戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (left1)

通し番号をクリックするとPubMedの該当ページを表示します
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
11      By examining the 5' UTRs of HIF-1alpha, FGF-9, and p53 mRNAs and using fluorescence anisotropy b
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
20 f BRD4 decreased NRP1 expression and ablated FGF-mediated tumor cell growth.
21               Although ligands that activate FGF receptors have antidepressant and anxiolytic effects
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
24  PSCs can be recapitulated without affecting FGF-MEK signalling or global DNA methylation.
25      However, it remains unknown whether all FGF activities depend on this canonical signal transduct
26 in of 120 amino acids (aa) is flanked in all FGFs by highly divergent amino-terminal and carboxy-term
27                                           An FGF-Foxf pathway acts in multipotent progenitors to esta
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
30  contribute to mesoderm heterogeneity via an FGF receptor-dependent positive feedback mechanism.
31  sequenced the fin whale genome and analysed FGFs from 8 cetaceans.
32                                   GDF-15 and FGF-21 were measured in serum from 24 patients with TK2
33 lly, intraarticular treatment with FGF-2 and FGF-8 was found to suppress joint inflammation.
34 data identify CREB activation via PGE(2) and FGF-2 as a previously unrecognized molecular controller
35 (BMAC) and growth factors (BMP-2, FGF-2, and FGF-8) and 2) increase matrix strength retention.
36 ls were cultured and treated with VEGF A and FGF 2 and the mRNA expression pattern of EGR family memb
37              It was observed that VEGF A and FGF 2 induced angiogenesis, cell proliferation and stero
38 ole of EGR mediated regulation of VEGF A and FGF 2 signaling in buffalo luteal cells.
39 owever, their role in controlling VEGF A and FGF 2 signaling in the CL of water buffalo is not known.
40 then cultured and stimulated with VEGF A and FGF 2.
41 hough both PGE(2) (via protein kinase A) and FGF-2 (via protein kinase B, also known as AKT) depended
42 g, likely being involved in TGF-beta/BMP and FGF/EGF signaling pathways.
43                   How Na(V) -CaM, CaMKII and FGF/fibroblast growth factor homologous factor interacti
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
46  and increased circulating serum insulin and FGF-21 concentrations.
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
49      Decreased circulating FGF-21 levels and FGF-21 message expression in the liver were found in Gpr
50 anscriptional patterning of the mesoderm and FGF signaling for mesoderm migration.
51 ective activation of PI3K and MAPK, PDGF and FGF cooperate with and oppose each other to balance prog
52           As expected retinoic acid (RA) and FGF are able to modulate HOX expression in the posterior
53 des evidence convincingly that both VEGF and FGF mediate their biological action through a common int
54         During Xenopus gastrulation, Wnt and FGF signaling pathways cooperate to induce posterior str
55                                      Wnt and FGF signaling promote the differentiation of these putat
56 hPSCs using sequential modulation of Wnt and FGF signaling to generate second heart field progenitors
57  as a key regulator that antagonizes WNT and FGF signaling to regulate MSC lineage commitment.
58 al stem cell (MSC) fate by mediating WNT and FGF signaling.
59 e absence of SPRY1, FGF9, and FGF20, another FGF ligand, FGF8, promotes nephrogenesis.
60 transcription factors modulated enhancers at FGF gene loci.
61      Here, we demonstrate that the autocrine FGF/FGFR axis is essential for multiple myeloma cell sur
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
64 trating the antagonistic interaction between FGF-induced MAPK and PDGF-induced PI3K signaling.
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
67                          This is achieved by FGF-dependent control of c-MYC (MYC) expression that, in
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.
70 n the epithelialisation timing controlled by FGF activity.
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
74 ion of inner ear progenitors is initiated by FGF signalling.
75 ersus 2.5 h), but are similarly regulated by FGF, WNT, Notch and YAP signalling(5).
76  calcium concentrations, activation of cAMP, FGF, and R-spondin signaling with inhibition of bone mor
77                        Decreased circulating FGF-21 levels and FGF-21 message expression in the liver
78                      The polydopamine-coated FGF-loaded PXDDA samples were then characterized using F
79 g of FGF19, FGF21 and FGF23 to their cognate FGF receptors (FGFRs).
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
84  putative interactions between the endocrine FGFs and FGFR1/Klb, or FGF19 with FGFR4.
85  RNAseq) were used to investigate endogenous FGF expression profiles in these cultures over time.
86                              FGFBP1 enhances FGF signaling including angiogenesis during cancer progr
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
89                Yet, TAMS not T cells express FGF receptors.
90 lls constitutively produce the growth factor FGF-2, which activates tumor-infiltrating B cells to pro
91          Levels of fibroblast growth factor (FGF) 1, FGF2, and FGF7 were significantly upregulated in
92             BA and fibroblast growth factor (FGF) 19 levels (a surrogate for intestinal farnesoid X r
93 cies, by measuring fibroblast growth factor (FGF) 19/15 protein and mRNA levels, and 7alpha-hydroxy-4
94 reduced C-terminal fibroblast growth factor (FGF) 23 compared with control.
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
97                    Fibroblast Growth Factor (FGF) dependent signalling is frequently activated in can
98       For example, fibroblast growth factor (FGF) drives naive pluripotent cells into extraembryonic
99 s of the endocrine fibroblast growth factor (FGF) family designated FGF19, FGF21, and FGF23 mediate t
100 nce highlights the fibroblast growth factor (FGF) family in emotion modulation.
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
103                    Fibroblast growth factor (FGF) plays a vital role in the repair and regeneration o
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
110                The fibroblast growth factor (FGF) signaling cascade is a key signaling pathway in hep
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
114                    Fibroblast growth factor (FGF) signaling plays pivotal roles in generating and mai
115                    Fibroblast Growth Factor (FGF) signaling promotes self-renewal in progenitor cells
116 ymes downstream of fibroblast growth factor (FGF) signaling.
117 oderm cells due to fibroblast growth factor (FGF) signaling.
118                    Fibroblast growth factor (FGF) signalling in the distal limb primes the ZRS at ear
119          Regulated fibroblast growth factor (FGF) signalling is a prerequisite for the correct develo
120 beta (TGFbeta) and fibroblast growth factor (FGF) signalling pathways to co-induce cranial epithelial
121  in the absence of fibroblast growth factor (FGF) signalling.
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
125 uld be enhanced by fibroblast growth factor (FGF)1 or FGF2.
126                    Fibroblast growth factor (FGF)13, a nonsecreted, X-linked, FGF homologous factor,
127  and that required fibroblast growth factor (FGF)19 signaling via FGF receptor 4 for survival were mo
128 aily injections of fibroblast growth factor (FGF)19.
129 ts, mean levels of hepatocyte growth factor, FGF-13, and IGF-1, but not FGF-2, were significantly hig
130                   Fibroblast growth factors (FGF) act as proangiogenic and mitogenic cytokines in mul
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
133                   Fibroblast growth factors (FGFs) 21 and 23 are recently identified hormones regulat
134                   Fibroblast growth factors (FGFs) 9 and 10 are essential during the pseudoglandular
135 bnormal levels of fibroblast growth factors (FGFs) and FGF receptors (FGFRs) have been detected in va
136  by the supply of fibroblast growth factors (FGFs) from lymphatic endothelial cells.
137              Most fibroblast growth factors (FGFs) function as receptor ligands through their conserv
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 (
140                         Drosophila has fewer FGF genes, with only three identified to date, pyramus (
141 rthermore, genetic overexpression of the fly FGF branchless (bnl) in the tubules induces expression o
142              Flow-mediated dilatation (FMD), FGF-23, serum lipid, hsCRP levels, BMI and HOMA were ass
143  formation, which suggest a crucial role for FGF in survival/proliferation, and a requirement of BMP
144                               Strategies for FGF signalling-based treatment of osteoarthritis and for
145  DESIGN, SETTING, AND PARTICIPANTS: FORWARD (FGF-18 Osteoarthritis Randomized Trial with Administrati
146                                  Of the four FGF receptors (FGFRs 1-4), FGFR1 and FGFR3 are strongly
147 ion in the paracrine activation of Heartless FGF receptor.
148                                The Heartless FGF receptor acts cell-autonomously in ensheathing glia
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
151                               We report high FGF receptor (FGFR) expression in 17.7% (11 of 62) of he
152 after meal; for example insulin-like hormone FGF-19 levels were elevated at 240 min (p = 0.001).
153                                          How FGF activity is restricted to leading cells in this syst
154 mics approach, SILAC, is applied to identify FGF-regulated phosphorylation events in two triple- nega
155                             Here we identify FGF receptor (FGFR) signalling as a critical regulator o
156 g up the risk of aberrant differentiation if FGF is activated before Nodal.
157 ased activation of the MAP kinases ERK1/2 in FGF-2-stimulated cell lines of affected individuals that
158                           Focal adhesions in FGF-2-stimulated fibroblasts of affected individuals con
159  be hijacked by disease-causing mutations in FGF receptor (FGFR) during embryogenesis.
160 re, we describe a novel function of Rspo2 in FGF pathway regulation in vivo Overexpressed Rspo2 inhib
161                     Decreasing or increasing FGF signaling in a Notch loss-of-function context respec
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
165 nl), and all three encoding relatively large FGF proteins (~80 kDa).
166 wth factor (FGF)13, a nonsecreted, X-linked, FGF homologous factor, is differentially expressed in ad
167 sed a simple dopamine coating method to load FGF on the surface of PXDDA polymeric films.
168 litol dodecanedioic acid) (PXDDA) and loaded FGF on the PXDDA for sustained drug delivery.
169              We hypothesized that the longer FGF proteins present in Drosophila and other organisms m
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
177                 As heparan sulfate modulates FGF-mediated signaling, we found a significantly decreas
178 ss the role of Notch signaling in modulating FGF activity within the parapineal.
179  with other FGF/FGFR alterations, 18 with no FGF/FGFR alterations, and one with an undetermined FGF/F
180 er FGF/FGFR alterations, or patients with no FGF/FGFR alterations.
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
184  expressed in NPCs modulates the activity of FGF signaling and regulates NPC stemness.
185 higher species under the hormonal control of FGF-signaling.
186                               The decline of FGF-21 was less prominent and consistent.
187 kinase-ERK signal transduction downstream of FGF receptor activation.
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
190                Here, we examined a family of FGF-induced SRTFs - Etv1, Etv 4, and Etv 5 - in murine l
191                             The functions of FGF receptors (FGFRs) in early development of the cerebr
192 he PXDDA film enhanced the immobilization of FGF and controlled its sustained release.
193                         The potent impact of FGF-FGFR in multiple embryonic developmental processes m
194                   The observed inhibition of FGF signaling was accompanied by the downregulation of t
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
197                              Manipulation of FGF or Wnt signaling demonstrated that 'ring' genes are
198                                Modulation of FGF signaling achieves stratified squamous epithelium fr
199 k new avenues for discovery of modulators of FGF signalling that can slow or stop the progression of
200                                  Mutation of FGF receptor Heartless (Htl) has been shown to cause CVM
201         The in vitro drug release profile of FGF from PXDDA film and cell growth behavior were measur
202 ere TIMPs negatively regulate the release of FGF-2 from chondrocytes to allow IHH expression.
203 l as regulates the production and release of FGF-21 to control systemic energy homeostasis.
204 served discrepancies relating to the role of FGF/ERK signalling in PrE versus EPI specification betwe
205                       The inductive roles of FGF, Wnt, and BMP at the neural plate border are well es
206 ; investigation of the crystal structures of FGF-Klotho-FGFR complexes is paving the way for the deve
207 rescues the defects caused by suppression of FGF signalling.
208 that CDC42 is involved in the trafficking of FGF receptors to the cell membrane to regulate epicardiu
209                 An improved understanding of FGF signalling from a structural biology perspective, an
210  through competition for a limited supply of FGFs.
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
215 er than the other groups without coatings or FGF loading.
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
219               Our results suggest that other FGFs may be membrane tethered or multifunctional like Py
220                                    Paracrine FGF-ERK signalling induces heterogeneity, whereby cells
221 r effects appear to be mediated by paracrine FGF control of kidney FGFR1 and subsequent regulation of
222         Unlike the heparin-binding paracrine FGFs, eFGFs require a unique Klotho family protein to fo
223 l distribution and levels of this particular FGF protein are tightly regulated.
224 llular differentiation stimuli, particularly FGF-MEK signalling.
225  on multiple previously implicated pathways: FGF, Hh, Wnt and BMP.
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
231 ine astroglial development and in regulating FGF protein levels and interaction with HS.
232 le is known about the molecule(s) regulating FGF signaling during nephron development.
233 the inner cell mass (ICM), all cells relayed FGF/ERK signals with varying durations and magnitude.
234 t the nascent PR axon, which in turn release FGF to induce SGs' differentiation into WG.
235 ompanied by Erk phosphorylation and required FGF and Nodal but not Wnt signaling.
236 tors within the mammalian lower jaw requires FGF signaling.
237 alateral merging are attenuated by restoring FGF signaling specifically in the CVM, suggesting that m
238  parapineal through its capacity to restrict FGF pathway activation to a few leading cells.
239                      Furthermore, these same FGFs were downregulated over time in (R200Q)VSX2 hiPSC-O
240 tures were treated exogenously with selected FGFs and subjected to gene and protein expression analys
241                           We found that some FGFs - including FGF2, strongly increased GLT1 expressio
242 tor' Hh, whereas BMP and mesenchyme-specific-FGF signalling were incorporated once stripes were forme
243 rphogenesis; however, the inverse, supplying FGF to the TVM, does not rescue CVM mismigration.
244 that the normal role of Hs2st is to suppress FGF-mediated astroglial translocation.
245                          Id1 then suppresses FGF activity to delay differentiation.
246  our data suggest a model in which sustained FGF signaling acts to suppress cardiomyocyte plasticity
247             Furthermore, we demonstrate that FGF signalling controls the phase and period of oscillat
248 l and disease progression, and indicate that FGF targeting may represent a therapeutic approach for p
249                    Our results indicate that FGF/MAPK blockade may be particularly efficacious agains
250                    In addition, we show that FGF regulates integrin expression in both tissues, but o
251                                 We show that FGF-MAPK signalling maintains multipotency and promotes
252                          Our work shows that FGF signaling directs zonal patterning at the boundary b
253                                          The FGF inhibitory activity was mapped to the thrombospondin
254                                          The FGF ligand Pyramus is expressed broadly in the ectoderm,
255 ed number of parapineal cells activating the FGF pathway, global activation of Notch signaling decrea
256 fied by secreted signaling proteins from the FGF, Nodal, BMP and Wnt families.
257                        Null mutations in the FGF receptor heartless (htl), or its ligands, caused sig
258 network by which activating mutations in the FGF receptor inhibit bone growth.
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
261 targets of Pnhd are shared with those of the FGF pathway.
262                            Inhibitors of the FGF receptor (Fgfr) and ERK pathways reversed the skewed
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
265                    Aberrant signaling of the FGF/FGFR pathway occurs frequently in cancers and is an
266 ge priming is prevented by inhibition of the FGF/MAPK signalling pathway.
267                     Therefore, targeting the FGF-Klotho endocrine axes might have therapeutic benefit
268 ng ChIP-seq, we show, surprisingly, that the FGF signaling mediator Ets2 binds near all Wnt target ge
269           Growing evidence suggests that the FGF-Klotho endocrine system also has a crucial role in t
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
272 rs promote pinealogenesis by inhibiting this FGF activity.
273                                         Thus FGF signaling lowers cyclic GMP production in the growth
274                                        Thus, FGF-dependent regulation of endothelial glycolysis is a
275                             We identify TIMP/FGF-2/IHH as a novel nexus underlying bone lengthening w
276                                  Contrary to FGF receptor mutants that displayed loss of ERK signalin
277 n and rescue the proapoptotic effects due to FGF blockade.
278 kinase 2 (TK2) deficiency and compared it to FGF-21.
279 ranscription factor NF-kappaB in response to FGF and IL-1/TNF, respectively.
280 ubcellular branching as a direct response to FGF signalling.
281  explants and Erk1 activation in response to FGF.
282 nstrated that 'ring' genes are responsive to FGF signaling at the dorsal midline, whereas 'horseshoe'
283        This PDX model is highly sensitive to FGF receptor (FGFR) inhibition, and more so to combined
284 al were more sensitive to trametinib than to FGF receptor 4 inhibitors.
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
287 FR alterations, and one with an undetermined FGF/FGFR alteration.
288 s elegans Dicer1 is also phosphorylated upon FGF stimulation at conserved serines in mouse embryonic
289 -beta increased KL secretion and upregulated FGF receptor (FGFR) 1.
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
292 ween BMP target genes largely collapsed when FGF and Nodal signaling were inhibited.
293         Wnt signaling initiates EMT, whereas FGF signaling terminates this event.
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
297 edgehog morphogen signals are required, with FGF providing a directional cue.
298  Additionally, intraarticular treatment with FGF-2 and FGF-8 was found to suppress joint inflammation
299                  Furthermore, treatment with FGFs provides a robust means for expansion of functional
300 GF-induced signal transduction pathways, yet FGF functions such as cell-matrix and cell-cell adhesion

 
Page Top