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Littérature scientifique sur le sujet « Fibroblast Growth Factor 2 »

Auteur : Grafiati

Publié le 4 juin 2021

Mis à jour le 18 février 2022

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Articles de revues sur le sujet "Fibroblast Growth Factor 2"

Nugent, Matthew A., et Renato V. Iozzo. « Fibroblast growth factor-2 ». International Journal of Biochemistry & ; Cell Biology 32, n^o 2 (février 2000) : 115–20. http://dx.doi.org/10.1016/s1357-2725(99)00123-5.

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Okada-Ban, Mai, Jean Paul Thiery et Jacqueline Jouanneau. « Fibroblast growth factor-2 ». International Journal of Biochemistry & ; Cell Biology 32, n^o 3 (mars 2000) : 263–67. http://dx.doi.org/10.1016/s1357-2725(99)00133-8.

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EL-HARIRY, IMAN, MASSIMO PIGNATELLI et NICHOLAS LEMOINE. « FIBROBLAST GROWTH FACTOR 1 AND FIBROBLAST GROWTH FACTOR 2 IMMUNOREACTIVITY IN GASTROINTESTINAL TUMOURS ». Journal of Pathology 181, n^o 1 (janvier 1997) : 39–45. http://dx.doi.org/10.1002/(sici)1096-9896(199701)181:1<39 ::aid-path711>3.0.co;2-c.

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Kardami, Elissavet, Karen Detillieux, Xin Ma, Zhisheng Jiang, Jon-Jon Santiago, Sarah K. Jimenez et Peter A. Cattini. « Fibroblast growth factor-2 and cardioprotection ». Heart Failure Reviews 12, n^o 3-4 (22 mai 2007) : 267–77. http://dx.doi.org/10.1007/s10741-007-9027-0.

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Wakulich, Candice, Linda Jackson-Boeters, Tom D. Daley et George P. Wysocki. « Immunohistochemical localization of growth factors fibroblast growth factor-1 and fibroblast growth factor-2 and receptors fibroblast growth factor receptor-2 and fibroblast growth factor receptor-3 in normal oral epithelium, epithelial dysplasias, and squamous cell carcinoma ». Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontology 93, n^o 5 (mai 2002) : 573–79. http://dx.doi.org/10.1067/moe.2002.124461.

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Malot, Michel, Edith Browaeys-Poly, Franck Foumiertjt, Katia Cailliaul et Jean Pierre Vilain. « Ca2+Oscillations induced by fibroblast growth factor 2 inXenopusoocytes expressing fibroblast growth factor receptors ». Molecular Membrane Biology 14, n^o 4 (janvier 1997) : 205–10. http://dx.doi.org/10.3109/09687689709048183.

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Ridyard, Marc S., et Stephen M. Robbins. « Fibroblast Growth Factor-2-induced Signaling through Lipid Raft-associated Fibroblast Growth Factor Receptor Substrate 2 (FRS2) ». Journal of Biological Chemistry 278, n^o 16 (5 février 2003) : 13803–9. http://dx.doi.org/10.1074/jbc.m210245200.

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Taurustya, Hernita, Mae Sri Hartati Wahyuningsih et Indwiani Astuti. « Ethanolic Extract of Nerium indicum Mill. Decreases Transforming Growth Factor Beta-1 and Vascular Endothelial Growth Factor Expressions in Keloid Fibroblasts ». Open Access Macedonian Journal of Medical Sciences 8, A (15 avril 2020) : 297–301. http://dx.doi.org/10.3889/oamjms.2020.4292.

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BACKGROUND: Keloid is a benign fibroproliferative dermis tumor characterized by an increase in growth factors which induce fibroblast proliferation, excessive migration, and synthesis of collagen. Nerium indicum Mill. extract had been studied as a keloid therapy agent. 5α-oleandrin contained in N. indicum has antikeloid activity by inhibiting keloid fibroblast proliferation, fibroblast migration, collagen deposition, and transforming growth factor beta-1 (TGF-β1) synthesis. OBJECTIVE: This study aimed to determine the effect of administration of N. indicum extract on TGF-β1 and vascular endothelial growth factor (VEGF) expression in keloid fibroblast. METHODS: This research was a quasi-experimental research with a post-test only control group design. The research subjects were fibroblast cells passage IV-VII isolated from patients’ keloid tissue with explant techniques. Treatment groups received N. indicum extract with a serial concentration of 2 μg/ml, 1 μg/ml, and 0.5 μg/ml, and control group received medium only. The supernatant was obtained after 72 h incubation period. Examination of TGF-β1 and VEGF expressions was performed using ELISA procedure. RESULT: The expression of TGF-β1 in the treatment groups of the extract N. indicum (2 μg/ml, 1 μg/ml, and 0.5 μg/ml) was significantly lower than a control group of keloid fibroblasts (p < 0.05), according to increased concentration. VEGF expression in the treatment groups of N. indicum extract was lower compared to the control group of keloid fibroblasts. A significant decrease in keloid fibroblast VEGF levels occurred at extract concentrations of 2 μg/ml and 1 μg/ml (p < 0.05). CONCLUSION: N. indicum extract could decrease TGF-β1 and VEGF expressions compared to control medium in keloid fibroblast cultures.

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Bikfalvi, A. « Biological Roles of Fibroblast Growth Factor-2 ». Endocrine Reviews 18, n^o 1 (1 février 1997) : 26–45. http://dx.doi.org/10.1210/er.18.1.26.

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Bikfalvi, Andreas, Sharon Klein, Giuseppe Pintucci et Daniel B. Rifkin. « Biological Roles of Fibroblast Growth Factor-2* ». Endocrine Reviews 18, n^o 1 (1 février 1997) : 26–45. http://dx.doi.org/10.1210/edrv.18.1.0292.

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Thèses sur le sujet "Fibroblast Growth Factor 2"

Prabhudesai, Shirish G. « Fibroblast growth factor-2, chemoresistance and colorectal cancer ». Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/10163.

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Introduction: The role of fibroblast growth factor-2 (FGF-2) on colorectal cancer (CRC) cells exposed to chemotherapy has not been studied extensively. This thesis investigated whether FGF-2 mediates chemoresistance in primary (SW480) and metastatic (SW620) colon adenocarcinoma cell lines. Methods: Proliferation assays were used to assess the response of SW480 and SW620 colon cancer cell lines to varying concentrations of FGF-2 and to optimise the dose of 5- FU at which 50% cell death was observed. Cell survival assays were performed following 96 hours exposure to 5-FU ± FGF-2. Levels of chemotherapy induced apoptosis were determined using Caspase-3/7 assay. Expression of anti-apoptotic proteins (Bcl-2 and Bcl-XL) and FGFRs at both protein and gene level were determined to see if these contributed to the difference in chemoprotection observed. Results: At 0.25 ng/ml, FGF-2 did not affect proliferation in either cell lines. 25μM of 5-FU resulted in 50% kill in both cell lines. Significant cell survival was observed when FGF-2 (0.25 ng/ml) pre-treated SW620 cells were exposed to 5-FU (25 μM) compared to cells exposed to 5-FU alone (81% vs 60%, p=0.015). This chemoresistance was associated with attenuation of cellular apoptosis (p=0.04) with no significant change in expression of Bcl-2 and Bcl-XL at gene or protein level. This survival advantage was not seen in SW480 cells (59% vs 55%, p=0.35). There were no observed differences in the expression of FGFR1-4 in either cell lines. Conclusion: FGF-2 offers chemoresistance to SW620 and not to SW480 cells exposed to 5-FU. Both cell lines expressed fgf2 and fgfr1-4 genes, suggesting that fgfr expression does not account for the difference in chemoresistance. FGF-2 offered protection by causing significant reduction in chemotherapy induced apoptosis in SW620 colon cancer cell line; however this was not due to increased expression of anti-apoptotic proteins. The molecular mechanisms for this selective chemoprotection need to be investigated further.

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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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Shi-Lu, Chia. « The role of fibroblast growth factor-2 in articular cartilage degradation ». Thesis, Imperial College London, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.501425.

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Osteoarthritis (OA) is the most common form of joint disease and a leading cause of physical disability woridwide. Cartilage degradation in OA is due to an imbalance between synthesis and degradation of the extracellular matrix. Recent work from our laboratory has shown that the heparin-binding growth factor fibroblast growth factor2 (FGF-2) mediates key responses in cartilage following mechanical trauma and loading. It has also been shown that FGF-2 is localised within the pericellular matrix, attached to the heparan sulphate proteoglycan perlecan. The spatial modulator of chondrocyte function. The primary aim of this research was to define the role of FGF-2 in cartilage degradation in vivo. Mice with deletion of Fgf2, whilst morphologically indistinguishable from wild-type animals, exhibited accelerated spontaneous and surgically-induced OA. Surgically-induced OA in Fgf2 mice was suppressed to wild type levels by subcutaneous administration of recombinant FGF-2. Increased disease in Fgf2 mice was associated with increased expression of ADAMTS-5, the key murine aggrecanase, but not other matrix metalloproteinases. Explants from Fgf2 mice showed increased aggrecanolysis and ADAMTS-5 (a disintegrin and metalloproteinase with thrombospondin motif, type 5; aggrecanase-2) gene expression following interleukin-1 (IL-1) stimulation, and exogenous FGF-2 suppressed IL-1 induced aggrecanolysis in wild-type explants. These data identify FGF-2 as a novel endogenous chondroprotective agent, and as an inhibitor of aggrecan breakdown acting through suppression of ADAMTS-5.

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Vailes, McCauley T. « Post-Transfer Outcomes in Cultured Bovine Embryos Supplemented with Epidermal Growth Factor, Fibroblast Growth Factor 2, and Insulin-Like Growth Factor 1 ». Thesis, Virginia Tech, 2017. http://hdl.handle.net/10919/86273.

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The high incidence of pregnancy loss is a major issue facing the cattle industry. Use of in vitro fertilized (IVF) bovine embryos has become increasingly popular to help alleviate several of these reproductive issues and provide a means to enhance genetic gain for production traits. An uterine paracrine factor cocktail containing epidermal growth factor (EGF), fibroblast growth factor 2 (FGF2), and insulin-like growth factor 1 (IGF1) (collectively termed EFI) was recently identified as a means for improving in vitro derived bovine embryo development and trophectoderm cell numbers. The objectives of this work were to determine if EFI treatment during in vitro bovine embryo culture improves transferable embryo quality and post-transfer placental and fetal development. For each replicate (3 total), slaughterhouse-derived bovine oocytes were matured and fertilized in vitro. At day 4 post-fertilization, ≥8 cell embryos were harvested, pooled, and exposed to either the EFI treatment (10ng/ml EGF, 10ng/ml FGF2, 50ng/ml IGF1) or carrier only (1% Bovine Serum Albumin). At day 7, individual embryos were transferred to estrous synchronized beef cattle. Artificial insemination (AI) was completed on a subset of cows. The EFI treatment increased (P<0.05) the percentage of transferable embryos. Pregnancy rate at day 28 post-estrus was similar among treatments. Circulating concentrations of pregnancy-associated glycoproteins (PAGs) were determined from plasma harvested at day 28, 42 and 56. Transrectal ultrasonography was used to measure fetal crown-rump length (CRL) at day 42 and 56 and to determine fetal sex at day 60. There were no main effect differences observed across days for PAG concentration. Fetus sex by ET/AI group interactions were absent at day 28 but existed at days 42 and 56 (P<0.05). At both days, this interaction reflected fetus sex-dependent changes within the ET control group, where PAG concentrations were greater (P<0.05) in male fetuses than female fetuses. No CRL differences or interactions existed among fetal sex and pregnancy group. In summary, addition of the EFI cocktail during bovine embryo culture improved the quality of transferable embryos, but did not affect placental function or embryonic/fetal development. Increasing the numbers of transferable embryos is of value given the cost of in vitro embryo production, but no apparent increases in embryo or placental competency were detected. The EFI treatment increased (P<0.05) the percentage of transferable embryos.
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Dinsdale, Jennifer Anne. « In vivo effects of fibroblast growth factor - 2 on oligodendrocytes and myelin ». Thesis, King's College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.407573.

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Hannocks, Melanie-Jane. « The effects of fibroblast growth factor-2 om human bone marrow cells ». Doctoral thesis, University of Cape Town, 2003. http://hdl.handle.net/11427/2836.

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Boulle, Nathalie. « Analyse du système des insulin-like growth factors (IGF) et du fibroblast growth factor-2 (FGF-2) dans la tumorigenèse corticosurrenalienne ». Paris 11, 2000. http://www.theses.fr/2000PA11T006.

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Dans les tumeurs corticosurrénaliennes, des anomalies de la région 11p15 et une surexpression du gène d'IGF-11 sont contemporaines de l'acquisition du phénotype malin. Nous montrons que la surexpression du gène IGF-11 dans les tumeurs corticosurrénaliennes malignes s'accompagne d'une traduction efficace de la protéine, majoritairement sous forme de précurseurs d'IGF-11. Ces mêmes tumeurs surexpriment de manière spécifique IGFBP-2, protéine de liaison des IGF fréquemment associée à la prolifération tumorale. La caractérisation de la lignée H295R, dérivée d'un carcinome surrénalien, montre que celle-ci surexprime IGF-11 et IGFBP-2 et constitue un bon modèle in vitro d'ét•ude de la tumorigénèse corticosurrénalienne. Cette lignée a permis de démontrer qu'IGF-11 était impliqué dans la prolifération des cellules tumorales corticosurrénaliennes via le récepteur de type 1 des IGF. L'intérêt de I'IGFBP-2 plasmatique en tant que marqueur circulant des tumeurs corticosurrénaliennes malignes a été évalué. Nous montrons que les taux d'IGFBP-2 plasmatique s'élèvent spécifiquement chez les patients porteurs de tumeurs malignes mais que cette élévation survient à lin stade avancé de la maladie (stade métastatique), indiquant la faible sensibilité d'IGFBP-2 et son intérêt limité comme marqueur des carcinomes surrénaliens. Les effets de FGF-2 sur les cellules tumorales corticosurrénaliennes ont également été étudiés. Nos résultats montrent que FGF-2 a un effet prolifératif sur les cellules H295R mais que paradoxalement, il inhibe l'expression du système des IGF par ces cellules. L'inhibition d'IGFBP-2 se fait au niveau transcriptionnel, alors que celle d'IGF-11 est post-transcriptionnelle, par inhibition de la maturation des précurseurs d'IGF-11. Ainsi, si IGF-11 a un rôle indiscutable au stade tardif de la tumorigénèse corticosurrénalienne, différents facteurs sont susceptibles de moduler son expression (FGF-2) ou son activité (IGFBP-2) au sein du tissu tumoral
Ln adrenocortical tumors, malignant phenotype is associated with abnormalities at the 11p15 locus and overexpression of the IGF-11 gene. Here, we show that IGF-11 mRNA is efficiently translated and that malignant adrenocortical tumors contain large amounts of IGF-11 protein, mainly in its prohormone form. The same tumors exhibit a high content in IGFBP-2 protein, an IGFBP being frequently expressed in tumor cells. The H295R cell line, which is derived from a human adrenal carcinoma, express high levels of both IGF-11 and IGFBP-2 and represents a suitable in vitro model to study adrenocortical tumorigenesis. Using this cell line, we could demonstrate that IGF-11 is involved in the proliferation of adrenocortical tumor cells, after binding to the type 1 IGF receptor. The interest of plasma IGFBP-2 as a marker for adrenocortical carcinoma was evaluated. Our results show that high levels of IGFBP-2 are specifically detected in the plasma of patients with malignant adrenocortical tumors. However, the increase in IGFBP-2 levels occur at a late stage of tumor progression (metastatic stage). This indicates a poor sensitivity for plasma IGFBP-2, which may limit its interest as a tumor marker. We also studied the effects of FGF-2 on adrenocortical tumor cells. Our results indicate that FGF-2 is mitogenic for H295R cells, although it inhibits the expression of both IGF-11 and IGFBP-2 by these cells. The inhibition of IGFBP-2 expression occur at the transcriptional levels. Ln contrast, FGF-2 inhibits the secretion and the last steps of maturation of the IGF-11 precursor. Altogether, these results suggest that in malignant adrenocortical tumors, various factors may modulate the expression (FGF-2) or the effects (IGFBP-2) of IGF-11 on adrenocortical tumor cells

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Maucher, Tobias [Verfasser]. « Regulation des glialen Glutamattransports durch den Wachstumsfaktor ''Fibroblast growth factor 2'' (FGF-2) / Tobias Maucher ». Ulm : Universität Ulm. Medizinische Fakultät, 2004. http://d-nb.info/1015438520/34.

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SAKANAKA, MASAHIRO, SHIGERU KOBAYASHI, MINORU UEDA, TOSHIO SHIGETOMI, KENICHI KOSAKI, HIDEAKI KAGAMI et YOSHIYUKI HIRAMATSU. « THE LOCALIZATION OF BASIC FIBROBLAST GROWTH FACTOR (FGF-2) IN RAT SUBMANDIBULAR GLANDS ». Nagoya University School of Medicine, 1994. http://hdl.handle.net/2237/16076.

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Wagner, Andreas. « Identifizierung von Genen, die durch fibroblast growth factor receptor 2 (FGFR2) reguliert werden ». [S.l.] : [s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=961705361.

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Livres sur le sujet "Fibroblast Growth Factor 2"

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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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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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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Burgar, Helen Rachel. Fibroblast growth factor receptor signalling. Birmingham : University of Birmingham, 2002.

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Walters, Jean Elizabeth. Immunochemical studies on fibroblast growth factor-1 and fibroblast growth factor receptor 1. Oxford : Oxford Brookes University, 1998.

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Cocks, Helen Catherine. Fibroblast growth factor in the thyroid. Birmingham : University of Birmingham, 2003.

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Daley, Sandra J. Basic fibroblast growth factor mediates neointimal formation in porcine aortic explants. Ottawa : National Library of Canada = Bibliothèque nationale du Canada, 1997.

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Plowright, Elizabeth Emma. Expression of fibroblast growth factor receptor 3 in multiple myeloma causes II-6-independence and enhanced survival. Ottawa : National Library of Canada, 1999.

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Chapitres de livres sur le sujet "Fibroblast Growth Factor 2"

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

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

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Cronauer, Marcus V., et Wolfgang A. Schulz. « Fibroblast Growth Factors ». Dans Encyclopedia of Cancer, 1–2. Berlin, Heidelberg : Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_2175-2.

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Baird, Andrew. « The Regulation of Basic Fibroblast Growth Factor (FGF-2) Through Limited Bioavailability ». Dans 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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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 ». Dans 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 et 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 ». Dans 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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Guzmán-Casado, Mercedes, María M. García-Mira, Pedro Cano-Soldado, Guillermo Giménez-Gallego, Jose M. Sanchez-Ruiz et Antonio Parody-Morreale. « Energetics of the Interaction of Human Acidic Fibroblast Growth Factor with Heparin and the Functional Analogue Myo-Inositol Hexasulfate ». Dans Biocalorimetry 2, 133–50. Chichester, UK : John Wiley & Sons, Ltd, 2005. http://dx.doi.org/10.1002/0470011122.ch7.

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Tamulewicz, Anna, et Ewaryst Tkacz. « Human Fibroblast Growth Factor 2 Hot Spot Analysis by Means of Time-Frequency Transforms ». Dans 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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Salajegheh, Ali. « Fibroblast Growth Factors (Acidic : FGF-1 ; Basic : FGF-2) and Its Receptors (FGFR) ». Dans 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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Reuss, Bernhard. « The Role of Fibroblast Growth Factor 2 in the Establishment and Maintenance of the Blood-Brain Barrier ». Dans 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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Actes de conférences sur le sujet "Fibroblast Growth Factor 2"

Guzy, R., B. Ansbro, E. Reed et N. O. Dulin. « Fibroblast Growth Factor 2 Accelerates Myofibroblast Dedifferentiation in Primary Human Lung Fibroblasts ». Dans American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a4042.

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Patel, Nisha S., et 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 ». Dans 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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Feng, Shu, Wendong Yu, Yi Cai, Jianghua Wang, Patricia D. Castro et Michael M. Ittmann. « Abstract 1106 : Fibroblast growth factor FGF19 signaling promotes prostate cancer progression ». Dans 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.am2011-1106.

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Zenya, Naito, Yoko Matsuda, Wei-Xia Peng, Kazuya Yamahatsu, Junji Ueda, Yoko Kawamoto, Kiyoshi Teduka, Tomoko Seya, Yoshiharu Ohaki et Toshiyuki Ishiwata. « Abstract 1194 : Fibroblast growth factor receptor 2 as a novel therapeutic target for colorectal cancer cell growth ». Dans 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.am2011-1194.

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Kalghatgi, S. U., A. Fridman, G. Friedman et A. Morss Clyne. « Non-thermal plasma enhances endothelial cell proliferation through fibroblast growth factor-2 release ». Dans 2009 IEEE 36th International Conference on Plasma Science (ICOPS). IEEE, 2009. http://dx.doi.org/10.1109/plasma.2009.5227716.

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Morss, Alisa, Michael Jonas et Elazer R. Edelman. « Elevated Basement Membrane Fibroblast Growth Factor-2 Protects Endothelial Cells in High Glucose ». Dans ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176187.

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Vascular disease is the primary cause of morbidity and mortality in diabetics. Diabetic vascular disease is disseminated and includes renal capillary hypertrophy, reduced wound repair, impaired angiogenesis, and rapid and excessive hyperplasia after endovascular intervention [1, 2]. No single biochemical aberration unifies the diffuse nature of diabetic vascular disease. Hyperglycemia has been implicated, and yet glucose effects persist long after restoration of euglycemia. It is possible that acute fluctuations in glucose concentration have prolonged cell and tissue effects.

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Khalil, N., Y. Xu, R. O'Connor, H. Behzad et 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). » Dans 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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Kage, Hidenori, Yosuke Amano, Rie Ishikawa, Mitsuhiro Sunohara, Masanori Kawakami, Noriko Emoto, Kousuke Watanabe et al. « Crosstalk Between Alveolar Epithelial Cells And Fibroblasts Through Transforming Growth Factor B1 And Prostaglandin Synthase 2 Results In Suppression Of Fibroblast Growth ». Dans American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3497.

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Sun, Liwei, Hao Feng, Rui Jiang, Liping Niu, Yu Song, Kai Feng et Chao Qi. « The effects of Ce3+and Ce4+on the stability of fibroblast growth factor-2 ». Dans Photonics Asia 2010, sous la direction de Qingming Luo, Ying Gu et Xingde Li. SPIE, 2010. http://dx.doi.org/10.1117/12.868223.

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Gust, Kilian M., David J. McConkey, Paul K. Hegarty, Jolanta E. Bondaruk, Bogdan A. Czerniak, Colin P. Dinney et Peter C. Black. « Abstract 234 : Fibroblast growth factor receptor (FGFR)-3 as a suitable target in bladder cancer ». Dans 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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Rapports d'organisations sur le sujet "Fibroblast Growth Factor 2"

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, octobre 2009. http://dx.doi.org/10.21236/ada564059.

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Welling, Bradley. Fibroblast Growth Factor Regeneration of Tympanic Membrane Perforations. Fort Belvoir, VA : Defense Technical Information Center, octobre 2013. http://dx.doi.org/10.21236/ada591173.

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Ittmann, Michael M. Fibroblast Growth Factor Receptor-4 and Prostate Cancer Progression. Fort Belvoir, VA : Defense Technical Information Center, octobre 2005. http://dx.doi.org/10.21236/ada446482.

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Ittmann, Michael M. Fibroblast Growth Factor Receptor-4 and Prostate Cancer Progression. Fort Belvoir, VA : Defense Technical Information Center, octobre 2006. http://dx.doi.org/10.21236/ada462818.

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Ittmann, Michael M. Fibroblast Growth Factor Receptor-4 and Prostate Cancer Progression. Fort Belvoir, VA : Defense Technical Information Center, octobre 2007. http://dx.doi.org/10.21236/ada476956.

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Kagan, Benjamin L. Growth Factor Regulation of an Angiogenic Factor, the Fibroblast Growth Factor-Binding Protein (FGF-BP), in Breast Cancer. Fort Belvoir, VA : Defense Technical Information Center, août 2001. http://dx.doi.org/10.21236/ada398106.

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Wieder, Robert. The Role of Basic Fibroblast Growth Factor in Human Breast Cancer. Fort Belvoir, VA : Defense Technical Information Center, septembre 1995. http://dx.doi.org/10.21236/ada302241.

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