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1 inity signaling complexes with their cognate FGF receptor.
2 action between different FGF ligands and the FGF receptor.
3 aling through this pathway downstream of the FGF receptor.
4 dependent expression of the breathless (btl) FGF receptor.
5 ltikinase inhibitor that targets BCR-ABL and FGF receptor.
6 that Cubn is a novel, interspecies-conserved Fgf receptor.
7 e to their different binding affinities with FGF receptors.
8 ly sensitive to small molecule inhibitors of FGF receptors.
9 ble FGF traps or a dominant inhibitor of all FGF receptors.
10 d ability of FGF23 to signal via its cognate FGF receptors.
11 nductive activity due to higher affinity for Fgf receptors.
12 ished binding of a subset of FGF proteins to FGF receptors.
13 forms of the mutant but not of the wild-type FGF receptors.
14 at BMP signaling is required at the level of FGF receptors.
15 sine-kinase inhibitor that inhibits VEGF and FGF receptors.
16 We created two lines of mice lacking both FGF receptor 1 (Fgfr1) and Fgfr2 in oligodendrocyte-line
19 we show using signal transduction mutants of FGF receptor 1 (FGFR1) expressed in rat VSMC that the ad
24 e defect had been identified: a heterozygous FGF receptor 1 (FGFR1) mutation in pedigree 1 and a comp
25 nce suggests that bFGF selectively activates FGF receptor 1 (FGFR1) to exert degradative effects in b
28 tified SK1 as a target of the canonical FGF2/FGF receptor 1 activation pathway in endothelial cells a
30 functions by blocking FGF2 signaling through FGF receptor 1 and syndecan-4 and downstream effectors p
31 r, rPAI-1(23) blocked FGF2 signaling through FGF receptor 1 and syndecan-4, inhibiting cell migration
32 signaling in animal caps, did interact with Fgf receptor 1 in cultured cells and, according to conte
34 lt, 12 hits were identified including FGFR1 (FGF receptor 1), TrkB, and TrkC as well as components of
35 sumably mediated by activation of the FGFR1 (FGF receptor 1), which is expressed in mammalian brain m
37 mice had significantly reduced expression of FGF receptor 1, hypoxia-inducible factor-1alpha, vascula
41 activation of the fibroblast growth factor (FGF) receptor 1 (FGFR1) are a feature of stem cell leuke
42 (BMP) receptor or fibroblast growth factor (FGF) receptor 1, we demonstrate that the BMP and FGF sig
43 growth factor (bFGF) and its major receptor FGF receptor-1 (FGFR-1) play an important role in the de
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
51 on Cre-mediated recombination to investigate FGF receptor 2 (Fgfr2) function in the postnatal mammary
55 mb development, we conditionally inactivated fgf receptor 2 (Fgfr2) in the mouse AER to terminate all
56 st on the endothelium, and downregulation of FGF receptor 2 (FGFR2) on PMNs rescued host defense in t
60 ere, we present the crystal structure of the FGF receptor 2 kinases caught in the act of trans-phosph
62 dy brings up the intriguing possibility that FGF receptor 2, in the oligodendrocyte/myelin compartmen
63 utation (S252W) in fibroblast growth factor (FGF) receptor 2 (FGFR2), which leads to abnormal FGF/FGF
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 ion and differentiation by signaling through FGF receptor 3 (FGFR3) and to regulate osteogenesis by s
67 revealed that the proximal tubule expresses FGF receptor 3 (FGFR3) but not FGFR1, FGFR2, or FGFR4.
71 verexpression, or intensified signaling from FGF receptor 3, occurs in 70%-90% of these tumors in hum
74 both short- and long-term assays through the FGF receptor 3/RAS/c-RAF/mitogen-activated protein kinas
75 ating mutations in fibroblast growth factor (FGF) receptor 3 and inactivating mutations in the NPR2 g
76 the expression of Fibroblast Growth Factor (FGF) Receptor 3 and responsiveness of progenitors to FGF
77 In contrast, the tyrosine kinase receptor FGF receptor-3 (FGFR3) and the transcription factor fork
78 lkaline phosphatase (Tnap) transcription via FGF receptor-3 (FGFR3) signaling, leading to inhibition
79 e report that FGF19 and its cognate receptor FGF receptor 4 (FGFR4) are coexpressed in primary human
81 nd gall bladder filling; FGF19 binds only to FGF receptor 4 (FGFR4), but its liver-specific activity
82 studies demonstrate that FGF signalling, via FGF receptor 4 (Fgfr4), mediates a signal-transduction p
84 kdown of SCUBE3 in C2C12 myoblasts inhibited FGF receptor 4 expression and FGF signaling, thus result
86 antagonizes transcription of the breathless FGF receptor, a known target of Trh in the tracheal syst
90 ting up a gradient of CXCL12a, and trailing (FGF receptor active) cells moving actively by chemotaxis
91 the lead positions, whereas those with less FGF receptor activity assume subsidiary positions and fo
92 , we have generated transgenic fish in which Fgf receptor activity can be experimentally manipulated.
93 nd link tissue subdivision (Wnt receptor and FGF receptor activity domains) to receptor-ligand parame
94 tween cells such that those with the highest FGF receptor activity take the lead positions, whereas t
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 a region on FGF2 that binds heparin and the FGF receptor and is important in FGF2 central cavity for
100 t2 interacts specifically with the activated FGF receptor and is required for a rapid phase of recept
101 from fibroblast growth factor (FGF) via the FGF receptor and its effectors in the Ras-MAPK pathway.
102 led to autocrine activation of Stat3 via the FGF receptor and JAK kinases, and pharmacological inhibi
103 the ability of VE-cadherin to associate with FGF receptor and the density-enhanced phosphatase-1 (Dep
104 ERK, which is sensitive to dominant-negative FGF receptor and to the inhibitors SU5402 and U0126, and
106 isolated lamprey homologs of FGF3, FGF8 and FGF receptors and asked whether these functions are ance
108 Using mice with tissue-specific ablation of FGF receptors and FGF receptor substrate 2alpha (Frs2alp
109 ressed in response to Wnt signaling activate FGF receptors and initiate proto-neuromast formation.
110 , which, respectively, activate cell surface FGF receptors and intranuclear FGFR1, to determine the r
112 expressed in thymic stromal cells along with FGF receptors and its obligate coreceptor, betaKlotho.
113 tion of Shh responses requires activation of FGF receptors and of ERK and JNK kinases, because it can
115 t physical interaction between the A(2A) and FGF receptors and the robust physiological consequences
117 tor cooperation between integrin beta(3) and FGF receptor, and triggered a downstream cascade includi
120 at some of the FGF ligands together with the FGF receptors are altered in individuals with affective
121 rs2alpha-Shp2 complex and its recruitment to FGF receptors are crucial for downstream ERK signaling i
122 g several FGF ligands and the four classical FGF receptors are detectable in the lens-forming ectoder
123 to induce diabetes remission and that brain FGF receptors are potential pharmacological targets for
125 inases and nonraft fibroblast growth factor (FGF) receptors are implicated in cell adhesion molecule-
126 road evidence that fibroblast growth factor (FGF) receptors are important in prostate cancer initiati
129 receptor substrate 2alpha (FRS2alpha) is an FGF receptor-associated protein required for activation
132 d embryos with FGF8b blocking antibody or an FGF receptor blocker rescues secondary heart field myoca
133 ished animal model of CKD, treatment with an FGF-receptor blocker attenuated LVH, although no change
135 pertrophy of isolated rat cardiomyocytes via FGF receptor-dependent activation of the calcineurin-NFA
141 blocked by expression of a dominant-negative Fgf receptor, epicardial EMT and coronary neovasculariza
144 events are highly correlated with changes in FGF receptor expression from FGFR3 to FGFR2 as OL progen
145 ligand availability, coupled with changes in FGF receptor expression, yield a changing repertoire of
146 vestigate the regulation of renal Klotho and FGF receptor (FEFR)-1 in healthy and uremic rats induced
147 ) to sub-mesothelial mesenchyme through both FGF receptor (FGFR) 1 and FGFR2 to induce proliferation.
150 s renal phosphate reabsorption by activating FGF receptor (FGFR) 1c in a Klotho-dependent fashion.
152 and signals to an epithelial splice form of FGF receptor (FGFR) 2 to regulate epithelial budding.
153 e that directly targets cardiac myocytes via FGF receptor (FGFR) 4 thereby inducing hypertrophic myoc
155 t a functional FGF19 receptor may consist of FGF receptor (FGFR) and heparan sulfate complexed with e
156 which is essential for the formation of FGF2/FGF receptor (FGFR) and VEGF(165)/VEGF receptor signalin
159 or Nurr1 or expressing the dominant-negative FGF receptor (FGFR) identified orphan nuclear receptor N
161 Finally, we examined anxiety behavior in FGF receptor (FGFR) KO mice; however, FGFR1, FGFR2, and
164 lectivity in their requirement for mediating FGF receptor (FGFR) signaling and activating downstream
166 n Xenopus embryos, we found that both RA and FGF receptor (FGFR) signaling ventralize the eye, by exp
168 al activities by activation of transmembrane FGF receptor (FGFR) tyrosine kinases and their coupled i
170 fferent signaling pathways downstream of the FGF receptor (FGFR), and consequently different developm
171 indings indicate that CIMA-1 antagonizes the FGF receptor (FGFR), and does so most likely by inhibiti
172 multiprotein complex formation between FGF, FGF receptor (FGFR), and heparan sulfate proteoglycan on
173 (RTKs), such as EGF receptor (EGFR), ErbB-2, FGF receptor (FGFR), and many others, has been reported
177 a prototypical SH2 containing substrate, by FGF receptors (FGFR) entails formation of an allosteric
178 on, to act as coreceptors along with classic FGF receptors (FGFR) to mediate potent biologic activity
179 mpeting models for fibroblast growth factor (FGF) receptor (FGFR) dimerization have recently emerged
181 Here, we identify fibroblast growth factor (FGF) receptor (FGFR)-3 as a novel Prox1 target gene.
185 ll-surface receptor composed of one of three FGF receptors (FGFR1c, FGFR2c or FGFR3c) in complex with
186 ct isoforms of the fibroblast growth factor (FGF) receptor FGFR2-IIIb and FGFR2-IIIc varying their ex
189 find that although both are able to activate FGF receptors (FGFRs) 1c, 2c, and 3c, only FGF19 activat
191 led that bone marrow stromal cells express 5 FGF receptors (FGFRs) among the 7 known FGFR subtypes.
194 ibroblast growth factor (FGF) family and the FGF receptors (FGFRs) have been implicated in mediating
196 role of fibroblast growth factors (FGFs) and FGF receptors (FGFRs) in establishing and maintaining co
198 roblast growth factors (FGFs) signal through FGF receptors (FGFRs) mediating a broad range of cellula
199 (mKL) that forms heteromeric complexes with FGF receptors (FGFRs) to initiate intracellular signalin
200 ctor (FGF) signaling through cross-talk with FGF receptors (FGFRs), but the mechanism underlying the
201 predominant effector pathway downstream from Fgf receptors (Fgfrs), but these receptors can also sign
202 e, we show that distinct sets of overlapping FGF receptors (FGFRs), FGFR2b and FGFR1b, mediate excita
203 -23 (FGF-23) activates complexes composed of FGF receptors (FGFRs), including FGFR1, and alpha-Klotho
204 n may not form stable ternary complexes with Fgf receptors (FgfRs), it acts together with and/or is n
212 Targeted inhibition of Ets1/2 activity or FGF receptor function also blocks heart specification.
214 re, we show that conditional deletion of the FGF receptor gene Fgfr1 abolishes FGF signaling in the m
215 ns included novel hypomorphic alleles of the FGF receptor gene, breathless, and the ETS-domain transc
220 monstrate that the Fibroblast growth factor (FGF) receptor Heartless autonomously controls astrocyte
221 genetically engineered a model of inducible FGF receptor (iFGFR) signaling in the context of the wel
224 the observation that DSTYK colocalizes with FGF receptors in the ureteric bud and metanephric mesenc
225 Here, we found that transgenic inhibition of Fgf receptors in uninjured zebrafish caused severe atrop
226 urnover of surface fibroblast growth factor (FGF) receptor, increased extracellular signal-regulated
230 ion was blocked by Fibroblast growth factor (Fgf) receptor inhibition, high miR-133 levels were quick
231 e studies with a Mek inhibitor, U0126, and a Fgf receptor inhibitor, SU5402, indicate that the timing
234 uced by 80% by the fibroblast growth factor (FGF) receptor inhibitor PD173074 and by 70% by the IKK i
235 DU 145 cells, treatment with a pharmacologic FGF-receptor inhibitor or a neutralizing anti-FGFR1 anti
237 d VEGF/platelet-derived growth factor (PDGF)/FGF receptor inhibitors, paracrine ERK activation in fib
240 sruption of matrix adhesion promotes uniform FGF receptor internalization and degradation while enhan
241 Here, we show that adhesion inhibits mitotic FGF receptor internalization, leading to receptor enrich
243 n, and that combined inhibition of VEGF/PDGF/FGF receptors is sufficient to inhibit mitogenic signali
244 this case mediated by a transporter and the FGF receptor, is vital to preserve embryonically derived
248 2alpha (FRS2), an adaptor protein that links FGF receptor kinases to multiple signaling pathways, med
251 ns cell differentiation, it is unclear which FGF receptors mediate these processes during different s
254 e found some directed dorsal migration in an FGF receptor mutant, which suggests that additional sign
255 y reported that the expression of activating FGF receptor mutations in osteoblasts downregulated the
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 ction mutations in fibroblast growth factor (FGF) receptors result in chondrodysplasia and craniosyno
265 reveal a previously unrecognized function of FGF receptor signaling in oligodendrocytes that contribu
266 levels of proteins known to be regulated by FGF receptor signaling, but proteins known to be importa
270 elicited similar phenotypes, suggesting that Fgf receptor signalling promotes Erk-mediated polarisati
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
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 e are deficient in expression of hippocampal FGF receptor subtype 1 mRNA, most notably in the dentate
282 inhibitors of YAP (such as verteporfin) and FGF receptors (such as BGJ398) can provide a novel thera
285 aptic SDC2 presents FGF22 to the presynaptic FGF receptor to promote presynaptic differentiation.
286 d 4, thereby increasing the ability of these FGF receptors to bind FGF21 and activate the MAP kinase
287 that CDC42 is involved in the trafficking of FGF receptors to the cell membrane to regulate epicardiu
288 onal ablation of this receptor-type, but not FGF receptor type 1 (FGFR1), resulted in attenuation of
290 ritically important to identify the specific FGF receptor type and its downstream signaling molecules
292 t into the signaling molecules downstream of FGF receptor tyrosine kinases in cardiac progenitors.
294 ors associate with fibroblast growth factor (FGF) receptor tyrosine kinases (FGFRs) to enable signali
296 Using a pharmacological inhibitor of the FGF receptor, we show that reducing FGF signalling parti
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
300 ted whether administering agents that act on FGF receptors would have antidepressant-like effects in
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