Littérature scientifique sur le sujet « BFGF receptor »
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Articles de revues sur le sujet "BFGF receptor"
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Moscatelli, D., et N. Quarto. « Transformation of NIH 3T3 cells with basic fibroblast growth factor or the hst/K-fgf oncogene causes downregulation of the fibroblast growth factor receptor : reversal of morphological transformation and restoration of receptor number by suramin. » Journal of Cell Biology 109, no 5 (1 novembre 1989) : 2519–27. http://dx.doi.org/10.1083/jcb.109.5.2519.
Texte intégralRésumé :
When NIH 3T3 cells were transfected with the cDNA for basic fibroblast growth factor (bFGF), most cells displayed a transformed phenotype. Acquisition of a transformed phenotype was correlated with the expression of high levels of bFGF (Quarto et al., 1989). Cells that had been transformed as a result of transfection with bFGF cDNA had a decreased capacity to bind 125I-bFGF to high affinity receptors. NIH 3T3 cells transfected with bFGF cDNA that expressed lower levels of bFGF were not transformed and had a normal number of bFGF receptors. NIH 3T3 cells transfected with the hst/Kfgf oncogene, which encodes a secreted molecule with 45% homology to bFGF, also displayed a transformed phenotype and decreased numbers of bFGF receptors. However, NIH 3T3 cells transfected with the H-ras oncogene were transformed but had a normal number of bFGF receptors. Thus, transformation by bFGF-like molecules resulted in downregulation of bFGF receptors. Receptor number was not affected by cell density for both parental NIH 3T3 cells and transformed cells. In the cells transfected with bFGF cDNA that were not transformed, the receptors could be downregulated in response to exogenous bFGF. Conditioned medium from transformed transfected cells contained sufficient quantities of bFGF to downregulate bFGF receptors on parental NIH 3T3 cells. Thus, the downregulation of bFGF receptors seemed related to the presence of bFGF in an extracytoplasmic compartment. Treatment of the transformed transfected NIH 3T3 cells with suramin, which blocks the interaction of bFGF with its receptor, reversed the morphological transformation and restored receptors almost to normal numbers. These results demonstrate that in these cells bFGF transforms cells by interacting with its receptor and that bFGF and hst/K-fgf may use the same receptor.
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Bikfalvi, A., S. Klein, G. Pintucci, N. Quarto, P. Mignatti et D. B. Rifkin. « Differential modulation of cell phenotype by different molecular weight forms of basic fibroblast growth factor : possible intracellular signaling by the high molecular weight forms. » Journal of Cell Biology 129, no 1 (1 avril 1995) : 233–43. http://dx.doi.org/10.1083/jcb.129.1.233.
Texte intégralRésumé :
To study possible functional differences of the 18-kD and high molecular weight forms of basic fibroblast growth factor (bFGF), we have examined the effect of endogenous production of different bFGF forms on the phenotype of NIH 3T3 cells. Cells transfected with cDNAs coding for either 18-kD bFGF (18-kD bFGF) or all four molecular forms (18, 22, 22.5, 24 kD; wild type [WT] bFGF) exhibit increased migration and decreased FGF receptor number compared to parental cells. However, migration and FGF receptor number of cells transfected with a cDNA coding only for high molecular weight bFGF (22, 22.5, and 24 kD; HMW bFGF) were similar to that of parental cells transfected with vector alone. Cells expressing HMW, 18 kD, or WT bFGF grew to high saturation densities in 10% serum. However, only cells expressing HMW or WT bFGF grew in low serum. Cell surface or metabolic labeling of the different cell types followed by immunoprecipitation with anti-bFGF antibody showed primarily cell surface-associated 18-kD bFGF. In addition, when cells expressing exclusively HMW bFGF were transfected with a cDNA coding for 18-kD bFGF, migration was increased, bFGF receptors were down-regulated, and 18-kD bFGF was found on the cell surface. Cells expressing 18-kD bFGF transfected with a cDNA encoding FGF receptor-2 lacking the COOH-terminal domain (dominant negative bFGF receptor) exhibited a flat morphology and decreases in migration and saturation density. Cells expressing HMW bFGF transfected with the dominant negative bFGF receptor continued to grow to a high saturation density, proliferated in low serum, and exhibited no morphological changes. These results indicate that increased cell migration and FGF receptor down-regulation are mediated by the extracellular interaction of 18-kD bFGF with its cell surface receptor. Growth in low serum may be stimulated by the intracellular action of HMW bFGF through mechanisms independent of the presence of a cell surface receptor. Thus, the different molecular forms of bFGF may act through distinct but convergent pathways.
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Miyaji, Katsuya, Eiichi Tani, Atsuhisa Nakano, Hideyasu Ikemoto et Keizo Kaba. « Inhibition by 5′-methylthioadenosine of cell growth and tyrosine kinase activity stimulated by fibroblast growth factor receptor in human gliomas ». Journal of Neurosurgery 83, no 4 (octobre 1995) : 690–97. http://dx.doi.org/10.3171/jns.1995.83.4.0690.
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✓ Stimulation of three human glioma cell lines with basic fibroblast growth factor (bFGF) led to the enhancement of cell growth and the rapid tyrosine phosphorylation of cellular proteins, including major substrates of 90 kD. A methyltransferase inhibitor, 5′-methylthioadenosine (MTA), inhibited dose dependently the bFGF-stimulated cell growth and protein tyrosine phosphorylation in glioma cells by blocking both receptor autophosphorylation and substrate phosphorylation, as shown by immunoblotting with antiphosphotyrosine antibodies and cross-linking bFGF to receptors. The antiproliferative activity of MTA correlated quantitatively with its potency as an inhibitor of bFGF-stimulated protein tyrosine kinase activity. The methyltransferase inhibitor MTA had no effect on either epidermal growth factor— or platelet-derived growth factor—stimulated protein tyrosine phosphorylation in glioma cells, but inhibited specifically bFGF-stimulated protein tyrosine kinase activity. The concentration of MTA required for inhibition of protein methylation correlated well with the concentration required for inhibition of bFGF-stimulated cell growth and protein tyrosine phosphorylation. Because MTA had no effect on numbers and dissociation constants of high- and low-affinity bFGF receptors, the inhibition of bFGF-stimulated bFGF receptor tyrosine kinase activity is not likely to be the result of a reduction in bFGF receptor and bFGF binding capacity. In fact, MTA delayed and reduced the internalization and nuclear translocation of bFGF, and the internalized bFGF was submitted to a limited proteolysis that converted it to lower molecular peptides whose presence remained for at least 22 hours. The effect of MTA on bFGF-stimulated tyrosine phosphorylation was immediate and readily reversible.
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Reiland, J., et A. C. Rapraeger. « Heparan sulfate proteoglycan and FGF receptor target basic FGF to different intracellular destinations ». Journal of Cell Science 105, no 4 (1 août 1993) : 1085–93. http://dx.doi.org/10.1242/jcs.105.4.1085.
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Basic FGF is a prototype of a family of heparin binding growth factors that regulate a variety of cellular responses including cell growth, morphogenesis and differentiation. At least two families of receptors bind bFGF and could mediate its response: (1) tyrosine kinase-containing FGF receptors, designated FGFR-1 to FGFR-4, and (2) heparan sulfate proteoglycans that bind bFGF through their heparan sulfate chains. Both are known to undergo internalization and thus bFGF bound to the different receptors may be internalized via more than one pathway. It is not known whether the intracellular fate of bFGF differs depending upon which receptor binds it at the cell surface. To investigate the respective roles of these receptors in the intracellular targeting of bFGF, we utilized NMuMG cells that bind and internalize bFGF through their heparan sulfate proteoglycans, but do not express detectable levels of FGFRs nor respond to bFGF. Basic FGF conjugated to saporin (bFGF-saporin) was used as a probe to study targeting of bFGF by the different receptors. Saporin is a cytotoxin that has no effect on cells if added exogenously. However, it kills cells if it gains access to the cytoplasm. The NMuMG cells internalize bFGF-saporin but are not killed. Transfecting these cells with FGFR-1 results in bFGF-responsive cells, which bind and internalize bFGF through FGFR-1, and are killed. Removing the heparan sulfate from these cells eliminates killing by bFGF-saporin.(ABSTRACT TRUNCATED AT 250 WORDS)
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Liuzzo, JP, et D. Moscatelli. « Human leukemia cell lines bind basic fibroblast growth factor (FGF) on FGF receptors and heparan sulfates : downmodulation of FGF receptors by phorbol ester ». Blood 87, no 1 (1 janvier 1996) : 245–55. http://dx.doi.org/10.1182/blood.v87.1.245.245.
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Abstract Basic fibroblast growth factor (bFGF) has been identified as an important cytokine for blood cells. To determine whether hematopoietic cells have receptors that recognize bFGF, the ability of human leukemia cell lines to bind 125I-bFGF was investigated. Specific bFGF-binding sites were identified on K562 and HL60 cells, but not on U937 cells. DAMI cells bound low amounts of 125I-bFGF specifically. Binding of 125I- bFGF to K562 cell surfaces was reduced in a dose-dependent manner by unlabeled bFGF or by heparin. Scatchard analysis of binding to K562 cells revealed two classes of binding sites: 1,650 high affinity binding sites per cell with a dissociation constant (kd) of 192 pmol/L, and 36,600 low affinity sites per cell with a kd of 9.3 nmol/L. Chemical crosslinking experiments with K562, HL60, and DAMI cells revealed receptor-growth factor complexes with molecular masses of 140 to 160 kD, similar in size to complexes formed by known receptor species. Binding of 125I-bFGF to K562 cells was sensitive to heparinase treatment but not to chondroitinase treatment, suggesting that heparan sulfate proteoglycans (HSPGs) may be responsible for the low affinity binding sites. To further investigate whether K562 cells make HSPG, the incorporation of 35SO4 into proteoglycans was assessed. Metabolically labeled cell-surface proteoglycans with molecular masses of 180 to 300 kD were identified in K562 cells. These proteoglycans were sensitive to heparinase, demonstrating that K562 cells synthesize bFGF-binding HSPG. Treatment of K562 cells with phorbol-12-myristate-13-acetate (PMA) caused a loss of bFGF-binding capacity. This decreased binding capacity reflected a rapid loss of high affinity receptors. The ability to form bFGF-receptor complexes decreased by 65% to 70% within 1 hour and declined continuously thereafter. The decrease in binding of bFGF was not due to an autocrine downregulation of bFGF receptors, because there was no increase in bFGF after PMA treatment as detected by Western blotting, and suramin, which blocks bFGF binding to receptors, did not prevent the loss of receptors after exposure to PMA. In addition, inhibitors of either protein synthesis or protease activity did not prevent the loss of bFGF receptors in PMA-treated cells. In summary, this work demonstrates that leukemia cell lines have receptors that specifically bind bFGF and supports the hypothesis that bFGF acts directly on certain blood cells to stimulate their proliferation.
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Liuzzo, JP, et D. Moscatelli. « Human leukemia cell lines bind basic fibroblast growth factor (FGF) on FGF receptors and heparan sulfates : downmodulation of FGF receptors by phorbol ester ». Blood 87, no 1 (1 janvier 1996) : 245–55. http://dx.doi.org/10.1182/blood.v87.1.245.bloodjournal871245.
Texte intégralRésumé :
Basic fibroblast growth factor (bFGF) has been identified as an important cytokine for blood cells. To determine whether hematopoietic cells have receptors that recognize bFGF, the ability of human leukemia cell lines to bind 125I-bFGF was investigated. Specific bFGF-binding sites were identified on K562 and HL60 cells, but not on U937 cells. DAMI cells bound low amounts of 125I-bFGF specifically. Binding of 125I- bFGF to K562 cell surfaces was reduced in a dose-dependent manner by unlabeled bFGF or by heparin. Scatchard analysis of binding to K562 cells revealed two classes of binding sites: 1,650 high affinity binding sites per cell with a dissociation constant (kd) of 192 pmol/L, and 36,600 low affinity sites per cell with a kd of 9.3 nmol/L. Chemical crosslinking experiments with K562, HL60, and DAMI cells revealed receptor-growth factor complexes with molecular masses of 140 to 160 kD, similar in size to complexes formed by known receptor species. Binding of 125I-bFGF to K562 cells was sensitive to heparinase treatment but not to chondroitinase treatment, suggesting that heparan sulfate proteoglycans (HSPGs) may be responsible for the low affinity binding sites. To further investigate whether K562 cells make HSPG, the incorporation of 35SO4 into proteoglycans was assessed. Metabolically labeled cell-surface proteoglycans with molecular masses of 180 to 300 kD were identified in K562 cells. These proteoglycans were sensitive to heparinase, demonstrating that K562 cells synthesize bFGF-binding HSPG. Treatment of K562 cells with phorbol-12-myristate-13-acetate (PMA) caused a loss of bFGF-binding capacity. This decreased binding capacity reflected a rapid loss of high affinity receptors. The ability to form bFGF-receptor complexes decreased by 65% to 70% within 1 hour and declined continuously thereafter. The decrease in binding of bFGF was not due to an autocrine downregulation of bFGF receptors, because there was no increase in bFGF after PMA treatment as detected by Western blotting, and suramin, which blocks bFGF binding to receptors, did not prevent the loss of receptors after exposure to PMA. In addition, inhibitors of either protein synthesis or protease activity did not prevent the loss of bFGF receptors in PMA-treated cells. In summary, this work demonstrates that leukemia cell lines have receptors that specifically bind bFGF and supports the hypothesis that bFGF acts directly on certain blood cells to stimulate their proliferation.
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Steinfeld, R., H. Van Den Berghe et G. David. « Stimulation of fibroblast growth factor receptor-1 occupancy and signaling by cell surface-associated syndecans and glypican. » Journal of Cell Biology 133, no 2 (15 avril 1996) : 405–16. http://dx.doi.org/10.1083/jcb.133.2.405.
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The formation of distinctive basic FGF-heparan sulfate complexes is essential for the binding of bFGF to its cognate receptor. In previous experiments, cell-surface heparan sulfate proteoglycans extracted from human lung fibroblasts could not be shown to promote high affinity binding of bFGF when added to heparan sulfate-deficient cells that express FGF receptor-1 (FGFR1) (Aviezer, D., D. Hecht, M. Safran, M. Eisinger, G. David, and A. Yayon. 1994. Cell 79:1005-1013). In alternative tests to establish whether cell-surface proteoglycans can support the formation of the required complexes, K562 cells were first transfected with the IIIc splice variant of FGFR1 and then transfected with constructs coding for either syndecan-1, syndecan-2, syndecan-4 or glypican, or with an antisense syndecan-4 construct. Cells cotransfected with receptor and proteoglycan showed a two- to three- fold increase in neutral salt-resistant specific 125I-bFGF binding in comparison to cells transfected with only receptor or cells cotransfected with receptor and anti-syndecan-4. Exogenous heparin enhanced the specific binding and affinity cross-linking of 125I-bFGF to FGFR1 in receptor transfectants that were not cotransfected with proteoglycan, but had no effect on this binding and decreased the yield of bFGFR cross-links in cells that were cotransfected with proteoglycan. Receptor-transfectant cells showed a decrease in glycophorin A expression when exposed to bFGF. This suppression was dose-dependent and obtained at significantly lower concentrations of bFGF in proteoglycan-cotransfected cells. Finally, complementary cell-free binding assays indicated that the affinity of 125I-bFGF for an immobilized FGFR1 ectodomain was increased threefold when the syndecan-4 ectodomain was coimmobilized with receptor. Equimolar amounts of soluble syndecan-4 ectodomain, in contrast, had no effect on this binding. We conclude that, at least in K562 cells, syndecans and glypican can support bFGF-FGFR1 interactions and signaling, and that cell-surface association may augment their effectiveness.
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Liu, L., K. B. Pasumarthi, R. R. Padua, H. Massaeli, R. R. Fandrich, G. N. Pierce, P. A. Cattini et E. Kardami. « Adult cardiomyocytes express functional high-affinity receptors for basic fibroblast growth factor ». American Journal of Physiology-Heart and Circulatory Physiology 268, no 5 (1 mai 1995) : H1927—H1938. http://dx.doi.org/10.1152/ajpheart.1995.268.5.h1927.
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As a first step in addressing the question of function for basic fibroblast growth factor (bFGF) in the adult myocardium, expression of bFGF receptors by adult rat myocytes was investigated. Cross-linking of 125I-labeled bFGF to purified sarcolemmal vesicles from adult hearts indicated specific binding to 90- to 104-kDa proteins, whereas equilibrium binding studies revealed the presence of "low"-affinity (1 nM) and "high"-affinity (115 pM) sites. Adult myocytes were found to express short and long variants of bFGF receptor 1 (FGFR-1, tyrosine kinase) mRNA. Adult heart overall levels of FGFR-1 mRNA were decreased by about one-third of corresponding fetal values. Several lines of evidence indicated that bFGF receptors in adult cardiomyocytes in situ and/or in isolation are functional. Isolated adult myocytes were found to be capable of heparin-resistant internalization of 125I-labeled bFGF, to lose their viability after interaction with bFGF-saporin (a mitotoxin known to kill cells after entry via the bFGF receptor), and to respond to bFGF by activation of mitogen-activated protein kinase. In addition, introduction of exogenous bFGF into the myocardium by Langendorff perfusion resulted in stimulation of tyrosine phosphorylation in association with cardiomyocyte intercalated disks, as assessed by immunofluorescence. It is concluded that adult cardiomyocytes express functionally coupled high-affinity bFGF receptors and that they are capable of a biologic response to bFGF in vivo.
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Quarto, N., D. Talarico, R. Florkiewicz et D. B. Rifkin. « Selective expression of high molecular weight basic fibroblast growth factor confers a unique phenotype to NIH 3T3 cells. » Cell Regulation 2, no 9 (septembre 1991) : 699–708. http://dx.doi.org/10.1091/mbc.2.9.699.
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The phenotypes of NIH 3T3 cells transfected with basic fibroblast growth factor (bFGF) cDNAs that express only the high molecular weight (HMW) forms of bFGF, the 18-kDa form, or all forms were examined. Cells producing the 18 kDa or all forms of bFGF were transformed at high levels of growth factor expression but were nontransformed at low levels. Cell producing low levels of HMW forms of bFGF were growth impaired when compared with the parental cells. These cells tended to form multinucleated giant cells, did not grow in soft agar, were nontumorigenic, had a normal bFGF receptor number, and had a nontransformed morphology. Cells expressing high levels of HMW bFGFs had a transformed morphology and were tumorigenic. These data suggest a specific functional role for HMWbFGF.
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Moscatelli, D. « Metabolism of receptor-bound and matrix-bound basic fibroblast growth factor by bovine capillary endothelial cells. » Journal of Cell Biology 107, no 2 (1 août 1988) : 753–59. http://dx.doi.org/10.1083/jcb.107.2.753.
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Bovine capillary endothelial (BCE) cells were incubated at 4 degrees C with 5 ng/ml 125I-basic fibroblast growth factor (bFGF) to equilibrate 125I-bFGF with high affinity cell surface receptors and low affinity matrix binding sites. 67% of the added 125I-bFGF bound to the matrix and 7% bound to receptors. The fate of bound bFGF was followed after cells were incubated in bFGF-free medium and were shifted to 37 degrees C to restore cell metabolism. 125I-bFGF bound to receptors decreased rapidly while the amount of 125I-bFGF bound to matrix was reduced more slowly. The rapid decrease in receptor-bound 125I-bFGF appeared to be due to a down-regulation of bFGF receptors; cells that had been treated for 5 h with bFGF had 60% fewer high affinity receptors than untreated cells. Despite the initial high level of 125I-bFGF binding to matrix, most of this 125I-bFGF was mobilized and metabolized by the cells. 125I-bFGF was internalized by the cells at 37 degrees C, leading to a constant accumulation of 125I-bFGF within the cell. Internalized bFGF was rapidly cleaved from an 18-kD form to a 16-kD form. The 16-kD form was more slowly degraded with a half-life of approximately 8 h. Degradation of internalized 125I-bFGF was inhibited by chloroquine, suggesting that the digestion occurred in a lysosomal compartment. The role of matrix binding sites in the internalization process was investigated. Binding to matrix sites seemed not to be directly involved in the internalization process, since addition of heparin at a concentration that blocked 95% of the binding to matrix had no effect on the initial rate of internalization of bFGF. BCE cells also released a substance that competed for the binding of bFGF to matrix but not to receptors. This substance bound to DEAE-cellulose and was sensitive to heparinase treatment, suggesting that it was a heparinlike molecule. Thus, heparinlike molecules produced by BCE cells can modulate the cellular interaction with bFGF. Matrix-associated heparinlike molecules bind bFGF which can later be metabolized by the cell, and secreted heparinlike molecules release bFGF from matrices.
Thèses sur le sujet "BFGF receptor"
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Preissler, Thales. « Interação funcional entre o receptor do peptídeo liberador de gastrina (GRPR) e o fator de crescimento de fibroblastro básico (bFGF) na formação da memória no hipocampo dorsal ». reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2008. http://hdl.handle.net/10183/15478.
Texte intégralRésumé :
O peptídeo liberador da gastrina (GRP), pertencente à família dos peptídeos semelhantes à bombesina, e seus receptores (GRPR) estão presentes em todo o sistema nervoso central, em particular em áreas límbicas cerebrais como o hipocampo e a amídala, as quais estão envolvidas de forma importante na regulação emocional, na função cognitiva e, possivelmente, em transtornos neuropsiquiátricos e neurodegenerativos. Crescentes evidências indicam que o receptor do peptídeo liberador de gastrina (GRPR) está envolvido na regulação da plasticidade sináptica e formação da memória no hipocampo e em outras áreas cerebrais. Entretanto, o mecanismo molecular do efeito prejudicial da memória do antagonismo do GRPR não está claro. O fator de crescimento de fibroblasto básico (bFGF/FGF-2), é um peptídeo que possui efeitos estimulatórios na proliferação, diferenciação e motilidade de diferentes tipos celulares. Em neurônios atua como um fator neurotrófico que estimula a sobrevida neuronal e neurogênese. Evidências de interações entre o bFGF e o GRPR foram dadas por estudos que mostraram que antagonistas do GRPR inibiam a expressão do bFGF em tumores. Neste trabalho mostramos que o fator de crescimento de fibroblasto básico (bFGF/FGF-2) recupera o prejuízo da memória induzida pelo antagonismo do GRPR no hipocampo dorsal de ratos. O antagonista [D-Tpi6, Leu13 psi(CH2NH)-Leu14] bombesin (6–14) (RC- 3095) na dose de 1.0 Tg prejudica, enquanto o bFGF na dose de 0,25 Tg aumenta a retenção da esquiva inibitória (um tipo de tarefa de condicionamento aversivo) quando infundidos imediatamente após o treino, na área CA1 do hipocampo dorsal em ratos machos. A coinfusão com uma dose sem efeito de bFGF bloqueou o efeito amnésico do RC- 3095. Estes achados sugerem que o efeito prejudicial dos antagonistas do GRPR devem ser parcialmente mediados pela inibição da função e/ou expressão do bFGF neuronal e pela diminuição da ativação das cascatas de proteína cinases intracelulares associadas com a sinalização do bFGF.Gastrin-releasing peptide (GRP), a bombesin-like peptide, and its receptor, GRP receptor (GRPR) are found throughout the central nervous system (CNS), including limbic areas such as the hippocampus and amygdala, which are significantly involved in emotional responses, cognitive function, and, possibly, neurodegenerative and neuropsychiatric disorders. Increasing evidence indicates that the gastrin releasing peptide receptor (GRPR) is implicated in regulating synaptic plasticity and memory formation in the hippocampus and other brain areas. However, the molecular mechanisms underlying the memory-impairing effects of GRPR antagonism have remained unclear. bFGF is a polypeptide displaying stimulatory actions on proliferation, differentiation and motility of different cell types. In neurons, bFGF acts as neurotrophic factor that stimulates neuronal survival, and neurogenesis. Evidence of functional interactions between bFGF and the GRPR was provided by studies showing that GRPR antagonists inhibit the expression of bFGF in tumours. Here we report that basic fibroblast growth factor (bFGF/FGF-2) rescues the memory impairment induced by GRPR antagonism in the rat dorsal hippocampus. The GRPR antagonist [D-Tpi6, Leu13 psi(CH2NH)-Leu14] bombesin (6–14) (RC-3095) at 1.0g impaired, whereas bFGF at 0.25g enhanced, 24 h retention of inhibitory avoidance (IA) when infused immediately after training into the CA1 hippocampal area in male rats. Coinfusion with an otherwise ineffective dose of bFGF blocked the memory-impairing effect of RC-3095. These findings suggest that the memory-impairing effects of GRPR antagonists might be partially mediated by an inhibition in the function and/or expression of neuronal bFGF or diminished activation of intracellular protein kinase pathways associated with bFGF signaling.
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Chen, Cheng. « Presynaptic differentiation at the neuromuscular junction : regulation by a novel bFGF-p120 catenin signaling pathway / ». View abstract or full-text, 2007. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202007%20CHEN.
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Herre, Jürgen. « Dectin-1 : receptor internalisation, trafficking and biological effects in macrophages ». Thesis, University of Oxford, 2004. http://ora.ox.ac.uk/objects/uuid:bb525976-bfbf-4817-926b-c3686da071b5.
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In host defence, pattern recognition plays an essential role by enabling the immune system to discriminate self from pathogenic non-self. Pattern recognition is mediated by leukocyte expressed pattern recognition molecules (PRMs), which recognise pathogen associated molecular patterns (PAMPs) on pathogens. Phagocytosis is a critical event for anti-microbial defence and its contribution is not limited to the clearance and killing of pathogens, but extends to the activation of adaptive immunity through production of pro-inflammatory mediators and antigen presentation. Anti- fungal immunity is extremely efficient and operates via recognition, phagocytosis and killing of fungal pathogens by leukocytes. We have examined Dectin-1, a non-opsonic pattern recognition receptor that recognises live fungi and fungal derived particles and that is highly expressed on various leukocyte populations. We wanted to establish whether Dectin-1 contributes to anti-fungal defence by analysing various aspects of the receptor biology. Using both confocal microscopy and flow-cytometry, we demonstrate that Dectin-1 is a phagocytic receptor. Furthermore, using cell lines expressing receptor mutants, we show that this capacity is mediated by the membrane proximal tyrosine residue located in the ITAM-like motif. This makes Dectin-1 the first described phagocytic leukocyte expressed receptor for unopsonised fungi and fungal derived particles, and the first pattern recognition receptor that mediates phagocytic uptake through a tyrosine based motif. We demonstrate that the mechanisms by which Dectin-1 mediates cytoskeletal activation and actin polymerisation are novel, and not shared with the canonical IT AM containing Fc(gamma)Rs. In particular the observation that Syk kinase plays not role in Dectin- 1 mediated phagocytosis in macrophages. We show that Dectin-1 mediates cellular activation in response to zymosan particles and that these (beta)-glucan dependent biological effects require collaboration with toll-like receptors (TLRs) at the cell surface. We also show that ligand size determines intracellular receptor trafficking following internalisation. Furthermore, we show that when biologically active soluble glucans are internalised by Dectin-1, the receptor is retained intracellularly yet, when biologically silent glucans are used, Dectin-1 is recycled. Dectin-1 is thus established as both an important phagocytic fungal pattern recognition receptor with pro- inflammatory abilities and an additional tool with which to study the diversity of signalling processes associated with leukocyte expressed receptors.
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Pallarés, Quixal Judit. « Expresión de los factores angiogénicos VEGF y bFGF, y de los receptores FLK/ KDR y Flt-1 en la neoplasia intraepitelial prostática ». Doctoral thesis, Universitat Autònoma de Barcelona, 2004. http://hdl.handle.net/10803/4226.
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El proceso de angiogénesis es necesario para el crecimiento de los tumores por encima de los 2-3mm y para el desarrollo de metástasis a distancia. El Factor de Crecimiento vascular endotelial (VEGF) es el factor angiogénico más potente conocido. Puede actuar de forma sinérgica junto al Factor de crecimiento fibroblástico básico (bFGF) en algunos modelos tumorales. VEGF ejerce sus funciones principalmente en las células endoteliales a través de dos receptores con acción tirosín quinasa FLK/ KDR (VEGFR2) y Flt-1( VEGFR2).
En el cáncer prostático se ha demostrado un aumento de la densidad vascular o angiogénesis en el carcinoma respecto al tejido normal, correlacionándose con otros marcadores pronósticos del cáncer prostático ya conocidos. Nuestro estudio ha demostrado un incremento de la densidad vascular y de la expresión de los factores angiogénicos VEGF y bFGF, y de los receptores FLK/ KDR y Flt-1 en la lesión precursora del cáncer de prostático, la neoplasia intraepitelial de alto grado (PINAG). Además, el aumento de la angiogénesis se ha correlacionado con los adenocarninomas prostáticos de alto grado de Gleason y estadios avanzados (pT3).
El aumento de la angiogénesis y la expresión de los factores angiogénicos y de sus receptores en la neoplasia intraepitelial de alto grado, apoya un papel de esta lesión como precursora en el cáncer prostático, y plantea su posible aplicación en biopsia por aguja en la próstata como marcador pronóstico adicional del adenocarcinoma prostático.
The process of angiogenesis is necessary for tumor growth beyond 2-3mm and for the development of metastasis. Vascular endothelial growth factor (VEGF) is the most potent angiogenic factor so far detected, and can function synergistically with Basic Fibroblastic growth factor (bFGF) inducing angiogenesis. VEGF acts upon binding to two tyrosine kinase receptors FLK/ KDR (VEGFR2) and Flt-1 (VEGFR2).
In prostate cancer the study of angiogenesis has revealed an increase in the microvessels density in the carcinoma compared to normal prostatic glands, and its has been correlated with pathological stage. Our results demostrated an increase in the vessels density and in the expression of the angiogenic factors VEGF and bFGF, and the receptors FLK/ KDR and Flt-1 in the prostatic intraepithelial neoplasia. Interestingly, angiogenesis also correlated with tumor grade and pathological stage (pT3).
The increased angiogenesis and expression of the angiogenic factors and their receptors in the prostatic intraepithelial neoplasia, support a premalignant role for this lesion, and suggest their application in prostatic core-biopsies as an additional prognostic factor in prostatic cancer.
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Campos, Danila Barreiro. « Imunolocalização do VEGF, bFGF e seus receptores na placenta bovina e influência destes fatores sobre a produção de progesterona pelas células placentárias em cultura ». Universidade de São Paulo, 2005. http://www.teses.usp.br/teses/disponiveis/10/10132/tde-05072006-093115/.
Texte intégralRésumé :
O estabelecimento e perfeito funcionamento da placenta são fatores dependentes da intensa vascularização ocorrida no órgão. Os processos de vasculogênese e angiogênese placentária são modulados por diversos fatores, incluindo o VEGF (fator de crescimento vascular endotelial) e bFGF (fator de crescimento fibroblástico básico). Apesar da importância do VEGF e bFGF durante a vascularização estar estabelecida, vários estudos indicam a participação desses fatores de crescimento como moduladores locais em outras funções fisiológicas, como por exemplo o controle da produção hormonal em tecidos esteroidogênicos. Animais clonados podem apresentar alterações na expressão de determinados genes durante seu desenvolvimento, o que pode alterar a função placentária. Os objetivos deste estudo são determinar a localização tecidual do VEGF, bFGF e seus receptores na placenta bovina e avaliar a influência destes fatores de crescimento sobre a produção de progesterona placentária em bovinos não clonados e clonados. Placentomas de 90, 150 e 210 dias de gestação foram obtidos em abatedouro e placentônios de gestações aos 270 dias provenientes de bovinos clonados e não clonados foram coletados após cesarianas. As amostras foram fixadas em formol tamponado 4%, desidratadas e incluídas em parafina. Cortes foram submetidos a imuno-histoquímica para posterior localização das proteínas do VEGF, bFGF e seus receptores. Sob condições assépticas, as células foram mecanicamente dispersas e cultivadas em placas de 96 cavidades. Os fatores foram adicionados em concentrações de 10 e 50 ηg/ml de bFGF e VEGF, respectivamente. Amostras de meio de cultura e as células dos grupos controle, bFGF, VEGF e VEGF mais bFGF foram coletadas 24, 48 e 96 horas após a adição dos fatores. A progesterona foi dosada por radioimunoensaio e o conteúdo protéico pelo método de Lowry. Os dados foram analisados utilizando-se o programa estatístico SAS (Statistical Analysis System), as diferenças estatísticas encontradas foram comparadas pelo teste de variação múltipla de Duncan. O VEGF, bFGF e seus receptores foram localizados em células do epitélio e estroma maternos e fetais e células endoteliais vasculares em bovinos não clonados e clonados. As células placentárias apresentaram diferentes capacidades de síntese de progesterona ao longo da gestação. Aos 90 e 210 dias de gestação o VEGF estimulou a produção de progesterona, enquanto aos 270 dias de gestação o fator inibiu a produção deste hormônio. O bFGF estimulou a produção de progesterona pelas células placentárias aos 90 dias de gestação. A adição dos dois fatores de crescimento conjuntamente determinou um estímulo na produção de progesterona aos 210 dias de gestação. A produção de progesterona pelas células de bovinos clonados foi semelhante àquela observada em células de bovinos não clonados na mesma idade gestacional e os fatores de crescimento não influenciaram essa produção. Conclui-se que o VEGF e bFGF, atuando localmente no tecido placentário, funcionam como moduladores do processo de esteroidogênese, influenciando de maneira tempo-dependente a produção de progesterona deste órgão.Placental establishment and function are dependent on intense vascularization. Placental vasculogenesis and angiogenesis are modulated by several factors, including VEGF (vascular endothelial growth factor) and bFGF (basic fibroblast growth factor). Although the role of VEGF and bFGF during vascularization is already well established, some studies have indicated the participation of these growth factors as local modulators in other physiological functions, such as control of hormonal production in steroidogenic tissues. Cloned animals may exhibit alterations in gene expression during development modifying placental function. The aims of this study are to determine the tissue localization of VEGF, bFGF and their receptors in the bovine placenta and to evaluate the influence of bFGF and VEGF on placental progesterone production in non-cloned and cloned bovines. Placentomes from days 90, 150 and 210 of pregnancy were obtained at local slaughterhouse and placentomes from cloned and non-cloned gestations at 270 days were obtained after cesarean sections. Samples were fixed in 4% buffered formol solution, dehydrated and included in paraffin. Sections were subimitted to immunohistochemistry for subsequent localization of VEGF, bFGF and their receptors proteins. Under aseptic conditions, cells were mechanically dispersed and then cultivated in a 96-well plate. Growth factors were added at concentrations of 10 and 50 ηg/ml for bFGF and VEGF, respectively. Samples of culture medium and cells from control, bFGF, VEGF and bFGF plus VEGF groups were collected 24, 48 and 96 hours after growth factor addition. Progesterone concentrations were assessed by radioimmunoassay and protein content was measured by Lowry?s method. Data were analyzed by SAS (Statistical Analysis System) program, significant differences were compared by Duncan?s range multiple test. VEGF, bFGF and their receptors were localized in maternal and fetal epithelial and stromal cells and vascular endothelial cells during pregnancy in non-cloned animals and in cloned bovine placenta at 270 days of pregnancy. Bovine placental cells were able to produce different amounts of progesterone during pregnancy. Growth factors were able to influence progesterone production in placental cells only after 24 hours in culture. At 90 and 210 days of pregnancy VEGF stimulated progesterone production, while at 270 days of pregnancy the growth factor inhibited production of this hormone. bFGF stimulated progesterone production in placental cells from 90 days of pregnancy. Both growth factors together determined an increase in progesterone production in placental cells from 210 days of pregnancy. Progesterone production in placental cells from cloned cattle is similar when compared with non-cloned placental cells at the same gestational age and growth factors did not influence progesterone production in these cells. VEGF and bFGF, acting locally in the placental tissue, are modulators of the steroidogenic process, influencing in a time-dependent manner the progesterone production in this organ.
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RIGACCI, STEFANIA. « Studio della distribuzione intracellulare e dei substrati in vivo della fosfotirosina proteina fosfatasi a basso peso molecolare ». Doctoral thesis, 2000. http://hdl.handle.net/2158/822776.
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« Imunolocalização do VEGF, bFGF e seus receptores na placenta bovina e influência destes fatores sobre a produção de progesterona pelas células placentárias em cultura ». Tese, Biblioteca Digital de Teses e Dissertações da USP, 2005. http://www.teses.usp.br/teses/disponiveis/10/10132/tde-05072006-093115/.
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Бень, Анжела Михайлівна. « Особливості поетики сучасної літературної казки (на матеріалі «ВДВ» Роальда Дала) ». Магістерська робота, 2021. https://dspace.znu.edu.ua/jspui/handle/12345/5488.
Texte intégralRésumé :
Бень А. М. Особливості поетики сучасної літературної казки (на матеріалі «ВДВ» Роальда Дала) : кваліфікаційна робота магістра спеціальності 035 "Філологія" / наук. керівник Н. М. Торкут. Запоріжжя : ЗНУ, 2021. 57 с.EN : The work is presented on 57 pages of printed text. The list of references includes 53 sources. The thesis presents the comprehensive study of the poetic features of the novel “BFG” by the famous modern British writer Roald Dahl whose books are very popular among young readers all over the world. The text of this novel is considered in the genre paradigm of centuries-old fairy-tale tradition. The study determines the interaction of the poetical elements of folk tales and literary tales written by some well-known English writers as well as to the author's innovation of R. Dahl. The work provides some insights into the problem of tale poetics in order to identify the features of folklore and literary tales. Special attention is paid to elucidating the formation of R. Dahl's creative personality and creating a holistic historical and literary vision of the creative work of this author against the background of the tradition of English literary tales. The target of this paper is to highlight the main features of the poetics of folk tales and to clarify the specifics of the transformation of the genre canon in the fairy tale by R. Dahl "BFG". A thorough analysis of the peculiarities of aesthetic tastes and intellectual demands of modern children has been conducted and it helps to discover the secrets of the immense popularity of “BFG” among the young readership. The study determines the special narrative strategies of Dahl which allow him to bring the text as close as possible to children's perception. The writer is proved to use the cinematographic principle of the plot sequence representation, numerous puns, black humor jokes, irony and specific author's neologisms, which form the original stylistic palette of the work. The practical significance of the thesis is that its results and conclusions can be used in the preparation of lectures on the theory of literature, history of foreign literature of the twentieth century, in the development of special courses on the history of English literature, and can be interesting for school teachers of foreign literature.
UA : Робота викладена на 57 сторінках друкованого тексту. Перелік посилань включає 53 джерела Об’єкт дослідження: казкова поетика в аспекті діахронії, від народно-поетичних зразків до сучасних літературних казок, зокрема, поетологічні особливості літературної казки-повісті відомого сучасного англійського письменника Р. Дала «ВДВ», які розглядаються під жанрологічним кутом зору. Мета роботи: виокремивши основні риси поетики фольклорної казки, з’ясувати специфіку трансформації жанрового канону в казковій повісті Р. Дала «ВДВ». Теоретико-методологічні засади: фундаментальні праці вітчизняних і зарубіжних вчених (Буслаєв і О. Афанасьєв, О. Веселовський, В. Пропп, С. Еплярд, С. Бремон, Л. І. Скуратовська, Ю. М. Романенко, І. В. Цикушева та ін.), сфокусовані на теоретичних та історико-літературних аспектах вивчення казки як жанру, а також наукові розвідки, присвячені творчості Р. Дала. Отримані результати: виявлено поетикальні особливості фольклорної та літературної казки; здійснено аналіз дефініцій та способів класифікації фольклорної та літературної казки; сформовано цілісне уявлення про специфіку формування творчої особистості Р. Дала та створено цілісну історико-літературну візію творчого доробку цього англійського автора на тлі традиції англійської літературної казки ; проаналізувано поетику повісті «ВДВ», виявлено її спільність з літературними традиціями та відмінності від них; а також окреслено кореляцію елементів казкової поетики «ВДВ» із запитами сучасного дитячого читацького загалу.
Chapitres de livres sur le sujet "BFGF receptor"
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Isacchi, A., L. Bergonzoni, M. Statuto, R. Chiesa, M. Rusnati, M. Presta, G. Ragnotti et P. Sarmientos. « Activation of the tyrosine kinase receptor is not sufficient for the full biological activity of bFGF ». Dans Experientia Supplementum, 101–6. Basel : Birkhäuser Basel, 1992. http://dx.doi.org/10.1007/978-3-0348-7001-6_17.
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Presta, Marco, Marco Rusnati, Jeanette A. M. Maier, Chiara Urbinati, Massimo Statuto, Anna Gualandris, Ambra Pozzi et Giovanni Ragnotti. « Basic Fibroblast Growth Factor and Endothelial Cells : Receptor Interaction, Signal Transduction, Cellular Response-Dissociation of the Mitogenic Activity of bFGF from its Plasminogen Activator-Inducing Capacity ». Dans Angiogenesis in Health and Disease, 79–89. Boston, MA : Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3358-0_7.
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Savion, Naphtali, Anat Beit-Or, Shlomo Kotev-Emeth et Sandu Pitaru. « Dexamethasone Modulates the Response of Rat Stromal Bone Marrow Derived Bone-Like Cells to bFGF and Igf-I ». Dans Growth Factors, Peptides and Receptors, 115–26. Boston, MA : Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2846-3_12.
Texte intégralActes de conférences sur le sujet "BFGF receptor"
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Saksela, O., D. Moscatelli et D. B. Rifkin. « THE OPPOSING OF BASIC FIBROBLAST GROWTH FACTOR AND TRANSFORMING GROWTH FACTOR BETA ON THE REGULATION OF PLASMINOGEN ACTIVATOR ACTIVITY IN CAPILLARY ENDOTHELIAL CELLS ». Dans XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644660.
Texte intégralRésumé :
Basic fibroblast growth factor (bFGF), a potent inducer of angio-genesis in vivo, stimulates the production of both the cell-associated and the secreted forms of urokinase-and tissue-type plasminogen activators (PA) in cultured bovine capillary endothelial cells. This stimulation was counteracted by picogram amounts of transforming growth factor beta The stimulatory effect of bFGF was not completely abolished by increasing the amount of TGFb However, the inhibition by TGFb was greatly enhanced if the cells were pretreated for 1-3 hours with TGFb before addition of bFGF, and the inhibition was almost total, if the' preincubationtime with TGFb was 6 hours.Sequential chanqes of serum-containing medium prior to addition ofbFGF also blocked the PA stimulatory effect of bFGF. This inhibitory activity of serum was reduced by incubation of the serum with anti-TGFb-IgG. After pro-longed incubation of cultures treated simultaneously with bFGF' and TGFb, the inhibitory effect of the added bFGF dominated as assayed by PAlevels. TGFbdid not alter the receptor binding of labeled bFGF, nor did a 6 hour pretreatment with TGFb reducethe amount of bound bFGF. The major difference between effects by bFGF and TGFb was thatwhile bFGF effectively enhanced PA-activi-ty expressed by the cells, TGF decreased the amounts of both cell-associated and secreted PA activity by decreasing enzyme production and proenzyme activation. Both bFGF and TGFb increased the secretion of the endothelial type 1 plasminogen activatorinhibitor (PAI 1). The highest concentration of TGFb is found in platelets, and it is known to be released during clot formation. The suppression of PA production by theendothelium by the release of TGFb shouldresult in a decrease in the fibrinolytic activity and promote clot maintenance. In addition, the rapid stimulation of high levels of PAI 1 secretion from the surrounding capillarycells by platelet released TGFb may further suppress fibrinolysis'. The reversabil it.y of theTGFb effect and domination of bFGF stimulation may be important in relation to the subsequentonset of clot lysis or angiogenesis leadino to thrombus reorganization and wound healing.