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1 ion in the paracrine activation of Heartless FGF receptor.
2 ltikinase inhibitor that targets BCR-ABL and FGF receptor.
3 that Cubn is a novel, interspecies-conserved Fgf receptor.
4 inity signaling complexes with their cognate FGF receptor.
5 action between different FGF ligands and the FGF receptor.
6 aling through this pathway downstream of the FGF receptor.
7 dependent expression of the breathless (btl) FGF receptor.
8 sine-kinase inhibitor that inhibits VEGF and FGF receptors.
9 e to their different binding affinities with FGF receptors.
10 ly sensitive to small molecule inhibitors of FGF receptors.
11 ble FGF traps or a dominant inhibitor of all FGF receptors.
12 d ability of FGF23 to signal via its cognate FGF receptors.
13 nductive activity due to higher affinity for Fgf receptors.
14 ished binding of a subset of FGF proteins to FGF receptors.
15 at BMP signaling is required at the level of FGF receptors.
16                Yet, TAMS not T cells express FGF receptors.
17    We created two lines of mice lacking both FGF receptor 1 (Fgfr1) and Fgfr2 in oligodendrocyte-line
18                                     NgR1 and FGF receptor 1 (FGFR1) are colocalized to synapses, and
19          While loss-of-function mutations in FGF receptor 1 (FGFR1) cause human GnRH deficiency, to d
20 we show using signal transduction mutants of FGF receptor 1 (FGFR1) expressed in rat VSMC that the ad
21                             Here we examined FGF receptor 1 (FGFR1) expression and investigated its i
22                                              FGF receptor 1 (FGFR1) expression is restricted to MMCm
23 mal transition (EndMT) and its key regulator FGF receptor 1 (FGFR1) in atherosclerosis.
24                      Morpholino knockdown of FGF receptor 1 (Fgfr1) in zebrafish cell-autonomously re
25 e defect had been identified: a heterozygous FGF receptor 1 (FGFR1) mutation in pedigree 1 and a comp
26 nce suggests that bFGF selectively activates FGF receptor 1 (FGFR1) to exert degradative effects in b
27 ctive factors include FGFs via activation of FGF receptor 1 (FGFR1).
28 nase (ERK)-cFos pathway after binding to the FGF receptor 1 (FGFR1).
29 tified SK1 as a target of the canonical FGF2/FGF receptor 1 activation pathway in endothelial cells a
30       Moreover, a differential expression of Fgf Receptor 1 and 2 resembling that previously found in
31 functions by blocking FGF2 signaling through FGF receptor 1 and syndecan-4 and downstream effectors p
32 r, rPAI-1(23) blocked FGF2 signaling through FGF receptor 1 and syndecan-4, inhibiting cell migration
33  signaling in animal caps, did interact with Fgf receptor 1 in cultured cells and, according to conte
34 c activity and is mediated predominantly via FGF receptor 1 signalling.
35 lt, 12 hits were identified including FGFR1 (FGF receptor 1), TrkB, and TrkC as well as components of
36 sumably mediated by activation of the FGFR1 (FGF receptor 1), which is expressed in mammalian brain m
37 homeostasis and eating/drinking behavior via FGF receptor 1/Klothobeta (FGFR1/KLB) complexes expresse
38                                              FGF receptors 1 and 2 (Fgfr1 and Fgfr2) are both express
39 llar development are primarily transduced by FGF receptors 1 and 2.
40                                              FGF receptors 1, 2, and 3 (Fgfrs) are expressed in the e
41 eceptors 1-3, PDGF receptors alpha and beta, FGF receptors 1-3, and Src and Abl kinases, which are al
42  activation of the fibroblast growth factor (FGF) receptor 1 (FGFR1) are a feature of stem cell leuke
43  (BMP) receptor or fibroblast growth factor (FGF) receptor 1, we demonstrate that the BMP and FGF sig
44  or intra-DMS blockade of the FGF2 receptor, FGF receptor-1 (FGFR1), suppresses alcohol consumption,
45 nity heparan sulfate co-receptor and blocked FGF receptor-1 autophosphorylation and p42/44 MAP kinase
46  antithrombin blocked the formation of FGF-2-FGF receptor-1 ectodomain-heparin ternary complexes, and
47 in (FN), activates fibroblast growth factor (FGF) receptor-1 (FGFR1) independent of FGF ligand in liv
48 n of the catalytic tyrosine kinase domain of FGF-receptor-1 (FGFR1) is mediated by a sequential and p
49 r 2 (FGF-2) and its receptor tyrosine kinase FGF receptor 1c.
50         BetaKlotho physically interacts with FGF receptors 1c and 4, thereby increasing the ability o
51  SUM52, that exhibit amplified expression of FGF receptor 2 (FGFR2) and are dependent on continued FG
52 on Cre-mediated recombination to investigate FGF receptor 2 (Fgfr2) function in the postnatal mammary
53                                              FGF receptor 2 (FGFR2) has a significant role in the pro
54           Conditionally deleting one copy of FGF receptor 2 (FGFR2) in adult mouse airway basal cells
55 n fibroblast growth factor 10 (FGF10) and in FGF receptor 2 (FGFR2) in LADD syndrome.
56                     Furthermore, deletion of Fgf receptor 2 (Fgfr2) in the epithelium also leads to s
57 mb development, we conditionally inactivated fgf receptor 2 (Fgfr2) in the mouse AER to terminate all
58 st on the endothelium, and downregulation of FGF receptor 2 (FGFR2) on PMNs rescued host defense in t
59                       Aberrant activation of FGF receptor 2 (FGFR2) signaling, through overexpression
60            BSS is caused by mutations in the FGF receptor 2 (FGFR2), but the molecular mechanisms tha
61 ere, we present the crystal structure of the FGF receptor 2 kinases caught in the act of trans-phosph
62 fgf8 (fibroblast growth factor 8) and fgfr2 (fgf receptor 2) transcripts.
63 dy brings up the intriguing possibility that FGF receptor 2, in the oligodendrocyte/myelin compartmen
64 nockdown changes the alternative splicing of FGF receptor-2 (FGFR2) transcripts, altering the incorpo
65 hed, and fibroblast growth factor 10 (FGF10)/FGF receptor 2b (FGFR2b) signaling directly regulates th
66  revealed that the proximal tubule expresses FGF receptor 3 (FGFR3) but not FGFR1, FGFR2, or FGFR4.
67                Gain-of-function mutations in FGF receptor 3 (FGFR3) have been implicated in severe sk
68                                              FGF receptor 3 (FGFR3) is activated by mutation or over-
69                            Overexpression of FGF receptor 3 (FGFR3) is implicated in the development
70 verexpression, or intensified signaling from FGF receptor 3, occurs in 70%-90% of these tumors in hum
71  on Sulf 1 and Sulf 2 expression, to control FGF receptor 3-IIIb-mediated astrocytic responses.
72 both short- and long-term assays through the FGF receptor 3/RAS/c-RAF/mitogen-activated protein kinas
73 ating mutations in fibroblast growth factor (FGF) receptor 3 and inactivating mutations in the NPR2 g
74  the expression of Fibroblast Growth Factor (FGF) Receptor 3 and responsiveness of progenitors to FGF
75    In contrast, the tyrosine kinase receptor FGF receptor-3 (FGFR3) and the transcription factor fork
76 lkaline phosphatase (Tnap) transcription via FGF receptor-3 (FGFR3) signaling, leading to inhibition
77 ism independent of adipogenesis and involves FGF receptor-3 (FGFR3), prostaglandin-E2 and interaction
78 e report that FGF19 and its cognate receptor FGF receptor 4 (FGFR4) are coexpressed in primary human
79 A stimulated tyrosine phosphorylation of the FGF receptor 4 (FGFR4) in hepatocytes.
80 nd gall bladder filling; FGF19 binds only to FGF receptor 4 (FGFR4), but its liver-specific activity
81 studies demonstrate that FGF signalling, via FGF receptor 4 (Fgfr4), mediates a signal-transduction p
82 corresponded with constitutive activation of FGF receptor 4 (FGFR4)-dependent ERK/AKT-p70S6K-S6 signa
83                      FGF19 uniquely binds to FGF receptor 4 (FGFR4).
84 kdown of SCUBE3 in C2C12 myoblasts inhibited FGF receptor 4 expression and FGF signaling, thus result
85 broblast growth factor (FGF)19 signaling via FGF receptor 4 for survival were more sensitive to trame
86 al were more sensitive to trametinib than to FGF receptor 4 inhibitors.
87                     Protein levels of FGF19, FGF receptor 4, FXR and short heterodimer partner were i
88  antagonizes transcription of the breathless FGF receptor, a known target of Trh in the tracheal syst
89                                              FGF receptor activation upregulates expression of these
90 ion as a co-factor permitting FGF21 mediated FGF receptor activation.
91 kinase-ERK signal transduction downstream of FGF receptor activation.
92 ha), a key link in fibroblast growth factor (FGF) receptor activation of ERK1/2.
93 ting up a gradient of CXCL12a, and trailing (FGF receptor active) cells moving actively by chemotaxis
94 nd link tissue subdivision (Wnt receptor and FGF receptor activity domains) to receptor-ligand parame
95                                The Heartless FGF receptor acts cell-autonomously in ensheathing glia
96                                   Activating FGF receptors acutely had an antidepressant-like effect
97 data that show that an SMC deletion of a pan-FGF receptor adaptor Frs2alpha (fibroblast growth factor
98 e demonstrate that skin hyperplasia requires FGF receptor adaptor protein Frs2alpha and tyrosine phos
99 t2 interacts specifically with the activated FGF receptor and is required for a rapid phase of recept
100  from fibroblast growth factor (FGF) via the FGF receptor and its effectors in the Ras-MAPK pathway.
101 led to autocrine activation of Stat3 via the FGF receptor and JAK kinases, and pharmacological inhibi
102 the ability of VE-cadherin to associate with FGF receptor and the density-enhanced phosphatase-1 (Dep
103 ERK, which is sensitive to dominant-negative FGF receptor and to the inhibitors SU5402 and U0126, and
104  isolated lamprey homologs of FGF3, FGF8 and FGF receptors and asked whether these functions are ance
105                                          The FGF receptors and co-receptors for these three FGF molec
106  Using mice with tissue-specific ablation of FGF receptors and FGF receptor substrate 2alpha (Frs2alp
107 ressed in response to Wnt signaling activate FGF receptors and initiate proto-neuromast formation.
108 , which, respectively, activate cell surface FGF receptors and intranuclear FGFR1, to determine the r
109                 This response is mediated by FGF receptors and involves the activation of IkappaBalph
110 expressed in thymic stromal cells along with FGF receptors and its obligate coreceptor, betaKlotho.
111 tion of Shh responses requires activation of FGF receptors and of ERK and JNK kinases, because it can
112 lying the control of transphosphorylation of FGF receptors and other receptor tyrosine kinases.
113 t physical interaction between the A(2A) and FGF receptors and the robust physiological consequences
114 r IHH-associated genes, including kal-1, the FGF receptor, and FGF.
115 tor cooperation between integrin beta(3) and FGF receptor, and triggered a downstream cascade includi
116 cient zebrafish embryos can be rescued by an FGF receptor antagonist SU5402.
117                                The action of FGF receptors appears to be through increasing self-rene
118 at some of the FGF ligands together with the FGF receptors are altered in individuals with affective
119 rs2alpha-Shp2 complex and its recruitment to FGF receptors are crucial for downstream ERK signaling i
120 g several FGF ligands and the four classical FGF receptors are detectable in the lens-forming ectoder
121  to induce diabetes remission and that brain FGF receptors are potential pharmacological targets for
122                                 We find that FGF receptors are required for neural stem-cell maintena
123 inases and nonraft fibroblast growth factor (FGF) receptors are implicated in cell adhesion molecule-
124 road evidence that fibroblast growth factor (FGF) receptors are important in prostate cancer initiati
125       Mutations in fibroblast growth factor (FGF) receptors are responsible for a variety of skeletal
126         Because small molecule inhibitors of Fgf-receptors are in human clinical trials, this suggest
127 eptor tyrosine kinases (RTKs), including the FGF receptor, are TRIAD1 substrates that are possibly re
128  receptor substrate 2alpha (FRS2alpha) is an FGF receptor-associated protein required for activation
129              The in vivo data, together with FGF receptor binding analysis, indicate that the in vivo
130 d embryos with FGF8b blocking antibody or an FGF receptor blocker rescues secondary heart field myoca
131 ished animal model of CKD, treatment with an FGF-receptor blocker attenuated LVH, although no change
132        Moreover, in older mice, an activated FGF receptor can rescue the age-related decline in neuro
133 nents of endocrine fibroblast growth factor (FGF) receptor complexes, as they are required for the hi
134 pertrophy of isolated rat cardiomyocytes via FGF receptor-dependent activation of the calcineurin-NFA
135  contribute to mesoderm heterogeneity via an FGF receptor-dependent positive feedback mechanism.
136                      Furthermore, SU5402, an FGF receptor-dependent protein kinase inhibitor, inhibit
137            Expression of a dominant-negative FGF receptor (DN-Fgfr1), treatment with SU5402 (a pharma
138                   The Caenorhabditis elegans FGF receptor, EGL-15, is alternatively-spliced to yield
139                        Two inhibitors of the Fgf receptor elicited similar phenotypes, suggesting tha
140 blocked by expression of a dominant-negative Fgf receptor, epicardial EMT and coronary neovasculariza
141                                              Fgf receptor/Erk signalling is known to be required for
142 arised primitive endoderm layer requires the Fgf receptor/Erk signalling pathway.
143 vestigate the regulation of renal Klotho and FGF receptor (FEFR)-1 in healthy and uremic rats induced
144                  We further demonstrate that Fgf receptor (Fgfr) 1 signaling within the developing se
145 -beta increased KL secretion and upregulated FGF receptor (FGFR) 1.
146 s renal phosphate reabsorption by activating FGF receptor (FGFR) 1c in a Klotho-dependent fashion.
147 th factor (FGF) 1 and FGF2 signaling through FGF receptor (FGFR) 1c.
148 e that directly targets cardiac myocytes via FGF receptor (FGFR) 4 thereby inducing hypertrophic myoc
149                            Inhibitors of the FGF receptor (Fgfr) and ERK pathways reversed the skewed
150 t a functional FGF19 receptor may consist of FGF receptor (FGFR) and heparan sulfate complexed with e
151 which is essential for the formation of FGF2/FGF receptor (FGFR) and VEGF(165)/VEGF receptor signalin
152 d activating binary complexes composed of an FGF receptor (FGFR) bound to either alpha-Klotho or beta
153  be hijacked by disease-causing mutations in FGF receptor (FGFR) during embryogenesis.
154                               We report high FGF receptor (FGFR) expression in 17.7% (11 of 62) of he
155  anterior neural plate via deletion of three FGF receptor (FGFR) genes.
156 or Nurr1 or expressing the dominant-negative FGF receptor (FGFR) identified orphan nuclear receptor N
157            We demonstrate that activation of Fgf receptor (Fgfr) induces intracellular Ras-MAPK, whic
158        This PDX model is highly sensitive to FGF receptor (FGFR) inhibition, and more so to combined
159     Finally, we examined anxiety behavior in FGF receptor (FGFR) KO mice; however, FGFR1, FGFR2, and
160 single-cell transcriptomics of wild-type and Fgf receptor (Fgfr) mutant embryos.
161 etic skeletal disorders caused by activating FGF receptor (FGFR) mutations.
162 g complex composed of alpha-Klotho (KLA) and FGF receptor (FGFR) resulting in kinase activation, regu
163 lectivity in their requirement for mediating FGF receptor (FGFR) signaling and activating downstream
164                  We investigated the role of FGF receptor (Fgfr) signaling in Schwann cells and the c
165                             Here we identify FGF receptor (FGFR) signalling as a critical regulator o
166 al activities by activation of transmembrane FGF receptor (FGFR) tyrosine kinases and their coupled i
167                                  Of the four FGF receptor (FGFR) tyrosine kinases, only FGFR4 is expr
168 indings indicate that CIMA-1 antagonizes the FGF receptor (FGFR), and does so most likely by inhibiti
169  multiprotein complex formation between FGF, FGF receptor (FGFR), and heparan sulfate proteoglycan on
170 (RTKs), such as EGF receptor (EGFR), ErbB-2, FGF receptor (FGFR), and many others, has been reported
171 Gs) via a ternary complex with FGF-2 and the FGF receptor (FGFR).
172 basic fibroblast growth factor 2 (FGF2b) and FGF receptor (FGFR)1 in LMC formation.
173       The migratory response was mediated by FGF receptors (FGFR) 1 and 3 and MAPK/ERK intracellular
174  a prototypical SH2 containing substrate, by FGF receptors (FGFR) entails formation of an allosteric
175 on, to act as coreceptors along with classic FGF receptors (FGFR) to mediate potent biologic activity
176                    Fibroblast growth factor (FGF) receptor (FGFR) substrate 2 (FRS2) is an adaptor pr
177                            Deletion of three FGF receptors (Fgfr1-3) early in lens development demons
178                                         Four FGF receptors (FGFR1-4) have been cloned and characteriz
179 tabolism in target organs through activating FGF receptors (FGFR1-4).
180 ll-surface receptor composed of one of three FGF receptors (FGFR1c, FGFR2c or FGFR3c) in complex with
181 ct isoforms of the fibroblast growth factor (FGF) receptor FGFR2-IIIb and FGFR2-IIIc varying their ex
182                               Among the four FGF receptors, FGFR2 showed two highly specific patterns
183                                  Of the four FGF receptors (FGFRs 1-4), FGFR1 and FGFR3 are strongly
184 tively spliced forms of four tyrosine kinase FGF receptors (FGFRs 1-4).
185 find that although both are able to activate FGF receptors (FGFRs) 1c, 2c, and 3c, only FGF19 activat
186                                      Whether FGF receptors (FGFRs) accomplish such varied tasks in pa
187 led that bone marrow stromal cells express 5 FGF receptors (FGFRs) among the 7 known FGFR subtypes.
188         Fibroblast growth factors (FGFs) and FGF receptors (FGFRs) are known for their potent effects
189                                          The FGF receptors (FGFRs) control a multitude of cellular pr
190 vels of fibroblast growth factors (FGFs) and FGF receptors (FGFRs) have been detected in various neur
191 F signaling, with only three ligands and two FGF receptors (FGFRs) identified.
192                             The functions of FGF receptors (FGFRs) in early development of the cerebr
193 role of fibroblast growth factors (FGFs) and FGF receptors (FGFRs) in establishing and maintaining co
194 pecific fibroblast growth factors (FGFs) and FGF receptors (FGFRs) in NSCLC cell lines.
195 roblast growth factors (FGFs) signal through FGF receptors (FGFRs) mediating a broad range of cellula
196  (mKL) that forms heteromeric complexes with FGF receptors (FGFRs) to initiate intracellular signalin
197 ctor (FGF) signaling through cross-talk with FGF receptors (FGFRs), but the mechanism underlying the
198 predominant effector pathway downstream from Fgf receptors (Fgfrs), but these receptors can also sign
199 e, we show that distinct sets of overlapping FGF receptors (FGFRs), FGFR2b and FGFR1b, mediate excita
200 -23 (FGF-23) activates complexes composed of FGF receptors (FGFRs), including FGFR1, and alpha-Klotho
201 n may not form stable ternary complexes with Fgf receptors (FgfRs), it acts together with and/or is n
202     Because FGF9 and FGF10 activate distinct FGF receptors (FGFRs), we hypothesized that they would c
203 nly known ligand that signals to mesenchymal FGF receptors (FGFRs).
204 g of FGF19, FGF21 and FGF23 to their cognate FGF receptors (FGFRs).
205 inal phosphotyrosine-binding domain (PTB) to FGF receptors (FGFRs).
206 efinitive endoderm through activation of the FGF receptors (FGFRs).
207 verexpress dominant-negative forms of Bmp or Fgf receptors following heat-shock induction.
208              Here we show, however, that the FGF receptors form dimers in the absence of ligand, and
209 al for lens fiber differentiation, different FGF receptors function redundantly.
210 re, we show that conditional deletion of the FGF receptor gene Fgfr1 abolishes FGF signaling in the m
211                                  Here, three FGF receptor genes are simultaneously deleted during cor
212               Although ligands that activate FGF receptors have antidepressant and anxiolytic effects
213       Multiple gain-of-function mutations in FGF receptors have been implicated in a variety of sever
214                    Fibroblast growth factor (Fgf) receptors have a recognized role in mammary ductal
215                                  Mutation of FGF receptor Heartless (Htl) has been shown to cause CVM
216                        Null mutations in the FGF receptor heartless (htl), or its ligands, caused sig
217 (FGF) 8/17/18 subfamily, are ligands for the FGF receptor Heartless (Htl).
218 monstrate that the Fibroblast growth factor (FGF) receptor Heartless autonomously controls astrocyte
219  genetically engineered a model of inducible FGF receptor (iFGFR) signaling in the context of the wel
220 modulatory coligand with FGF to activate the FGF receptor in an HS-dependent manner.
221 able of binding and activating their cognate FGF receptor in vitro and in living cells.
222  the observation that DSTYK colocalizes with FGF receptors in the ureteric bud and metanephric mesenc
223 Here, we found that transgenic inhibition of Fgf receptors in uninjured zebrafish caused severe atrop
224 tic astrocyte in vivo, identifies a role for Fgf receptors in vertebrate astrocytes and establishes z
225 urnover of surface fibroblast growth factor (FGF) receptor, increased extracellular signal-regulated
226 network by which activating mutations in the FGF receptor inhibit bone growth.
227        Conversely, miR-133 antagonism during Fgf receptor inhibition accelerated regeneration through
228 t FGF2-mediated resistance is interrupted by FGF receptor inhibition.
229 ion was blocked by Fibroblast growth factor (Fgf) receptor inhibition, high miR-133 levels were quick
230 e studies with a Mek inhibitor, U0126, and a Fgf receptor inhibitor, SU5402, indicate that the timing
231  cell development in a manner similar to the FGF receptor inhibitor.
232 arly stages of cochlear development using an FGF receptor inhibitor.
233 uced by 80% by the fibroblast growth factor (FGF) receptor inhibitor PD173074 and by 70% by the IKK i
234 DU 145 cells, treatment with a pharmacologic FGF-receptor inhibitor or a neutralizing anti-FGFR1 anti
235        ES cells lacking Fgf4 or treated with FGF receptor inhibitors resist neural and mesodermal ind
236 d VEGF/platelet-derived growth factor (PDGF)/FGF receptor inhibitors, paracrine ERK activation in fib
237 on principle in both endocrine and paracrine FGF receptor interaction and activation.
238                     Further understanding of FGF/receptor interactions may allow the development of e
239 sruption of matrix adhesion promotes uniform FGF receptor internalization and degradation while enhan
240 Here, we show that adhesion inhibits mitotic FGF receptor internalization, leading to receptor enrich
241                Therefore, while signaling by FGF receptors is essential for lens fiber differentiatio
242 n, and that combined inhibition of VEGF/PDGF/FGF receptors is sufficient to inhibit mitogenic signali
243  this case mediated by a transporter and the FGF receptor, is vital to preserve embryonically derived
244                   FGFR4 is the major hepatic FGF receptor isoform and is responsible for the hepatic
245             The identity and location of the FGF receptor isotypes that mediate these effects are unc
246                                              FGF-receptor kinase inhibitors blocked these effects.
247 2alpha (FRS2), an adaptor protein that links FGF receptor kinases to multiple signaling pathways, med
248                   Neuronal expression of the FGF receptor ligand Pyramus is also required for the gen
249 ressed genes, including multiple Wnt and ndk/FGF receptor-like (ndl/FGFRL) genes.
250 ns cell differentiation, it is unclear which FGF receptors mediate these processes during different s
251       Furthermore, through the activation of FGF receptor-mediated intracellular MAPK pathway, FGF16
252                                         This FGF receptor-mediated stimulation of mature oligodendroc
253 e found some directed dorsal migration in an FGF receptor mutant, which suggests that additional sign
254                                  Contrary to FGF receptor mutants that displayed loss of ERK signalin
255 y reported that the expression of activating FGF receptor mutations in osteoblasts downregulated the
256 fation-dependent FGF signaling mechanism via FGF receptors on astrocytes.
257  in the assembly of signaling complexes with FGF-receptors on the plasma membrane.
258 ing by expression of a constitutively active FGF receptor only partially rescued the lacrimal gland d
259 onditionally express an activated form of an FGF receptor or delete the FGF receptors that are expres
260 og or Dpp pathways, nor did Fas2 inhibit the FGF receptor or Torso, indicating specificity in the inh
261 402, or by activation of a dominant negative FGF receptor, or by activation of expression of the Wnt
262  activation of the fibroblast growth factor (FGF) receptor, phospholipase C (PLC), protein kinase C (
263 tral activation of fibroblast growth factor (FGF) receptors regulates peripheral glucose homeostasis
264 ction mutations in fibroblast growth factor (FGF) receptors result in chondrodysplasia and craniosyno
265                    Pharmacologic blockade of FGF receptors resulted in a comparable increase in plasm
266 reveal a previously unrecognized function of FGF receptor signaling in oligodendrocytes that contribu
267  levels of proteins known to be regulated by FGF receptor signaling, but proteins known to be importa
268                                              FGF receptor signaling, in turn, inhibits Wnt signaling.
269 on to CB1 cannabinoid receptor regulation of FGF receptor signaling.
270                                      We used FGF-receptor signaling to identify EGR1 as a locus that
271 elicited similar phenotypes, suggesting that Fgf receptor signalling promotes Erk-mediated polarisati
272 d by PD173074, a small molecule inhibitor of FGF receptor signalling.
273  the actions of FGF19 on target tissues, its FGF receptor specificity, and the contributions of other
274 introducing endothelial-specific deletion of FGF receptor substrate 2 alpha (Frs2a) in atheroscleroti
275 issue-specific ablation of FGF receptors and FGF receptor substrate 2alpha (Frs2alpha) in heart proge
276                                              FGF receptor substrate 2alpha (FRS2alpha) is an FGF rece
277                                              FGF receptor substrate 2alpha (FRS2alpha) is an FGFR int
278 expression, and decreased phosphorylation of FGF receptor substrate 2alpha, a major FGF-23 receptor s
279 bility of FGF23 to induce phosphorylation of FGF receptor substrate and ERK in various types of cells
280 ch, unlike other FGF peptides, activates all FGF receptor subtypes.
281  inhibitors of YAP (such as verteporfin) and FGF receptors (such as BGJ398) can provide a novel thera
282        A dominant-negative form of the Ciona FGF receptor suppresses the formation of polarized actin
283 ivated form of an FGF receptor or delete the FGF receptors that are expressed in these cells.
284 aptic SDC2 presents FGF22 to the presynaptic FGF receptor to promote presynaptic differentiation.
285 d 4, thereby increasing the ability of these FGF receptors to bind FGF21 and activate the MAP kinase
286 that CDC42 is involved in the trafficking of FGF receptors to the cell membrane to regulate epicardiu
287 onal ablation of this receptor-type, but not FGF receptor type 1 (FGFR1), resulted in attenuation of
288                           Here, we show that FGF receptor type 2 (FGFR2) is highly enriched at the pa
289 ritically important to identify the specific FGF receptor type and its downstream signaling molecules
290 activities by activating diverse isotypes of FGF receptor tyrosine kinases (FGFRs).
291 t into the signaling molecules downstream of FGF receptor tyrosine kinases in cardiac progenitors.
292 les that specifically inhibit GSK3, MEK, and FGF receptor tyrosine kinases.
293 ors associate with fibroblast growth factor (FGF) receptor tyrosine kinases (FGFRs) to enable signali
294 of VEGF, PDGF, and fibroblast growth factor (FGF) receptor tyrosine kinases.
295     Using a pharmacological inhibitor of the FGF receptor, we show that reducing FGF signalling parti
296 ural cell adhesion molecule (NCAM) activates FGF receptors, we asked whether peripherally administere
297 ctivation of brain fibroblast growth factor (FGF) receptors, we explored the antidiabetic efficacy of
298 ot targeted by Cre-mediated recombination of Fgf receptors, were also misplaced in FGFR DKO mice, pos
299 r tyrosine kinase receptors, such as EGF and FGF receptors, were not activated by GCs.
300 ted whether administering agents that act on FGF receptors would have antidepressant-like effects in

 
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