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1 FGF 23, FMD and hsCRP can stratify the risk of early CVD
2 FGF and Hedgehog morphogen signals are required, with FG
3 FGF signaling has emerged as a significant "late-stage"
4 FGF signaling induces JNK-dependent proteasomal degradat
5 FGF signaling promotes epicardium formation in vivo, and
6 FGF signalling pathways are found to be flexible in arch
7 FGF signals are thus essential regulators of myotube gui
8 FGF-mediated PM induction in NMPs functions in tight coo
9 FGF/ERK signaling is crucial for the patterning and prol
10 FGFs are key developmental regulators that engage a sign
12 (2) (PGE(2)) and fibroblast growth factor 2 (FGF-2) -mediators known to influence fibroblast activati
13 ds to VEGF-A and fibroblast growth factor-2 (FGF-2) in human plasma and colocalizes with VEGF-A in EC
14 oncentrate (BMAC) and growth factors (BMP-2, FGF-2, and FGF-8) and 2) increase matrix strength retent
15 baseline, only fibroblast growth factor 21 (FGF-21) predicted weight loss, and none helped individua
16 rmone (PTH) and fibroblast growth factor 23 (FGF-23) were studied up to 24-hours after Npt2a-I treatm
17 alyses revealed lower group levels of FGF-5, FGF-19 and SPOCK1 in multiple system atrophy compared wi
18 ha [HIF-1alpha], fibroblast growth factor 9 [FGF-9], and p53) is still translated by an unknown, cap-
19 lage, as evidenced by the fact that aberrant FGF signalling contributes to the maldevelopment of join
22 ural cell adhesion molecule (NCAM) activates FGF receptors, we asked whether peripherally administere
23 ther revealed its initiation by 'activators' FGF and Wnt, and 'inhibitor' Hh, whereas BMP and mesench
26 in of 120 amino acids (aa) is flanked in all FGFs by highly divergent amino-terminal and carboxy-term
28 its role in Wnt signaling, Rspo2 acts as an FGF antagonist during mesoderm formation and patterning.
29 d activating binary complexes composed of an FGF receptor (FGFR) bound to either alpha-Klotho or beta
34 data identify CREB activation via PGE(2) and FGF-2 as a previously unrecognized molecular controller
36 ls were cultured and treated with VEGF A and FGF 2 and the mRNA expression pattern of EGR family memb
39 owever, their role in controlling VEGF A and FGF 2 signaling in the CL of water buffalo is not known.
41 hough both PGE(2) (via protein kinase A) and FGF-2 (via protein kinase B, also known as AKT) depended
44 ed the functional divergence between Etv and FGF in lens development, demonstrating that these SRTFs
45 vels of fibroblast growth factors (FGFs) and FGF receptors (FGFRs) have been detected in various neur
47 g complex composed of alpha-Klotho (KLA) and FGF receptor (FGFR) resulting in kinase activation, regu
48 vestigate the regulation of renal Klotho and FGF receptor (FEFR)-1 in healthy and uremic rats induced
51 ective activation of PI3K and MAPK, PDGF and FGF cooperate with and oppose each other to balance prog
53 des evidence convincingly that both VEGF and FGF mediate their biological action through a common int
56 hPSCs using sequential modulation of Wnt and FGF signaling to generate second heart field progenitors
62 eceptors 1-3, PDGF receptors alpha and beta, FGF receptors 1-3, and Src and Abl kinases, which are al
63 ors (serum, ascorbic acid, insulin, and beta-FGF) are examined to study their effects on the differen
65 portant in organogenesis (Wnt, TGFbeta/ BMP, FGF, Notch, SHH, Erbb) were differentially expressed bet
66 ted changes in genes regulating TGF-beta/BMP/FGF signaling, as well as in genes controlling ECM struc
68 get for cancer therapy, FGF/FGFR blockade by FGF trapping or tyrosine kinase inhibitor impaired the g
69 this pathway is activated in chondrocytes by FGF signaling, a critical regulator of skeletal growth.
71 ands from the embryonic node and executed by FGF signals in nascent mesoderm to control anterior meso
72 nscription factor, ETV4, which is induced by FGF signalling and acts as a repressor of ZRS activity,
73 but inactive state of the ZRS is induced by FGF signalling and in combination with balanced histone
76 calcium concentrations, activation of cAMP, FGF, and R-spondin signaling with inhibition of bone mor
80 as receptor ligands through their conserved FGF domain, but sequences outside this domain vary and a
81 ta-catenin, and that N-cadherin also dampens FGF activity and consequently stabilises neural fate.
82 Because FGF9 and FGF10 activate distinct FGF receptors (FGFRs), we hypothesized that they would c
83 neral mechanism for recognition of endocrine FGFs by Klotho proteins and regulatory interactions with
87 he signaling mutations abrogated established FGF-induced signal transduction pathways, yet FGF functi
88 actor (FGF) signaling pathway, and exogenous FGF rescues the myogenic differentiation defects upon lo
90 lls constitutively produce the growth factor FGF-2, which activates tumor-infiltrating B cells to pro
93 cies, by measuring fibroblast growth factor (FGF) 19/15 protein and mRNA levels, and 7alpha-hydroxy-4
95 regulating hormone fibroblast growth factor (FGF) 23 have emerged as powerful risk factors for cardio
96 relies on coupled fibroblast growth factor (FGF) and bone morphogenetic protein (BMP) signalling tog
99 s of the endocrine fibroblast growth factor (FGF) family designated FGF19, FGF21, and FGF23 mediate t
101 s of the endocrine-fibroblast growth factor (FGF) family, FGF19, 21, and 23 are circulating hormones
102 Here, we show that fibroblast growth factor (FGF) ligands FGF8, FGF17 and FGF18 are essential for thi
104 lly with canonical fibroblast growth factor (FGF) proteins that signal through the extracellular sign
105 ating mutations in fibroblast growth factor (FGF) receptor 3 and inactivating mutations in the NPR2 g
106 nents of endocrine fibroblast growth factor (FGF) receptor complexes, as they are required for the hi
107 activation of the fibroblast growth factor (FGF) receptor, phospholipase C (PLC), protein kinase C (
108 tral activation of fibroblast growth factor (FGF) receptors regulates peripheral glucose homeostasis
109 ne a Hedgehog (Hh)-fibroblast growth factor (FGF) signaling axis required for anterior mesoderm linea
111 nal attenuation of fibroblast growth factor (FGF) signaling is essential for the establishment of the
112 components of the Fibroblast Growth Factor (FGF) signaling pathway were enriched in nascent myotubes
113 is mediated by the fibroblast growth factor (FGF) signaling pathway, and exogenous FGF rescues the my
120 beta (TGFbeta) and fibroblast growth factor (FGF) signalling pathways to co-induce cranial epithelial
122 f an intracellular fibroblast growth factor (FGF), FGF13, in the mouse DRG neurons selectively abolis
123 ere, by modulating fibroblast growth factor (FGF), transforming growth factor beta (TGF-beta), and WN
124 fying a network of fibroblast growth factor (FGF), wingless-related integration site (WNT), and bone
127 and that required fibroblast growth factor (FGF)19 signaling via FGF receptor 4 for survival were mo
129 ts, mean levels of hepatocyte growth factor, FGF-13, and IGF-1, but not FGF-2, were significantly hig
131 proteins (such as fibroblast growth factors (FGF) or CaM-dependent kinase II (CaMKII)) that can also
132 , we identify two fibroblast growth factors (FGF), FGF6 and FGF9, as potent inducers of UCP1 expressi
135 bnormal levels of fibroblast growth factors (FGFs) and FGF receptors (FGFRs) have been detected in va
138 demonstrate that fibroblast growth factors (FGFs) position the pineal progenitor domain within the n
139 te growth factor, fibroblast growth factors (FGFs)-2 and -13, and type 1 insulin-like growth factor (
141 rthermore, genetic overexpression of the fly FGF branchless (bnl) in the tubules induces expression o
143 formation, which suggest a crucial role for FGF in survival/proliferation, and a requirement of BMP
145 DESIGN, SETTING, AND PARTICIPANTS: FORWARD (FGF-18 Osteoarthritis Randomized Trial with Administrati
149 chment in canonical pathways included HIF1A, FGF/stemness, WNT signaling, interferon signaling and co
150 imposing this prepattern's condition of high FGF and low BMP activity across the entire skin reveals
152 after meal; for example insulin-like hormone FGF-19 levels were elevated at 240 min (p = 0.001).
154 mics approach, SILAC, is applied to identify FGF-regulated phosphorylation events in two triple- nega
157 ased activation of the MAP kinases ERK1/2 in FGF-2-stimulated cell lines of affected individuals that
160 re, we describe a novel function of Rspo2 in FGF pathway regulation in vivo Overexpressed Rspo2 inhib
162 on phenotype by pharmacologically inhibiting FGF signaling shows that the normal role of Hs2st is to
163 ism independent of adipogenesis and involves FGF receptor-3 (FGFR3), prostaglandin-E2 and interaction
164 actor-extracellular signal-regulated kinase (FGF -ERK) signalling drives differentiation of mouse emb
166 wth factor (FGF)13, a nonsecreted, X-linked, FGF homologous factor, is differentially expressed in ad
170 lved in PDGF, EGFR, VEGF, insulin/IGF/MAPKK, FGF, Hedgehog, TGFbeta, and PI3K signaling pathways.
171 nstrate that, during normal lung maturation, FGF signaling restricts expression of the elastogenic ma
172 lectivity in their requirement for mediating FGF receptor (FGFR) signaling and activating downstream
173 hanism that prepares Drosophila melanogaster FGF Branchless (Bnl) for cytoneme-mediated intercellular
174 t the embryonic mouse telencephalic midline, FGF/ERK signaling drives astroglial precursor somal tran
175 ant and anxiolytic effects in animal models, FGF ligands have a broad range of actions both in the br
176 n mice to understand whether SPRY1 modulates FGF signaling in NPCs and whether FGF8 functions with FG
179 with other FGF/FGFR alterations, 18 with no FGF/FGFR alterations, and one with an undetermined FGF/F
181 te growth factor, FGF-13, and IGF-1, but not FGF-2, were significantly higher by up to 7-fold than in
182 A decrease in HK2 levels in the absence of FGF signalling inputs results in decreased glycolysis, l
183 corresponded with constitutive activation of FGF receptor 4 (FGFR4)-dependent ERK/AKT-p70S6K-S6 signa
188 brane tension facilitates the endocytosis of FGF signaling components, which activate ERK signaling a
189 SUM52, that exhibit amplified expression of FGF receptor 2 (FGFR2) and are dependent on continued FG
195 This study expands the known landscape of FGF signalling and identifies many new targets for funct
196 ific analyses revealed lower group levels of FGF-5, FGF-19 and SPOCK1 in multiple system atrophy comp
199 k new avenues for discovery of modulators of FGF signalling that can slow or stop the progression of
204 served discrepancies relating to the role of FGF/ERK signalling in PrE versus EPI specification betwe
206 ; investigation of the crystal structures of FGF-Klotho-FGFR complexes is paving the way for the deve
208 that CDC42 is involved in the trafficking of FGF receptors to the cell membrane to regulate epicardiu
211 ntitative dependence of stem cell density on FGF dosage, the biased localization of stem cells toward
212 e demonstrate a selective action of Hs2st on FGF protein by showing that Hs2st (but not Hs6st1) norma
213 oblast cells attachment and proliferation on FGF-immobilized PXDDA films were much higher than the ot
214 high affinity ligand for FGFR3, is the only FGF-based drug currently in clinical trials for osteoart
216 ty and mechanism of action of FGF2 and other FGF family members, as well as neurotrophic and differen
217 FR2 fusions or rearrangements, 20 with other FGF/FGFR alterations, 18 with no FGF/FGFR alterations, a
218 sions or rearrangements, patients with other FGF/FGFR alterations, or patients with no FGF/FGFR alter
221 r effects appear to be mediated by paracrine FGF control of kidney FGFR1 and subsequent regulation of
226 ction experiments that the epiblast provides FGF signal that results in differential fate acquisition
227 or intra-DMS blockade of the FGF2 receptor, FGF receptor-1 (FGFR1), suppresses alcohol consumption,
228 med a small screen that revealed how reduced FGF signalling induces a short-tail phenotype in embryos
229 ression suggests that functionally redundant FGF ligands may contribute to vestibular hair cell diffe
230 ng of the molecular mechanisms that regulate FGF signalling during normal joint development and in th
233 the inner cell mass (ICM), all cells relayed FGF/ERK signals with varying durations and magnitude.
237 alateral merging are attenuated by restoring FGF signaling specifically in the CVM, suggesting that m
240 tures were treated exogenously with selected FGFs and subjected to gene and protein expression analys
242 tor' Hh, whereas BMP and mesenchyme-specific-FGF signalling were incorporated once stripes were forme
246 our data suggest a model in which sustained FGF signaling acts to suppress cardiomyocyte plasticity
248 l and disease progression, and indicate that FGF targeting may represent a therapeutic approach for p
255 ed number of parapineal cells activating the FGF pathway, global activation of Notch signaling decrea
259 eptor tyrosine kinases (RTKs), including the FGF receptor, are TRIAD1 substrates that are possibly re
260 y, we described that focal activation of the FGF pathway promotes the migration of the parapineal in
263 miRNAs collectively target components of the FGF signaling pathway, a central player in the process o
264 was accompanied by the downregulation of the FGF target genes tbxt/brachyury and cdx4, which mediate
268 ng ChIP-seq, we show, surprisingly, that the FGF signaling mediator Ets2 binds near all Wnt target ge
270 findings dissect the mechanism by which the FGF/FGFR system plays a nonredundant role in multiple my
271 x status can be a target for cancer therapy, FGF/FGFR blockade by FGF trapping or tyrosine kinase inh
282 nstrated that 'ring' genes are responsive to FGF signaling at the dorsal midline, whereas 'horseshoe'
285 the biased localization of stem cells toward FGF sources, and stem cell dynamics during regeneration
286 Pyr is the first demonstrated transmembrane FGF, that it has both extracellular and intracellular fu
288 s elegans Dicer1 is also phosphorylated upon FGF stimulation at conserved serines in mouse embryonic
290 homeostasis and eating/drinking behavior via FGF receptor 1/Klothobeta (FGFR1/KLB) complexes expresse
291 broblast growth factor (FGF)19 signaling via FGF receptor 4 for survival were more sensitive to trame
294 es new insights into the mechanisms by which FGF antagonists promote multiple myeloma cell death.
295 se results identify mechanisms through which FGF signaling regulates inner cell mass lineage restrict
296 ogether, these data support a model in which FGFs, possibly from axons, activate FGFR2 in the oligode
298 Additionally, intraarticular treatment with FGF-2 and FGF-8 was found to suppress joint inflammation
300 GF-induced signal transduction pathways, yet FGF functions such as cell-matrix and cell-cell adhesion