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Добірка наукової літератури з теми "Fibroblast growth factor 2 (FGF2)"

Автор: Grafiati
Опубліковано: 14 березня 2023

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Статті в журналах з теми "Fibroblast growth factor 2 (FGF2)"

1

Akimoto, Tetsu, and Marc R. Hammerman. "Fibroblast growth factor 2 promotes microvessel formation from mouse embryonic aorta." American Journal of Physiology-Cell Physiology 284, no. 2 (February 1, 2003): C371—C377. http://dx.doi.org/10.1152/ajpcell.00193.2002.

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To delineate the roles that oxygen and fibroblast growth factors (FGFs) play in the process of angiogenesis from the embryonic aorta, we cultured mouse embryonic aorta explants (thoracic level to lateral vessels supplying the mesonephros and metanephros) in a three-dimensional type I collagen gel matrix. During 8 days of culture under 5% O2, but not room air, the addition of FGF2 to explants stimulated the formation of Gs-IB4-positive, CD31-positive, and Flk-1-positive microvessels in a concentration-dependent manner. FGF2-stimulated microvessel formation was inhibited by sequestration of FGF2 via addition of soluble FGF receptor (FGFR) chimera protein or anti-FGF2 antibodies. FGFR1 and FGFR2 were present on explants. Levels of FGFR1, but not FGFR2, were increased in embryonic aorta cultured under 5% O2 relative to room air. Our data suggest that low oxygen upregulates FGFR1 expression in embryonic aorta in vitro and renders it more responsive to FGF2.
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2

Mejhert, Niklas, Jean Galitzky, Amanda T. Pettersson, Clara Bambace, Lennart Blomqvist, Anne Bouloumié, Keith N. Frayn, Ingrid Dahlman, Peter Arner, and Mikael Rydén. "Mapping of the Fibroblast Growth Factors in Human White Adipose Tissue." Journal of Clinical Endocrinology & Metabolism 95, no. 5 (May 1, 2010): 2451–57. http://dx.doi.org/10.1210/jc.2009-2049.

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Abstract Context: Fibroblast growth factors (FGFs) regulate the development of white adipose tissue (WAT). However, the secretion and cellular origin of individual FGFs in WAT as well as the influence of obesity are unknown. Objective: Our objective was to map FGFs in human sc WAT, the cellular source, and association with obesity. Design: Secretion, mRNA, and circulatory levels of FGFs in human abdominal sc WAT from nonobese and obese donors were examined by microarray, real-time quantitative PCR, and ELISA. The activity of FGFs in cultured human adipocytes was determined by phosphorylation assays. Results: Expression of five FGFs (FGF1, FGF2, FGF7, FGF9, and FGF18) and FGF homologous factor (FHF2) was identified in WAT. Only FGF1 was released in a time-dependent manner from sc WAT, and fat cells were the major source of FGF1 secretion. FGF1 expression increased and FGF2 decreased during adipocyte differentiation. Furthermore, FGF1 was not secreted into the circulation. Although FGF1 levels were 2-fold increased in obesity, they were unaltered by weight reduction. Only FGF1 and FGF2 induced a marked concentration-dependent phosphorylation of p44/42 in cultured human adipocytes. Conclusions: Of the investigated FGFs, only FGF1 is secreted from sc WAT and predominantly so from the adipocyte fraction. The activity in adipocyte cultures and lack of secretion into the circulation suggest that FGF1 acts as an auto- or paracrine factor. FGF1 levels are increased in obesity but unaffected by weight reduction, suggesting a primary defect in obese individuals. In conclusion, FGF1 may play a superior role among the FGFs in sc WAT and obesity development.
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3

Rusnati, Marco, Maura Camozzi, Emanuela Moroni, Barbara Bottazzi, Giuseppe Peri, Stefano Indraccolo, Alberto Amadori, Alberto Mantovani, and Marco Presta. "Selective recognition of fibroblast growth factor-2 by the long pentraxin PTX3 inhibits angiogenesis." Blood 104, no. 1 (July 1, 2004): 92–99. http://dx.doi.org/10.1182/blood-2003-10-3433.

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Abstract The long pentraxin PTX3 is a soluble pattern recognition receptor produced by monocytes and endothelial cells that plays a nonredundant role in inflammation. Several pathologic conditions are characterized by local production of both PTX3 and the angiogenic fibroblast growth factor-2 (FGF2). Here, solid-phase binding assays demonstrated that PTX3 binds with high affinity to FGF2 but not to a panel of cytokines and growth factors, including FGF1, FGF4, and FGF8. Accordingly, PTX3 prevented 125I-FGF2 binding to endothelial cell receptors, leading to specific inhibition of FGF2-induced proliferation. PTX3 hampered also the motogenic activity exerted by endogenous FGF2 on a wounded endothelial cell monolayer. Moreover, PTX3 cDNA transduction in FGF2-transformed endothelial cells inhibited their autocrine FGF2-dependent proliferation and morphogenesis in vitro and their capacity to generate vascular lesions when injected in nude mice. Finally, PTX3 suppressed neovascularization triggered by FGF2 in the chick embryo chorioallantoic membrane with no effect on physiologic angiogenesis. In contrast, the short pentraxin C-reactive protein was a poor FGF2 ligand/antagonist. These results establish the selective binding of a member of the pentraxin superfamily to a growth factor. PTX3/FGF2 interaction may modulate angiogenesis in various physiopathologic conditions driven by inflammation, innate immunity, and/or neoplastic transformation.
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4

Bellosta, Paola, Akiyo Iwahori, Alexander N. Plotnikov, Anna V. Eliseenkova, Claudio Basilico, and Moosa Mohammadi. "Identification of Receptor and Heparin Binding Sites in Fibroblast Growth Factor 4 by Structure-Based Mutagenesis." Molecular and Cellular Biology 21, no. 17 (September 1, 2001): 5946–57. http://dx.doi.org/10.1128/mcb.21.17.5946-5957.2001.

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ABSTRACT Fibroblast growth factors (FGFs) comprise a large family of multifunctional, heparin-binding polypeptides that show diverse patterns of interaction with a family of receptors (FGFR1 to -4) that are subject to alternative splicing. FGFR binding specificity is an essential mechanism in the regulation of FGF signaling and is achieved through primary sequence differences among FGFs and FGFRs and through usage of two alternative exons, IIIc and IIIb, for the second half of immunoglobulin-like domain 3 (D3) in FGFRs. While FGF4 binds and activates the IIIc splice forms of FGFR1 to -3 at comparable levels, it shows little activity towards the IIIb splice forms of FGFR1 to -3 as well as towards FGFR4. To begin to explore the structural determinants for this differential affinity, we determined the crystal structure of FGF4 at a 1.8-Å resolution. FGF4 adopts a β-trefoil fold similar to other FGFs. To identify potential receptor and heparin binding sites in FGF4, a ternary FGF4-FGFR1-heparin model was constructed by superimposing the FGF4 structure onto FGF2 in the FGF2-FGFR1-heparin structure. Mutation of several key residues in FGF4, observed to interact with FGFR1 or with heparin in the model, produced ligands with reduced receptor binding and concomitant low mitogenic potential. Based on the modeling and mutational data, we propose that FGF4, like FGF2, but unlike FGF1, engages the βC′-βE loop in D3 and thus can differentiate between the IIIc and IIIb splice isoforms of FGFRs for binding. Moreover, we show that FGF4 needs to interact with both the 2-O- and 6-O-sulfates in heparin to exert its optimal biological activity.
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5

Alan, Emel, and Yasin Kulak. "The immunoexpression patterns of fibroblast growth factors in the pregnant and postpartum rat ovary." Reproduction, Fertility and Development 33, no. 16 (2021): 817. http://dx.doi.org/10.1071/rd21025.

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Анотація:
Fibroblast growth factors (FGFs) are polypeptides involved in the regulation of oogenesis and folliculogenesis by inducing ovarian mitogenic, homeostatic and angiogenic activity. This study was aimed at determining the localisation of FGF ligands (FGF1 and FGF2) and FGF receptor 2 (FGFR2) in the rat ovary by immunohistochemical analyses, at pregnancy and the postpartum period. During pregnancy and the postpartum period, positive FGF1 immunoreactions were observed in the nucleus and cytoplasm of germinative epithelial cells, granulosa cells of follicles in different developmental stages, theca interna cells, interstitial cells, luteal cells and atretic follicles. FGF2 immunoreactivity was strong in the cytoplasm of the endothelial cells and smooth muscle cells of the ovarian blood vessels and in the smooth muscle cells of the ovarian cortex and medulla. Strong FGFR2 immunoreactivity was observed in the stromal cells surrounding the blood vessels and rete ovarii. Immunoreaction intensity of the FGF1, FGF2 and FGFR2 had relatively similar abundances between the periods examined. Considering that FGFs act as local regulators in oogenesis, folliculogenesis, follicular atresia, ovulation, corpus luteum formation and regression and angiogenesis, this study supports the idea that FGFs may also be involved in these physiological functions in rat ovaries during pregnancy and postpartum period.
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6

Nawrocka, Daria, Mateusz Adam Krzyscik, Łukasz Opaliński, Malgorzata Zakrzewska, and Jacek Otlewski. "Stable Fibroblast Growth Factor 2 Dimers with High Pro-Survival and Mitogenic Potential." International Journal of Molecular Sciences 21, no. 11 (June 9, 2020): 4108. http://dx.doi.org/10.3390/ijms21114108.

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Анотація:
Fibroblast growth factor 2 (FGF2) is a heparin-binding growth factor with broad mitogenic and cell survival activities. Its effector functions are induced upon the formation of 2:2 FGF2:FGFR1 tetrameric complex. To facilitate receptor activation, and therefore, to improve the FGF2 biological properties, we preorganized dimeric ligand by a covalent linkage of two FGF2 molecules. Mutations of the FGF2 WT protein were designed to obtain variants with a single surface-exposed reactive cysteine for the chemical conjugation via maleimide-thiol reaction with bis-functionalized linear PEG linkers. We developed eight FGF2 dimers of defined topology, differing in mutual orientation of individual FGF2 molecules. The engineered proteins remained functional in terms of FGFR downstream signaling activation and were characterized by the increased stability, mitogenic potential and anti-apoptotic activity, as well as induced greater migration responses in normal fibroblasts, as compared to FGF2 monomer. Importantly, biological activity of the dimers was much less dependent on the external heparin administration. Moreover, some dimeric FGF2 variants internalized more efficiently into FGFR overexpressing cancer cells. In summary, in the current work, we showed that preorganization of dimeric FGF2 ligand increased the stability of the growth factor, and therefore, enhanced its biological activity.
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7

Pinto-Bravo, Pedro, Maria Rosa Rebordão, Ana Amaral, Carina Fernandes, António Galvão, Elisabete Silva, Pedro Pessa-Santos, et al. "Microvascularization and Expression of Fibroblast Growth Factor and Vascular Endothelial Growth Factor and Their Receptors in the Mare Oviduct." Animals 11, no. 4 (April 12, 2021): 1099. http://dx.doi.org/10.3390/ani11041099.

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Анотація:
The oviduct presents the ideal conditions for fertilization and early embryonic development. In this study, (i) vascularization pattern; (ii) microvascular density; (iii) transcripts of angiogenic factors (FGF1, FGF2, VEGF) and their receptors—FGFR1, FGFR2, KDR, respectively, and (iv) the relative protein abundance of those receptors were assessed in cyclic mares’ oviducts. The oviductal artery, arterioles and their ramifications, viewed by means of vascular injection-corrosion, differed in the infundibulum, ampulla and isthmus. The isthmus, immunostained with CD31, presented the largest vascular area and the highest number of vascular structures in the follicular phase. Transcripts (qPCR) and relative protein abundance (Western blot) of angiogenic factors fibroblast growth factor 1 (FGF1) and 2 (FGF2) and vascular endothelial growth factor (VEGF), and their respective receptors (FGFR1, FGFR2, VEGFR2 = KDR), were present in all oviduct portions throughout the estrous cycle. Upregulation of the transcripts of angiogenic receptors FGF1 and FGFR1 in the ampulla and isthmus and of FGF2 and KDR in the isthmus were noted. Furthermore, in the isthmus, the relative protein abundance of FGFR1 and KDR was the highest. This study shows that the equine oviduct presents differences in microvascular density in its three portions. The angiogenic factors VEGF, FGF1, FGF2 and their respective receptors are expressed in all studied regions of the mare oviduct, in agreement with microvascular patterns.
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Britto, Jonathan A., Robert D. Evans, Richard D. Hayward та Barry M. Jones. "Toward Pathogenesis of Apert Cleft Palate: FGF, FGFR, and TGFβ Genes Are Differentially Expressed in Sequential Stages of Human Palatal Shelf Fusion". Cleft Palate-Craniofacial Journal 39, № 3 (травень 2002): 332–40. http://dx.doi.org/10.1597/1545-1569_2002_039_0332_tpoacp_2.0.co_2.

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Objective: Critical cellular events at the palatal medial edge epithelium (MEE) occur in unperturbed mammalian palatogenesis, the molecular control of which involves a number of growth factors including transforming growth factor β3 (TGFβ3). Apert syndrome is a monogenic human disorder in which cleft palate has been significantly correlated to the fibroblast growth factor receptor (FGFR) 2-Ser252Trp mutation. We report the relative expression of these genes in human palatogenesis. Methods: The expression of the IgIIIa/b and IgIIIa/c transcript isoforms of FGFR2 and the proteins FGFR1, FGFR2, and FGFR3 was studied in situ throughout the temporospatial sequence of human palatal shelf fusion and correlated with the expression of TGFβ3. In addition, the immunolocalization of the ligand FGFs 2, 4, and 7 was undertaken together with the intracellular transcription factor STAT1, which is activated by FGFR signaling. Results: FGFRs are differentially expressed in the mesenchyme and epithelia of fusing palatal shelves, in domains overlapping those of their ligands FGF4 and FGF2 but not FGF7. Coexpression is seen with TGFβ3, which is implicated in MEE dynamics and FGF and FGFR upregulation, and STAT1, an intracellular transcription factor that mediates apoptosis. Conclusions: The coregulation of molecules of the FGFR signaling pathway with TGFβ3 throughout the stages of human palatal fusion suggests their controlling influence on apoptosis and epitheliomesenchymal transdifferentiation at the MEE. Experimental evidence links FGFR2-IgIIIa/b loss of function with palatal clefting, and these correlated data suggest a unique pathological mechanism for Apert cleft palate.
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9

Iseki, S., A. O. Wilkie, J. K. Heath, T. Ishimaru, K. Eto, and G. M. Morriss-Kay. "Fgfr2 and osteopontin domains in the developing skull vault are mutually exclusive and can be altered by locally applied FGF2." Development 124, no. 17 (September 1, 1997): 3375–84. http://dx.doi.org/10.1242/dev.124.17.3375.

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Mutations in the human fibroblast growth factor receptor type 2 (FGFR2) gene cause craniosynostosis, particularly affecting the coronal suture. We show here that, in the fetal mouse skull vault, Fgfr2 transcripts are most abundant at the periphery of the membrane bones; they are mutually exclusive with those of osteopontin (an early marker of osteogenic differentiation) but coincide with sites of rapid cell proliferation. Fibroblast growth factor type 2 (FGF2) protein, which has a high affinity for the FGFR2 splice variant associated with craniosynostosis, is locally abundant; immunohistochemical detection showed it to be present at low levels in Fgfr2 expression domains and at high levels in differentiated areas. Implantation of FGF2-soaked beads onto the fetal coronal suture by ex utero surgery resulted in ectopic osteopontin expression, encircled by Fgfr2 expression, after 48 hours. We suggest that increased FGF/FGFR signalling in the developing skull, whether due to FGFR2 mutation or to ectopic FGF2, shifts the cell proliferation/differentiation balance towards differentiation by enhancing the normal paracrine down-regulation of Fgfr2.
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SAFRAN, Michal, Miriam EISENSTEIN, David AVIEZER, and Avner YAYON. "Oligomerization reduces heparin affinity but enhances receptor binding of fibroblast growth factor 2." Biochemical Journal 345, no. 1 (December 17, 1999): 107–13. http://dx.doi.org/10.1042/bj3450107.

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Анотація:
The biological response of cells to fibroblast growth factors (FGFs) depends on heparan sulphate glycosaminoglycans sharing particular structural motifs. Heparin induced FGF dimerization has been suggested to mediate receptor dimerization and activation. Here we demonstrate that heparin-derived oligosaccharides that promote receptor binding and activation specifically induce the dimerization of basic FGF (FGF2). These heparin-induced dimers of FGF2 acquire high affinity for receptor binding and are biologically active. Using biotinylated FGF2 bound to immobilized streptavidin gradually saturated with biotin, enabled a quantitative analysis of heparin-dependent and heparin-independent FGF2 monomers and oligomers. Streptavidin induced FGF2 dimers bind and activate FGF receptors only in the presence of heparin. An excess of streptavidin, forcing biotin-FGF2 into monomers, reduces receptor binding and blocks FGF-dependent cell proliferation. All these suggest predominant receptor binding and activation by heparin associated FGF2 oligomers. Unexpectedly, heparin induced dimers and higher order oligomers lose most of their affinity towards heparin. Direct binding of soluble FGF receptors (FGFRs) to either monomers or dimers of FGF2, immobilized on heparin, confirm the preferred association of FGFRs with dimers of FGF2. Computerized molecular docking predicts a cis-oriented FGF2 dimer, stabilized by heparin, which complies with all the experimental data.
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Більше джерел

Дисертації з теми "Fibroblast growth factor 2 (FGF2)"

1

Sullivan, Christopher James. "The role of fibroblast growth factor-2 (FGF2) in vascular remodeling and adaptation." Diss., The University of Arizona, 2002. http://hdl.handle.net/10150/284317.

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The goal of this dissertation was to test the hypothesis that fibroblast growth factor-2 (FGF2) is required during diseased-related vascular growth and remodeling in the adult organism. Given previous research, it is generally assumed that FGF2 is an important regulator of vessel growth during various pathophysiological processes (e.g. tissue ischemia, vessel injury, and flow-dependent remodeling). However, such studies only indirectly implicate FGF2 in vascular adaptation and remodeling. In contrast, experiments using mice with a targeted disruption of the Fgf2 gene have allowed direct determination of the biological roles of endogenous FGF2. Thus, experimental models of flow-dependent remodeling and ischemic revascularization were used to compare the responses of Fgf2⁻/⁻ and Fgf2⁺/⁺ mice to directly identify the function of FGF2 during vascular adaptation in the adult animal. Surprisingly, the lack of FGF2 did not appear to affect vascular growth in these models. First, using a novel model of flow-dependent remodeling, Fgf2⁻/⁻ mice had equivalent carotid artery adaptation in response to both high-flow and low-flow was as wildtype counterparts. Second, angiogenesis and arteriogenesis were not different between the ischemic limbs Fgf2⁺/⁺ and Fgf2⁻/⁻ mice, demonstrating that FGF2 is not required for vascular adaptation in response to ischemia. However, these experiments led to the observation that reactive hyperemia was impaired in ischemic limb of Fgf2⁻/⁻ mice. These results indicate that vessel responsiveness is altered in the collateral circulation of the ischemic Fgf2⁻/⁻ limb. This possible identification of FGF2 as a "functional" factor in the collateral circulation suggests a novel, non-mitogenic role for endogenous growth factors. Finally, Fgf2⁻/⁻ mice had altered gene expression in the ischemic limb as evaluated using cDNA microarrays. The significance of differential gene expression in the absence of FGF2 is unknown. It is unclear whether such changes in gene expression are related to the FGF2 hyperemia phenotype or whether they are related to an unknown phenotype present in the ischemic limb of Fgf2⁻/⁻ mice. Overall, this dissertation provides new evidence that endogenous FGF2 has important actions in the remodeling vasculature during ischemic revascularization. Specifically, endogenous FGF2 appears to modulate vascular reactivity of the collateral circulation of the hindlimb.
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2

Olson, Nels Eric. "FGF2 is weakly mitogenic for intimal smooth muscle cells : role of FGF receptor expression, cytoplasmic signaling and cell cycle regulation /." Thesis, Connect to this title online; UW restricted, 2000. http://hdl.handle.net/1773/6335.

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3

Kole, Denis. "Role of Fibroblast Growth Factor 2 in Maintenance of Multipotency in Human Dermal Fibroblasts Treated with Xenopus Laevis Egg Extract Fractions." Digital WPI, 2014. https://digitalcommons.wpi.edu/etd-dissertations/207.

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Анотація:
Current usage of human embryonic stem cells (hES) and induced pluripotent stem cells (iPS) in clinical therapies and personalized medicine are limited as a result of ethical, technical and medical problems that arise from isolation and generation of these cells. Isolation of hES cells faces ethical problems associated with their derivation from human pre-implantation embryos. The most controversial aspect of hES cell isolation targets the generation of autologous hES cell lines which requires the transfer of a somatic-cell nucleus from the patient to an enucleated oocyte. While already established embryonic stem cell lines from IVF embryos can be used in a similar manner, lack of genetic identity can cause therapy rejection from the host, and prevent their use in personalized medicine. Induced pluripotent stem cells on the other hand, are generated from somatic cells that have been reprogrammed in vitro to behave like stem cells. While these cells can potentially be used for personalized medicine without the risk of rejection by the host system, derivation methods prevent their therapeutic use. The most efficient method used to generate iPS cells involves usage of viral particles which can result in viral DNA being integrated in the host cell’s genome and render these cells non-compliant for clinical therapies. Other methods not involving viral particles exist as well, but the reprogramming efficiency is too low and technical problems with generating large enough numbers of cells prevent these methods from being feasible approaches for clinical therapies. Direct reprogramming of a differentiated cell into a developmentally more plastic cell would offer alternatives to applications in regenerative medicine that currently depend on either embryonic stem cells (ES), adult stem cells or iPS cells. We hypothesize that Xenopus laevis egg cytoplasmic extract contains critical factors needed for reprogramming that may allow for non-viral, chemically defined derivation of human induced pluripotent/multipotent cells which can be maintained by addition of exogenous FGF2. In this thesis we investigated a new method for generation of multipotent cells through determining the ability of select fractions of Xenopus laevis egg extract to induce multipotency in already differentiated cells. We were able to identify select fractions from the extract that in combination with exogenously added FGF2 can reprogram and maintain the reprogrammed cells in an undifferentiated state. The findings of this work also determined that Xenopus laevis egg extract mRNA is required for achieving full reprogramming. The body of work presented in this thesis showed the ability of FGF2 isoforms to bind and activate select FGF receptor tyrosine kinases, act as extracellular mitogenic factors to support growth of hES cells in an undifferentiated state as well bind to nuclear DNA and affect expression of endogenous genes. Moreover, we showed that all FGF2 isoforms can induce expression of stem cell specific proteins in human dermal fibroblasts as well as extend lifespan of human dermal fibroblasts in vitro. In this work we identified HECW1, the gene coding for E3 ubiquitin ligase NEDL1, as a novel nuclear target for all FGF2 isoforms and showed that overexpression of recombinant FGF2 isoforms in human dermal fibroblasts can down regulate expression of HECW1 gene.
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4

Kinkl, Norbert. "Mechanisms of action of fibroblast growth factor 2 (FGF2) in rat retinal cells : photoreceptor survival and intracellular signaling." Université Louis Pasteur (Strasbourg) (1971-2008), 2001. http://www.theses.fr/2001STR13166.

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Анотація:
La dégénérescence des photorécepteurs est à l'origine de nombreuses pathologies rétiniennes aboutissant à une malvoyance voire à la cécité. Les facteurs neurotrophiques représentent une approche thérapeutique potentielle. Au cours de cette thèse nous nous sommes intéressés aux mécanismes d'actions in vitro d'un facteur neurotrophique exprimé dans la rétine, le FGF2. Afin d'étudier les effets directs du FGF2 sur la survie des photorécepteurs, nous avons mis au point un nouveau modèle de culture pure en photorécepteurs à partir de rétine jeune de rat. La pureté en photorécepteurs des cultures est > 99,5%, les cellules gliales de Müller (CGM) représentant < 0,5% de la population cellulaire. Grâce à ce modèle, nous avons montré que le FGF2 stimule la survie des photorécepteurs in vitro et qu'un autre facteur neurotrophique, l'EGF, accélère leur dégénérescence, en activant leurs récepteurs respectifs à activité tyrosine kinase. Les FGFR1-4 ainsi que différentes protéines impliquées dans la transduction du signal du FGF2 (ERK1/2, MEK1, MEK2, PLCg1, SHPTP-2, SOS1, SOS2, Grb2, Shc, Akt), sont exprimés de façon ubiquitaire, mais possèdent des niveau d'expression distinct, selon les différentes populations de cellules rétiniennes (photorécepteurs, rétine interne et CGM) in vivo et in vitro. Néanmoins, le FGF2 y induit des cascades de signalisation distinctes. Ceci indique l'existence de différentes voies de transduction du signal au FGF2 dans la rétine aboutissant toutes à l'activation de ERK1/2. L'inhibition pharmacologique de MEK bloque l'activation de ERK1/2 dans les photorécepteurs et inhibe leur survie induit par le FGF2, alors qu'au niveau des cellules de la rétine interne et des CGM, le FGF2 stimule également des voies d'activation de ERK1/2 indépendantes de MEK. L'ensemble de ces résultats apporte des données originales concernant les effets du FGF2 sur la survie des photorécepteurs ainsi que sur sa signalisation dans la rétine de rat in vitro, et pourrait contribuer à une application potentielle du FGF2 dans une approche clinique.
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5

Hedlund, Eva-Maria. "Molecular mechanisms of angiogenic synergism between Fibroblast Growth Factor-2 and Platelet Derived Growth Factor-BB." Thesis, Södertörn University College, School of Life Sciences, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:sh:diva-932.

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6

RIZZO, ILARIA MARIA. "Biological role of sphingosine 1-phosphate in neuroblasts derived from otic vesicle." Doctoral thesis, Università di Siena, 2016. http://hdl.handle.net/11365/1009811.

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Анотація:
Hearing loss is a health and social problem, particularly common among older people. Deafness is associated with an irreversible loss of sensory hair cells and spiral ganglion neurons, which don’t have regenerative potential. To date, cochlear implants are the only possible therapy, even if not always effective. Therefore, there is an enormous research interest aimed at identifying factors that could prevent hearing loss. Sphingosine 1-phosphate (S1P) is a bioactive lipid involved in the regulation of many physiological and pathological processes. Most of S1P functions are mediated through a family of five G-protein coupled receptors. Cytokines and growth factors cross-talk with S1P pathway via the regulation of the expression levels and activity of the enzymes responsible for S1P production, sphingosine kinases (SK1 and SK2), and S1P receptors (S1P1-5) in different cellular types. Recently, a crucial role for S1P signaling axis has been demonstrated in hearing loss. S1P receptor 2 (S1p2) and Spinster-2 (Spns2, the S1P specific transporter) knock-out mice are deaf for defects in the stria vascularis. Nevertheless, the exact role of S1P in sensory hair cells and spiral ganglion neurons biology has not been clarified. In this study, the mouse otocyst cell line US/VOT-N33 has been used as experimental model of differentiation into neurons of the spiral ganglion. We have demonstrated that fibroblast growth factor 2 (FGF2) was able to induce the proliferation of US/VOT-N33 and to act as pro-survival factor in staurosporine-induced apoptosis. Moreover, SK1 and SK2 are required for FGF2-mediated proliferation and cell survival, measured by 3HThymidine incorporation and caspase-3 activity/cleavage assay respectively, demonstrating an involvement of S1P signaling axis in these effects. While S1P1 and S1P2 down-regulation affects proliferation, S1P receptor activation is not required for cell survival induced by FGF2. Additionally, the ERK1/2 MAPK signaling pathway was found to mediate the mitogenic action of FGF2. The cell counting of neurite-bearing cells and Western blotting analysis for Islet1/2 neuronal marker were performed to evaluate FGF2-induced neuronal differentiation of this cell line. Preliminary results showed that this effect exerted by FGF2 was reduced by concomitant addition of exogenous S1P. Furthermore, pro-differentiating role exerted by FGF2 was increased in presence of SK1 knockdown and when SPNS2 is silenced, presuming a negative role of S1P pathway in FGF2-induced neuritogenesis. Taken together, these findings demonstrate a crucial role for S1P signaling axis in proliferation and survival of otic vesicle neuroprogenitors, however further studies will be necessary in order to clarify the role of S1P pathway during the differentiation of the spiral ganglion neurons. This work could help to identify possible novel therapeutical approaches to prevent neuronal degeneration during hearing loss.
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Manning, Janet R. "Fibroblast growth factor 2-mediated cardioprotection: the kinase mediators and downstream targets of FGF2-induced protection from ischemia and reperfusion injury." University of Cincinnati / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1331296684.

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Aguiar, Rodrigo Barbosa de. "Aplicação diagnóstica e terapêutica de um novo anticorpo anti-FGF2 em processos de angiogênese em melanoma experimental." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/5/5155/tde-29102014-162446/.

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Evidências sugerem que o fator de crescimento de fibroblasto 2 (FGF2), produzido por melanomas, possui importante papel no crescimento tumoral, angiogênese e metástase. Assim, o uso de anticorpo monoclonal (mAb) que reconhece e bloqueia a atividade de FGF2 é uma abordagem a ser considerada em oncologia. O propósito desse estudo foi avaliar a aplicação diagnóstica e terapêutica de um novo anticorpo anti-FGF2, 3F12E7 IgG1, em melanoma experimental B16-F10. Para isso, camundongos C57Bl/6 foram implantados subcutaneamente (ou intravenosamente, para ensaios de metástase) com células de melanoma murino B16-F10 (5x105 células/animal). Quando tumores alcançaram 3-4 mm de diâmetro (ou 24 h pós-inóculo de células B16-F10, no caso de ensaios de metástase), camundongos foram tratados com anti-FGF2 3F12E7 IgG. Animais controle receberam igual volume do veículo ou quantidade de anticorpo controle de isotipo. Grupos: animais tratados com (1) anti-FGF2 3F12E7 IgG1; (2) ligante de CEA IgG1 (controle de isotipo); e (3) veículo. O tratamento dos camundongos portadores de tumor com anti-FGF2 IgG resultou, comparado com os controles salina e de isotipo, em uma redução no número de focos metastáticos nos pulmões (ANOVA, p < 0,05), em ensaios de metástase experimental, bem como em uma menor taxa de crescimento de tumores subcutâneos (n=7/grupo). Esse resultado é acompanhado por uma redução na densidade vascular do tumor, conforme determinado por imunomarcação para CD34 ou CD31. A captação tumoral de anti-FGF2 3F12E7 IgG foi avaliada por métodos de medicina nuclear, usando esse anticorpo radiomarcado com tecnécio-99m. Estudos SPECT/CT in vivo e de biodistribuição ex vivo revelaram que 99mTc-anti-FGF2 3F12E7 IgG pode atingir eficientemente tumores subcutâneos e metastáticos de B16-F10. Assim, esses dados sugerem que anti-FGF2 3F12E7 IgG pode ser uma estratégia antitumoral promissora para melanoma, bem como uma potencial ferramenta de imagem a ser explorada, atuando como um possível traçador para rastrear tumores FGF2-positivos e mapear esse estímulo angiogênico no microambiente tumoral. Aprovado pelo comitê de ética (CAPPesq): número 0942/09
Compelling evidence suggests that fibroblast growth factor 2 (FGF2), produced by melanomas, plays important role in tumor growth, angiogenesis and metastasis. Therefore, the use of a monoclonal antibody (mAb) that recognizes and blocks FGF2 activity is seen as an approach to be considered in oncology. The purpose of this study was to evaluate the diagnostic and therapeutic application of a new anti-FGF2 antibody, 3F12E7 IgG1, in experimental melanoma B16-F10. For this, C57Bl/6 mice were subcutaneously (or intravenously, for experimental metastasis assay) implanted with murine melanoma B16-F10 cells (5x105 cells/animal). When tumors reached 3-4 mm in diameter (or 24 h after B16-F10 cells injection, in the case of metastasis assay), mice started receiving anti-FGF2 3F12E7 IgG. Control mice received equal volume of vehicle or isotype control IgG amount. Groups: (1) anti-FGF2 3F12E7 IgG1-treated, (2) CEA-binding IgG1-treated (isotype control) and (3) vehicle-treated mice. The treatment of tumor-bearing mice with anti-FGF2 IgG, compared with saline and isotype controls, led to a reduction in the number of metastatic foci in the lungs (ANOVA test, p < 0.05), in experimental metastasis assays, as well as to a lower subcutaneous tumor growth rate (n=7 per group). This result is accompanied by a reduction in the tumor vascular density, as determined by CD34 or CD31 staining. The anti-FGF2 3F12E7 IgG tumor uptake was evaluated by nuclear medicine approaches, using this antibody radiolabeled with technetium-99m. In vivo SPECT/CT and ex vivo biodistribution studies reveled that 99mTc-anti-FGF2 IgG could efficiently achieved B16-F10 subcutaneous and metastatic tumors. Thus, these data suggest that the anti-FGF2 3F12E7 IgG may be a promising antitumor strategy for melanoma, as well as a potential imaging tool to be explored, working as a possible tracer to identify FGF2-positive tumors and map this angiogenic stimulus in the tumor microenvironment. Ethics committee (CAPPesq) approval number 0942/09
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Adeyemo, Adeola T. "The Roles of the High and Low Molecular Weight Isoforms of Fibroblast Growth Factor 2 in Ischemia-Induced Revascularization." University of Cincinnati / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1460444581.

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Ehrenfels, Yvonne. "Mutationen in den "fibroblast growth factor" (FGF)-Rezeptorgenen FGFR 1, 2 und 3 bei primären Craniosynostosen." [S.l.] : [s.n.], 2000. http://deposit.ddb.de/cgi-bin/dokserv?idn=960357629.

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Книги з теми "Fibroblast growth factor 2 (FGF2)"

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Thompson, Stuart David. Fibroblast growth factor 2 and its receptor, FGFR 1 in the normal thyroid and multinodular goitre. Birmingham: University of Birmingham, 2000.

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Lyn-Cook, Richard X. Cortical development in fibroblast growth factor 2 knockout mice. [New Haven, Conn: s.n.], 1999.

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Smith, Conrad. Developmental changes in the injury induced expression of fibroblast growth factor-2 and fibroblast growth factor receptor 1 in the rat brain. Birmingham: University of Birmingham, 1998.

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Wang, David I. Kuo. The effects of fibroblast growth factor 2 on the early stages on in vitro endothelial wound repair. Ottawa: National Library of Canada, 1998.

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Clarke, Wendy Elizabeth. Intracellular compartmentalisation of fibroblast growth factor-2 and associated high and low affinity receptors after cerebral injury to the adult rat brain. Birmingham: University of Birmingham, 1999.

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Duman, Ronald S. Neurotrophic Mechanisms of Depression. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0027.

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Early theories of depression and treatment response were centered on the monoamine neurotransmitters, but more recent work has focused on functional and structural synaptic plasticity and the role of neurotrophic factors, particularly brain derived neurotrophic factor (BDNF). Neurotrophic factors regulate all aspects of neuronal function, including adaptive plasticity, synapse formation, and neuronal survival. Chronic stress and depression cause reductions in levels of BDNF and other key factors, including vascular endothelial growth factor (VEGF) and fibroblast growth factor 2 (FGF2), in cortical regions that contribute to atrophy and loss of neurons observed in depressed patients and rodent stress models. In contrast, these neurotrophic factors are upregulated by chronic administration of typical antidepressants and are required for antidepressant responses. Moreover, fast acting, highly efficacious antidepressant agents such as ketamine rapidly increase BDNF release and synapse formation, paving the way for a new generation of medications for the treatment of depression.
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Steinfeld, R. Modulation of the Interaction Between Fibroblast Growth Factor-2 and Fibroblast Growth Factor Receptor-1 by Cell Surface Heparan Sulfate Proteoglycans. Leuven University Press, 1996.

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Wang, Zhouguang, Xiaokun Li, Li Lin, Saverio Bellusci, and Jin-San Zhang, eds. The Fibroblast Growth Factor Signaling Pathway in Metabolic Regulation, Development, Disease and Repair After Injury. Frontiers Media SA, 2020. http://dx.doi.org/10.3389/978-2-88966-128-2.

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Bardin, Thomas, and Tilman Drüeke. Renal osteodystrophy. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0149.

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Renal osteodystrophy (ROD) is a term that encompasses the various consequences of chronic kidney disease (CKD) for the bone. It has been divided into several entities based on bone histomorphometry observations. ROD is accompanied by several abnormalities of mineral metabolism: abnormal levels of serum calcium, phosphorus, parathyroid hormone (PTH), vitamin D metabolites, alkaline phosphatases, fibroblast growth factor-23 (FGF-23) and klotho, which all have been identified as cardiovascular risk factors in patients with CKD. ROD can presently be schematically divided into three main types by histology: (1) osteitis fibrosa as the bony expression of secondary hyperparathyroidism (sHP), which is a high bone turnover disease developing early in CKD; (2) adynamic bone disease (ABD), the most frequent type of ROD in dialysis patients, which is at present most often observed in the absence of aluminium intoxication and develops mainly as a result of excessive PTH suppression; and (3) mixed ROD, a combination of osteitis fibrosa and osteomalacia whose prevalence has decreased in the last decade. Laboratory features include increased serum levels of PTH and bone turnover markers such as total and bone alkaline phosphatases, osteocalcin, and several products of type I collagen metabolism products. Serum phosphorus is increased only in CKD stages 4-5. Serum calcium levels are variable. They may be low initially, but hypercalcaemia develops in case of severe sHP. Serum 25-OH-vitamin D (25OHD) levels are generally below 30 ng/mL, indicating vitamin D insufficiency or deficiency. The international KDIGO guideline recommends serum PTH levels to be maintained in the range of approximately 2-9 times the upper normal normal limit of the assay and to intervene only in case of significant changes in PTH levels. It is generally recommended that calcium intake should be up to 2 g per day including intake with food and administration of calcium supplements or calcium-containing phosphate binders. Reduction of serum phosphorus towards the normal range in patients with endstage kidney failure is a major objective. Once sHP has developed, active vitamin D derivatives such as alfacalcidol or calcitriol are indicated in order to halt its progression.
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Photochemical Systematic Evolution of Ligands by Exponential Enrichment (Photoselex) Employing the 5-BROMO-2'-Deoxyuridine Chromophore for the Basic Fibroblast Growth Factor Target. Storming Media, 1999.

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Частини книг з теми "Fibroblast growth factor 2 (FGF2)"

1

Baird, Andrew. "The Regulation of Basic Fibroblast Growth Factor (FGF-2) Through Limited Bioavailability." In Growth Factors and Wound Healing, 27–36. New York, NY: Springer New York, 1997. http://dx.doi.org/10.1007/978-1-4612-1876-0_3.

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Salajegheh, Ali. "Fibroblast Growth Factors (Acidic: FGF-1; Basic: FGF-2) and Its Receptors (FGFR)." In Angiogenesis in Health, Disease and Malignancy, 111–20. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-28140-7_18.

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3

Kardami, Elissavet, Karen A. Detillieux, Sarah K. Jimenez, and Peter A. Cattini. "Fibroblast Growth Factor-2." In Myocardial Ischemia, 145–66. Boston, MA: Springer US, 2006. http://dx.doi.org/10.1007/0-387-28658-6_7.

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4

Presta, Marco, Stefania Mitola, Patrizia Dell'Era, Daria Leali, Stefania Nicoli, Emanuela Moroni, and Marco Rusnati. "Fibroblast Growth Factor-2 in Angiogenesis." In Angiogenesis, 77–88. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-71518-6_7.

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Rowley, David R. "Reactive Stroma and Evolution of Tumors: Integration of Transforming Growth Factor-β, Connective Tissue Growth Factor, and Fibroblast Growth Factor-2 Activities". У Transforming Growth Factor-β in Cancer Therapy, Volume II, 475–505. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-293-9_30.

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Vogt, P. M., D. Wagner, M. Lehnhardt, A. Bosse, E. Eriksson, and H. U. Steinau. "Profile der Sekretion von Transforming Growth Factor-β 2(TGF-β 2) und Basic Fibroblast Growth Factor (bFGF) in Wundflüssigkeit chirurgischer Wunden." In Chirurgisches Forum ’95 für experimentelle und klinische Forschung, 647–52. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79621-0_131.

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Tamulewicz, Anna, and Ewaryst Tkacz. "Human Fibroblast Growth Factor 2 Hot Spot Analysis by Means of Time-Frequency Transforms." In Advances in Intelligent Systems and Computing, 147–59. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-39904-1_13.

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Guzmán-Casado, Mercedes, María M. García-Mira, Pedro Cano-Soldado, Guillermo Giménez-Gallego, Jose M. Sanchez-Ruiz, and Antonio Parody-Morreale. "Energetics of the Interaction of Human Acidic Fibroblast Growth Factor with Heparin and the Functional Analogue Myo-Inositol Hexasulfate." In Biocalorimetry 2, 133–50. Chichester, UK: John Wiley & Sons, Ltd, 2005. http://dx.doi.org/10.1002/0470011122.ch7.

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Brown, M. D., H. Walter, O. Hudlicka, F. M. Hansen-Smith, and J. B. Weiss. "Role of Fibroblast Growth Factor -2 and Endothelial Cell Stimulating Angiogenic Factor (ESAF) in Capillary Growth in Skeletal Muscles Exposed to Long-Term High Activity." In Angiogenesis, 137–47. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4757-9185-3_16.

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Reuss, Bernhard. "The Role of Fibroblast Growth Factor 2 in the Establishment and Maintenance of the Blood-Brain Barrier." In Blood-Brain Barriers, 237–46. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2007. http://dx.doi.org/10.1002/9783527611225.ch10.

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Тези доповідей конференцій з теми "Fibroblast growth factor 2 (FGF2)"

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Patel, Nisha S., and Alisa Morss Clyne. "A Computational Model of Fibroblast Growth Factor-2 Binding to Isolated and Intact Cell Surface Receptors: Effects of Fibroblast Growth Factor-2 Concentration, Flow and Delivery Mode." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80798.

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Fibroblast growth factor-2 (FGF2) plays an important role in both healthy vascular cell functions and pathogenesis in cancer, atherosclerosis and reduced perfusion in diabetes (1–4). FGF2 therapy and targeted drug delivery have great potential in the treatment of such diseases, but have had little clinical success. FGF2 binding kinetics to heparan sulfate proteoglycan (HSPG) and fibroblast growth factor receptors (FGFR) have been largely studied under static conditions (5), however FGF2 binding to endothelial cells occurs physiologically under fluid flow conditions. Understanding complex FGF2 binding kinetics would enable the development of new anti- and pro-angiogenic therapeutics. We developed a computational model of FGF2 binding to FGFR and HSPG with flow to investigate the effect of fluid flow and FGF2 delivery mode on FGF2 binding to isolated or combined binding sites.
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Miura, Kentaro, Ken-ichi Ito, Takaaki Oba, and Asumi Iesato. "Abstract 4027: Fibroblast growth factor 2 (FGF2) is associated with the development of resistance to pemetrexed in lung cancer cells." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-4027.

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Saxty, Gordon, R. Akkari, P. Angibaud, J. Arts, P. Benderitter, V. Berdini, P. Bonnet, et al. "Abstract 1361: Fragment based drug discovery of selective inhibitors of Fibroblast Growth Factor Receptor (FGFR)." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-1361.

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Gust, Kilian M., David J. McConkey, Paul K. Hegarty, Jolanta E. Bondaruk, Bogdan A. Czerniak, Colin P. Dinney, and Peter C. Black. "Abstract 234: Fibroblast growth factor receptor (FGFR)-3 as a suitable target in bladder cancer." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-234.

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Zhang, Hao, Bonnie Hylander, Charles LeVea, Elizabeth Repasky, Robert Straubinger, Alex Adjei, and Wen Wee Ma. "Abstract 1214: Effects of dovitinib on fibroblast growth factor receptor-2 (FGFR2) expressing pancreatic cancer." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1214.

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Khalil, N., Y. Xu, R. O'Connor, H. Behzad та X. Liu. "The Effects of Transforming Growth Factor-beta1 (TGF-β1) and Fibroblast Growth Factor-2 (FGF-2) on Proliferation of Fibroblasts from Lungs of Patients with Idiopathic Pulmonary Fibrosis (IPF)." У American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3466.

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Ishiwata, Toshiyuki, Yoko Matsuda, Kiyoko Kawahara, Tetsushi Yamamoto, Kiyoshi Teduka, Eiji Uchida, Murray Korc, and Zenya Naito. "Abstract 4101: Fibroblast growth factor receptor (FGFR) 2 IIIc, is a novel molecular target for suppressing pancreatic cancer cell growth and migration." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-4101.

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Yeh, Kun-Huei, Chia-Tung Shun, Chiu-Hua Kao, Yu-Lin Lin, Ying-Chun Shen, and Ann-Lii Cheng. "Abstract 1770: Overexpression of fibroblast growth factor receptor 2 (FGFR2) in gastric cancer and basis for future FGFR2-targeted cancer therapy." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1770.

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Bai, Ailin, Kristan Meetze, Nhi Y. Vo, Sriram Kollipara, Elizabeth K. Mazsa, William M. Winston, Solly Weiler, et al. "Abstract 4586: Essential role of fibroblast growth factor receptor 2 (FGFR2) in tumorigenesis of human cancers with activated FGFR2 signaling demonstrated by functional blocking antibodies." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-4586.

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Zamora, E., C. Aura, J. Perez-Garcia, L. Prudkin, A. Meire, E. Muñoz Cosuelo, J. Jimenez, et al. "Abstract P4-09-02: Concordance in fibroblast growth factor receptor 1 (FGFR1) and 2 (FGFR2) status in breast cancer during tumor progression." In Abstracts: Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 8-12, 2015; San Antonio, TX. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.sabcs15-p4-09-02.

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Звіти організацій з теми "Fibroblast growth factor 2 (FGF2)"

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Funkenstein, Bruria, and Shaojun (Jim) Du. Interactions Between the GH-IGF axis and Myostatin in Regulating Muscle Growth in Sparus aurata. United States Department of Agriculture, March 2009. http://dx.doi.org/10.32747/2009.7696530.bard.

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Growth rate of cultured fish from hatching to commercial size is a major factor in the success of aquaculture. The normal stimulus for muscle growth in growing fish is not well understood and understanding the regulation of muscle growth in fish is of particular importance for aquaculture. Fish meat constitutes mostly of skeletal muscles and provides high value proteins in most people's diet. Unlike mammals, fish continue to grow throughout their lives, although the size fish attain, as adults, is species specific. Evidence indicates that muscle growth is regulated positively and negatively by a variety of growth and transcription factors that control both muscle cell proliferation and differentiation. In particular, growth hormone (GH), fibroblast growth factors (FGFs), insulin-like growth factors (IGFs) and transforming growth factor-13 (TGF-13) play critical roles in myogenesis during animal growth. An important advance in our understanding of muscle growth was provided by the recent discovery of the crucial functions of myostatin (MSTN) in controlling muscle growth. MSTN is a member of the TGF-13 superfamily and functions as a negative regulator of skeletal muscle growth in mammals. Studies in mammals also provided evidence for possible interactions between GH, IGFs, MSTN and the musclespecific transcription factor My oD with regards to muscle development and growth. The goal of our project was to try to clarify the role of MSTNs in Sparus aurata muscle growth and in particular determine the possible interaction between the GH-IGFaxis and MSTN in regulating muscle growth in fish. The steps to achieve this goal included: i) Determining possible relationship between changes in the expression of growth-related genes, MSTN and MyoD in muscle from slow and fast growing sea bream progeny of full-sib families and that of growth rate; ii) Testing the possible effect of over-expressing GH, IGF-I and IGF-Il on the expression of MSTN and MyoD in skeletal muscle both in vivo and in vitro; iii) Studying the regulation of the two S. aurata MSTN promoters and investigating the possible role of MyoD in this regulation. The major findings of our research can be summarized as follows: 1) Two MSTN promoters (saMSTN-1 and saMSTN-2) were isolated and characterized from S. aurata and were found to direct reporter gene activity in A204 cells. Studies were initiated to decipher the regulation of fish MSTN expression in vitro using the cloned promoters; 2) The gene coding for saMSTN-2 was cloned. Both the promoter and the first intron were found to be polymorphic. The first intron zygosity appears to be associated with growth rate; 3) Full length cDNA coding for S. aurata growth differentiation factor-l I (GDF-II), a closely related growth factor to MSTN, was cloned from S. aurata brain, and the mature peptide (C-terminal) was found to be highly conserved throughout evolution. GDF-II transcript was detected by RT -PCR analysis throughout development in S. aurata embryos and larvae, suggesting that this mRNA is the product of the embryonic genome. Transcripts for GDF-Il were detected by RT-PCR in brain, eye and spleen with highest level found in brain; 4) A novel member of the TGF-Bsuperfamily was partially cloned from S. aurata. It is highly homologous to an unidentified protein (TGF-B-like) from Tetraodon nigroviridisand is expressed in various tissues, including muscle; 5) Recombinant S. aurata GH was produced in bacteria, refolded and purified and was used in in vitro and in vivo experiments. Generally, the results of gene expression in response to GH administration in vivo depended on the nutritional state (starvation or feeding) and the time at which the fish were sacrificed after GH administration. In vitro, recombinantsaGH activated signal transduction in two fish cell lines: RTHI49 and SAFI; 6) A fibroblastic-like cell line from S. aurata (SAF-I) was characterized for its gene expression and was found to be a suitable experimental system for studies on GH-IGF and MSTN interactions; 7) The gene of the muscle-specific transcription factor Myogenin was cloned from S. aurata, its expression and promoter activity were characterized; 8) Three genes important to myofibrillogenesis were cloned from zebrafish: SmyDl, Hsp90al and skNAC. Our data suggests the existence of an interaction between the GH-IGFaxis and MSTN. This project yielded a great number of experimental tools, both DNA constructs and in vitro systems that will enable further studies on the regulation of MSTN expression and on the interactions between members of the GHIGFaxis and MSTN in regulating muscle growth in S. aurata.
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Baird, Andrew. Fibroblast Growth Factor 2: An Epithelial Ductal Cell Growth Inhibitor That Drops Out in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2009. http://dx.doi.org/10.21236/ada564059.

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Baird, Andrew. Fibroblast Growth Factor 2: An Epithelial Ductal Cell Growth Inhibitor That Drops Out in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2010. http://dx.doi.org/10.21236/ada564060.

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Baird, Andrew. Fibroblast Growth Factor 2: An Epithelial Ductal Cell Growth Inhibitor That Drops Out in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2011. http://dx.doi.org/10.21236/ada564061.

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