) identified FGF and HH ligands as interacting molecular influences t
147 Finally, we examined anxiety behavior in FGF receptor (FGFR) KO mice; however, FGFR1, FGFR2, and
148 Further, culturing rat lens explants in FGF increased their expression of Prox1, and this was at
151 to act as a FGF trap molecule and to inhibit FGF-dependent receptor activation, cell proliferation, a
157 We show that deleting Ptpn11, which links FGF with the ERK pathway, prevents inferior colliculus f
159 nstrate that, during normal lung maturation, FGF signaling restricts expression of the elastogenic ma
160 eceptors and signaling pathways that mediate FGF-dependent presynaptic differentiation, and thereby p
161 lectivity in their requirement for mediating FGF receptor (FGFR) signaling and activating downstream
162 her analysis indicated that RPS15A modulated FGF signaling by enhancing Wnt/beta-catenin-mediated FGF
163 haracterize the effect of FGF-10 on LR-MSCs, FGF-10 was intratracheally delivered into the lungs of r
165 CP) system in the disc, and neither Dpp- nor FGF-receiving cytonemes extended over mutant disc cells
166 onal ablation of this receptor-type, but not FGF receptor type 1 (FGFR1), resulted in attenuation of
168 A decrease in HK2 levels in the absence of FGF signalling inputs results in decreased glycolysis, l
169 e detected in vivo and reflect the action of FGF signaling on downstream targets during bone developm
173 These results highlight the complexity of FGF signaling in the regulation of various metabolic pro
175 -23 (FGF-23) activates complexes composed of FGF receptors (FGFRs), including FGFR1, and alpha-Klotho
178 st on the endothelium, and downregulation of FGF receptor 2 (FGFR2) on PMNs rescued host defense in t
179 stablish the genetic hierarchy downstream of FGF by systematic analysis of many ear factors combined
180 lled by different strengths and durations of FGF signals originated from the so-called isthmic organi
181 te proliferation and the mitogenic effect of FGF signalling, which are only required after wound clos
182 gs, suggesting that the protective effect of FGF-10 might be mediated, in part, by the mobilization o
186 to be a general agreement on the effects of FGF signaling on the proliferation of pulp cells, there
191 ls to serum starvation is not due to lack of FGF synthesis but likely to effects of Psen1 on FGF rele
193 served discrepancies relating to the role of FGF/ERK signalling in PrE versus EPI specification betwe
197 that CDC42 is involved in the trafficking of FGF receptors to the cell membrane to regulate epicardiu
200 lts provide novel insights into the roles of FGFs in cetacean adaptation to the aquatic environment.
202 synthesis but likely to effects of Psen1 on FGF release onto the cell surface and impaired activatio
203 n which BMP keeps lens cells in an optimally FGF-responsive state and, reciprocally, FGF enhances BMP
204 inds of plasmid DNA encoding either BMP-2 or FGF-2 formulated into polyethylenimine (PEI) complexes.
205 nds on additional mechanisms, such as BMP or FGF signalling for the particular genes we investigated,
207 data that show that an SMC deletion of a pan-FGF receptor adaptor Frs2alpha (fibroblast growth factor
209 r effects appear to be mediated by paracrine FGF control of kidney FGFR1 and subsequent regulation of
210 d VEGF/platelet-derived growth factor (PDGF)/FGF receptor inhibitors, paracrine ERK activation in fib
211 n, and that combined inhibition of VEGF/PDGF/FGF receptors is sufficient to inhibit mitogenic signali
212 aptic SDC2 presents FGF22 to the presynaptic FGF receptor to promote presynaptic differentiation.
215 ein response (UPR), which profoundly reduces FGF signaling in cardiac progenitor cells of the second
217 e demonstrate that skin hyperplasia requires FGF receptor adaptor protein Frs2alpha and tyrosine phos
219 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
220 recombinant human FGF-2 (rh-FGF-2), 0.3% rh-FGF-2, and 0.4% rh-FGF-2 with beta-TCP-following scaling
221 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
222 n detected a plateau in the 0.3% and 0.4% rh-FGF-2/beta-TCP groups with significant improvements over
224 No increases in specific antibody to rh-FGF-2 were detected, and no serious adverse events relat
227 ritically important to identify the specific FGF receptor type and its downstream signaling molecules
228 e developmental roles.SIGNIFICANCE STATEMENT FGFs promote a range of developmental processes in many
229 cushion mesenchymal cells where it supports FGF-driven expansion of ECs and then AVC valve extracell
230 our data suggest a model in which sustained FGF signaling acts to suppress cardiomyocyte plasticity
236 in vivo SIGNIFICANCE STATEMENT: We find that FGF-1 elevates [Ca(2+)]i in spinal astrocytes, which cau
237 se spinal cord slices ex vivo, we found that FGF-1 treatment for 1 h increases the percentage of GFAP
239 8 and the isthmic organizer, indicating that FGF and Mek1(DD) initiate qualitatively and/or quantitat
240 dy brings up the intriguing possibility that FGF receptor 2, in the oligodendrocyte/myelin compartmen
249 d gain-of-function experiments, we show that FGF signalling is necessary and sufficient for stratific
250 GMP production in intact tibia, we show that FGF-induced dephosphorylation of NPR2 decreases its guan
251 cting Pten and Ras pathways and suggest that FGF-activated Ras-MAPK pathway is an effective therapeut
252 n factor brachyury We find in zebrafish that FGF is continuously required for paraxial mesoderm (PM)
256 veal a novel mode of cooperation between the FGF and BMP pathways in which BMP keeps lens cells in an
261 of FGF9 in relation to other members of the FGF family may prove key to understanding vulnerability
263 gnaling components, including members of the FGF pathway, EPHA3 and SPRY2, also contribute risk for i
281 ting up a gradient of CXCL12a, and trailing (FGF receptor active) cells moving actively by chemotaxis
287 e that directly targets cardiac myocytes via FGF receptor (FGFR) 4 thereby inducing hypertrophic myoc
288 lkaline phosphatase (Tnap) transcription via FGF receptor-3 (FGFR3) signaling, leading to inhibition
290 Unlike the majority of cell types where FGF signaling triggers proliferation, chondrocytes respo
294 se results identify mechanisms through which FGF signaling regulates inner cell mass lineage restrict
295 ogether, these data support a model in which FGFs, possibly from axons, activate FGFR2 in the oligode
296 ell understood, the mechanisms through which FGFs induce hepatic character within the endoderm are il
297 expressed in thymic stromal cells along with FGF receptors and its obligate coreceptor, betaKlotho.
298 rotein (BMP) and WNT signaling combined with FGF and retinoic acid treatments over the course of 18 d
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