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PMID |
Sentence |
1 |
8416827
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Single-stranded RNA probes for the three chicken fibroblast growth factor (FGF) receptors, cek-1, cek-2, and cek-3, in conjunction with in situ hybridization were used to characterize the distribution of the corresponding mRNAs in the developing chicken embryo.
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2 |
8416827
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Cek-1 was expressed diffusely in most tissues examined, whereas the expression of cek-2 and cek-3 was more restricted.
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3 |
8416827
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Single-stranded RNA probes for the three chicken fibroblast growth factor (FGF) receptors, cek-1, cek-2, and cek-3, in conjunction with in situ hybridization were used to characterize the distribution of the corresponding mRNAs in the developing chicken embryo.
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4 |
8416827
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Cek-1 was expressed diffusely in most tissues examined, whereas the expression of cek-2 and cek-3 was more restricted.
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5 |
9716527
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FGFR-3 and FGFR-4 function cooperatively to direct alveogenesis in the murine lung.
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6 |
9716527
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An examination of fgf receptor gene expression indicated that all four receptors (fgfr-1 to fgfr-4) are expressed in postnatal lungs at varying levels.
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7 |
9716527
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However, mice doubly homozygous for disruptions of the fgfr-3 and fgfr-4 genes display novel phenotypes not present in either single mutant, which include pronounced dwarfism and lung abnormalities.
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8 |
9716527
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Lungs of fgfr-3(-/-)fgfr-4(-/- )animals, which are normal at birth, are completely blocked in alveogenesis and do not form secondary septae to delimit alveoli.
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9 |
9716527
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These data revealed a cooperative function of FGFR-3 and FGFR-4 to promote the formation of alveoli during postnatal lung development.
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10 |
9716527
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FGFR-3 and FGFR-4 function cooperatively to direct alveogenesis in the murine lung.
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11 |
9716527
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An examination of fgf receptor gene expression indicated that all four receptors (fgfr-1 to fgfr-4) are expressed in postnatal lungs at varying levels.
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12 |
9716527
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However, mice doubly homozygous for disruptions of the fgfr-3 and fgfr-4 genes display novel phenotypes not present in either single mutant, which include pronounced dwarfism and lung abnormalities.
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13 |
9716527
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Lungs of fgfr-3(-/-)fgfr-4(-/- )animals, which are normal at birth, are completely blocked in alveogenesis and do not form secondary septae to delimit alveoli.
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14 |
9716527
|
These data revealed a cooperative function of FGFR-3 and FGFR-4 to promote the formation of alveoli during postnatal lung development.
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15 |
9716527
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FGFR-3 and FGFR-4 function cooperatively to direct alveogenesis in the murine lung.
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16 |
9716527
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An examination of fgf receptor gene expression indicated that all four receptors (fgfr-1 to fgfr-4) are expressed in postnatal lungs at varying levels.
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17 |
9716527
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However, mice doubly homozygous for disruptions of the fgfr-3 and fgfr-4 genes display novel phenotypes not present in either single mutant, which include pronounced dwarfism and lung abnormalities.
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18 |
9716527
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Lungs of fgfr-3(-/-)fgfr-4(-/- )animals, which are normal at birth, are completely blocked in alveogenesis and do not form secondary septae to delimit alveoli.
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19 |
9716527
|
These data revealed a cooperative function of FGFR-3 and FGFR-4 to promote the formation of alveoli during postnatal lung development.
|
20 |
9716527
|
FGFR-3 and FGFR-4 function cooperatively to direct alveogenesis in the murine lung.
|
21 |
9716527
|
An examination of fgf receptor gene expression indicated that all four receptors (fgfr-1 to fgfr-4) are expressed in postnatal lungs at varying levels.
|
22 |
9716527
|
However, mice doubly homozygous for disruptions of the fgfr-3 and fgfr-4 genes display novel phenotypes not present in either single mutant, which include pronounced dwarfism and lung abnormalities.
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23 |
9716527
|
Lungs of fgfr-3(-/-)fgfr-4(-/- )animals, which are normal at birth, are completely blocked in alveogenesis and do not form secondary septae to delimit alveoli.
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24 |
9716527
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These data revealed a cooperative function of FGFR-3 and FGFR-4 to promote the formation of alveoli during postnatal lung development.
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25 |
9846883
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AGE-binding receptors are: scavenger receptors types I and II, the receptor for advanced glycation endproducts (RAGE), oligosaccharyl transferase-48 (OST-48, AGE-R1), 80K-H phosphoprotein (AGE-R2) and galectin-3 (AGE-R3).
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26 |
9846883
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Scavenger receptors have only been shown to bind proteins modified by AGE to a much higher extent than found in vivo. 80K-H phosphoprotein is involved in FGFR3 signal transduction to MAP kinase, and may be involved in AGE-receptor signal transduction.
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27 |
10861287
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Increased expression of PATCHED: (PTC:) was observed, independent of unaltered expression of parathyroid hormone-related peptide (PTHrP) receptor and Indian Hedgehog (IHH:), suggesting a new regulatory role for Fgfr3 in embryos.
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28 |
11181569
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A Ser(365)-->Cys mutation of fibroblast growth factor receptor 3 in mouse downregulates Ihh/PTHrP signals and causes severe achondroplasia.
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29 |
11181569
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Missense mutations in fibroblast growth factor receptor 3 (FGFR3) result in several types of human skeletal dysplasia, including the neonatally lethal dwarfism known as thanatophoric dysplasia.
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30 |
11181569
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The receptor-activating mutation also resulted in downregulation of expression of the Indian hedgehog (IHH) and parathyroid hormone-related protein (PTHrP) receptor genes, both of which are important for bone growth.
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31 |
11181569
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Consistent with the in vivo observations, FGF2 inhibited bone growth in culture and induced downregulation of IHH and PTHrP receptor gene expression.
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32 |
11181569
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Furthermore, PTHrP partially reversed the inhibition of long bone growth caused by activation of FGFR3; however, it impaired the differentiation of chondrocytes in an FGFR3-independent manner.
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33 |
11181569
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A Ser(365)-->Cys mutation of fibroblast growth factor receptor 3 in mouse downregulates Ihh/PTHrP signals and causes severe achondroplasia.
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34 |
11181569
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Missense mutations in fibroblast growth factor receptor 3 (FGFR3) result in several types of human skeletal dysplasia, including the neonatally lethal dwarfism known as thanatophoric dysplasia.
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35 |
11181569
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The receptor-activating mutation also resulted in downregulation of expression of the Indian hedgehog (IHH) and parathyroid hormone-related protein (PTHrP) receptor genes, both of which are important for bone growth.
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36 |
11181569
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Consistent with the in vivo observations, FGF2 inhibited bone growth in culture and induced downregulation of IHH and PTHrP receptor gene expression.
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37 |
11181569
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Furthermore, PTHrP partially reversed the inhibition of long bone growth caused by activation of FGFR3; however, it impaired the differentiation of chondrocytes in an FGFR3-independent manner.
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38 |
11181569
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A Ser(365)-->Cys mutation of fibroblast growth factor receptor 3 in mouse downregulates Ihh/PTHrP signals and causes severe achondroplasia.
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39 |
11181569
|
Missense mutations in fibroblast growth factor receptor 3 (FGFR3) result in several types of human skeletal dysplasia, including the neonatally lethal dwarfism known as thanatophoric dysplasia.
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40 |
11181569
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The receptor-activating mutation also resulted in downregulation of expression of the Indian hedgehog (IHH) and parathyroid hormone-related protein (PTHrP) receptor genes, both of which are important for bone growth.
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41 |
11181569
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Consistent with the in vivo observations, FGF2 inhibited bone growth in culture and induced downregulation of IHH and PTHrP receptor gene expression.
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42 |
11181569
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Furthermore, PTHrP partially reversed the inhibition of long bone growth caused by activation of FGFR3; however, it impaired the differentiation of chondrocytes in an FGFR3-independent manner.
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43 |
12384452
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Short-term insulin treatment and aortic expressions of IGF-1 receptor and VEGF mRNA in diabetic rats.
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44 |
12384452
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Aortas from diabetic rats, but not those from insulin-treated diabetic rats, showed impaired endothelium-dependent relaxation in response to ACh (vs. untreated controls).
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45 |
12384452
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In diabetics, insulin treatment significantly increased the aortic expressions of endothelial nitric oxide synthase (eNOS) mRNA and VEGF mRNA.
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46 |
12384452
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The expression of IGF-1 mRNA was unaffected by diabetes or by insulin treatment.
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47 |
12384452
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In contrast, the mRNA for the aortic IGF-1 receptor was increased in diabetics and further increased in insulin-treated diabetics.
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48 |
12384452
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These results suggest that in STZ-diabetic rats, short-term insulin treatment can ameliorate endothelial dysfunction by inducing overexpression of eNOS and/or VEGF mRNAs possibly via IGF-1 receptors.
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49 |
12784193
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As the clinical and radiographic features suggested the diagnosis of a skeletal dysplasia, a DNA sequence analysis of the fibroblast growth factor receptor 3 gene on chromosome 4 p16.3 was performed, which identified the missense mutation C1620 G in the tyrosine kinase domain resulting in an Asn540Lys substitution.
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50 |
12784193
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We want to emphasise that in children with normal serum IGF-I and IGFBP-3 levels accurate measurements of body proportions and skeletal radiographs in disproportionate cases are more important than reiterative GH stimulation tests, which prepubertally and in the early phase of puberty often show subnormal responses.
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51 |
16082703
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Although 4p was significantly deleted on Giemsa banding, the 4p junction was distal to the WHS and FGFR3 but proximal to the D4S3360 marker.
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52 |
17192470
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In vitro studies showed that FGF9 is a very potent ligand for FGFR3 and activates extracellular signal-related kinases (ERKs) in pancreatic cell lines.
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53 |
18225590
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The expression of EGFR, erbB2, erbB3, FGFR-2, FGFR-3, c-myc, N-ras, ets-1, H-ras, c-fos and c-jun, the tumor suppressor genes p53 and p16, apoptosis markers Bax and Bcl-2, and the cell proliferation marker Ki-67 in the sequential stages of rat oral oncogenesis was investigated.
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54 |
18225590
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Diabetes seems to promote the activation of the Ras/Raf/MAPK signal transduction pathway mainly by induction of erbB2 and erbB3 receptors, leading to increased cell proliferation, while there was no difference in apoptosis levels during oncogenesis.
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55 |
19595708
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More surprisingly, the maximum vasorelaxation induced by exenatide (without Intralipid was only 3+/-2%, compared to the 23+/-4%, 38+/-4%, 79+/-3% and 97+/-4% relaxations induced by GLP-1, GLP-1 (9-36), ACh and SNP, respectively.
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56 |
19595708
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This unexpected finding prompted us to ascertain that the exenatide preparation was biologically active, and both exenatide (10(-11) mol/l) and GLP-1 (10(-9) mol/l) significantly increased insulin secretion in pancreatic beta-cells from ob/ob mice in vitro.
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57 |
20154258
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Prostacyclin was the predominant prostaglandin produced by ACh-stimulated CCAs, with greater than twofold more prostacyclin released from SHR versus WKY rats, and its production was unaffected by ROCK inhibition.
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58 |
20154258
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Augmentation of chemical superoxide quenching with tiron or inhibition of the NADPH oxidase-derived superoxide-producing pathway with apocynin reduced ACh-stimulated contractile activity in SHR more than in WKY rats, whereas the SOD mimetic tempol amplified the response.
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59 |
23262134
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Vascular contractions to phenylephrine and relaxation to ACh were assessed in aortas obtained from healthy WT and GDF15 KO mice.
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60 |
23262134
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Phenylephrine-induced contractions and ACh-mediated relaxations were similar in WT and GDF15 KO mice.
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61 |
23262134
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In cultured endothelial cells, GDF15 pretreatment caused a dissociation between caveolin-1 and endothelial NO synthase.
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62 |
23262134
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Vascular contractions to phenylephrine and relaxation to ACh were assessed in aortas obtained from healthy WT and GDF15 KO mice.
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63 |
23262134
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Phenylephrine-induced contractions and ACh-mediated relaxations were similar in WT and GDF15 KO mice.
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64 |
23262134
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In cultured endothelial cells, GDF15 pretreatment caused a dissociation between caveolin-1 and endothelial NO synthase.
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65 |
23918206
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Secretoneurin shows positive effects on in vitro angiogenesis, proliferation and apoptosis of these cells in a basic fibroblast growth factor dependent manner.
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66 |
23918206
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A small molecular weight inhibitor revealed fibroblast growth factor receptor 3 as the main receptor for secretoneurin mediated effects.
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67 |
23918206
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Additionally, we could identify heparan-sulfates as important co-factor of secretoneurin induced binding of basic fibroblast growth factor to human dermal endothelial cells.
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