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Journal articles on the topic 'FGF2 Signaling'

Author: Grafiati

Published: 4 June 2021

Last updated: 15 February 2022

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1

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 (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 com

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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 (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, a

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Kwabi-Addo, B., M. Ozen, and M. Ittmann. "The role of fibroblast growth factors and their receptors in prostate cancer." Endocrine-Related Cancer 11, no. 4 (2004): 709–24. http://dx.doi.org/10.1677/erc.1.00535.

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Prostate cancer is the most common malignancy in men in the USA and the second leading cause of cancer deaths. Fibroblast growth factors (FGFs), including FGF1 (acidic FGF), FGF2 (basic FGF), FGF6 and FGF8 are all expressed at increased levels in prostate cancer as paracrine and/or autocrine growth factors for the prostate cancer cells. In addition, increased mobilization of FGFs from the extracellular matrix in cancer tissues can increase the availability of FGFs to cancer cells. Prostate cancer epithelial cells express all four types of FGF receptors (FGFR-1 to -4) at variable frequencies. E

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Price, Christopher A. "Mechanisms of fibroblast growth factor signaling in the ovarian follicle." Journal of Endocrinology 228, no. 2 (2015): R31—R43. http://dx.doi.org/10.1530/joe-15-0414.

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Fibroblast growth factors (FGFs) have been shown to alter growth and differentiation of reproductive tissues in a variety of species. Within the female reproductive tract, the effects of FGFs have been focused on the ovary, and the most studied one is FGF2, which stimulates granulosa cell proliferation and decreases differentiation (decreased steroidogenesis). Other FGFs have also been implicated in ovarian function, and this review summarizes the effects of members of two subfamilies on ovarian function; the FGF7 subfamily that also contains FGF10, and the FGF8 subfamily that also contains FG

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Yeh, Brian K., Anna V. Eliseenkova, Alexander N. Plotnikov, et al. "Structural Basis for Activation of Fibroblast Growth Factor Signaling by Sucrose Octasulfate." Molecular and Cellular Biology 22, no. 20 (2002): 7184–92. http://dx.doi.org/10.1128/mcb.22.20.7184-7192.2002.

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ABSTRACT Sucrose octasulfate (SOS) is believed to stimulate fibroblast growth factor (FGF) signaling by binding and stabilizing FGFs. In this report, we show that SOS induces FGF-dependent dimerization of FGF receptors (FGFRs). The crystal structure of the dimeric FGF2-FGFR1-SOS complex at 2.6-Å resolution reveals a symmetric assemblage of two 1:1:1 FGF2-FGFR1-SOS ternary complexes. Within each ternary complex SOS binds to FGF and FGFR and thereby increases FGF-FGFR affinity. SOS also interacts with the adjoining FGFR and thereby promotes protein-protein interactions that stabilize dimerizati

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Karajannis, Matthias A., Loïc Vincent, Fan Zhang, et al. "Fibroblast Growth Factor Receptor-1 Expression and Signaling in Acute Myeloid Leukemia." Blood 104, no. 11 (2004): 4477. http://dx.doi.org/10.1182/blood.v104.11.4477.4477.

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Abstract Fibroblast growth factor receptors (FGFRs) are tyrosine kinase receptors affecting cell proliferation, motility and survival. Fibroblast growth factor 2 (FGF2, basic FGF) represents the prototype FGFR ligand. Expression of FGFRs has been demonstrated in a subset of acute myeloid leukemias (AMLs) and FGF2 is overexpressed in the bone marrow of AML patients. The role of FGF/FGFR signaling in AML however is controversial, and downstream signaling cascades activated by FGFR1 are not known. Therefore, we hypothesized that subsets of primary acute leukemic cells may express functional FGFR1

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Naimy, Hicham, Jo Ann Buczek-Thomas, Matthew A. Nugent, Nancy Leymarie, and Joseph Zaia. "Highly Sulfated Nonreducing End-derived Heparan Sulfate Domains Bind Fibroblast Growth Factor-2 with High Affinity and Are Enriched in Biologically Active Fractions." Journal of Biological Chemistry 286, no. 22 (2011): 19311–19. http://dx.doi.org/10.1074/jbc.m110.204693.

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Human fibroblast growth factor-2 (FGF2) regulates cellular processes including proliferation, adhesion, motility, and angiogenesis. FGF2 exerts its biological function by binding and dimerizing its receptor (FGFR), which activates signal transduction cascades. Effective binding of FGF2 to its receptor requires the presence of heparan sulfate (HS), a linear polysaccharide with N-sulfated domains (NS) localized at the cell surface and extracellular matrix. HS acts as a platform facilitating the formation of a functional FGF-FGFR-HS ternary complex. Crystal structures of the signaling ternary com

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Bei, M., and R. Maas. "FGFs and BMP4 induce both Msx1-independent and Msx1-dependent signaling pathways in early tooth development." Development 125, no. 21 (1998): 4325–33. http://dx.doi.org/10.1242/dev.125.21.4325.

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During early tooth development, multiple signaling molecules are expressed in the dental lamina epithelium and induce the dental mesenchyme. One signal, BMP4, has been shown to induce morphologic changes in dental mesenchyme and mesenchymal gene expression via Msx1, but BMP4 cannot substitute for all the inductive functions of the dental epithelium. To investigate the role of FGFs during early tooth development, we examined the expression of epithelial and mesenchymal Fgfs in wild-type and Msx1 mutant tooth germs and tested the ability of FGFs to induce Fgf3 and Bmp4 expression in wild-type an

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Kumar, Karthiga Santhana, Cyrill Brunner, Matthias Schuster, et al. "MODL-14. SMALL MOLECULE TARGETING OF ONCOGENIC FGF2-FGFR SIGNALING IN BRAIN TUMORS." Neuro-Oncology 22, Supplement_3 (2020): iii413—iii414. http://dx.doi.org/10.1093/neuonc/noaa222.588.

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Abstract FGF2, the ligand of FGF receptors (FGFRs), is expressed in the developing and adult brain. FGF2-FGFR1 signaling causes the induction and maintenance of cancer stem cells through ERK-dependent up-regulation of ZEB1 and Olig2 in glioblastoma. In SHH medulloblastoma, Olig2 triggers tumor initiation from GCPs, maintains quiescent stem-like cells during the disease and contributes to tumor outgrowth at recurrence. We found that FGF2-FGFR signaling causes increased growth and tissue invasion through the FGFR adaptor protein FRS2 in SHH and group-3 medulloblastoma 1. Thus, targeting of FGFR-

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Dettmer, Rabea, Karsten Cirksena, Julia Münchhoff, et al. "FGF2 Inhibits Early Pancreatic Lineage Specification during Differentiation of Human Embryonic Stem Cells." Cells 9, no. 9 (2020): 1927. http://dx.doi.org/10.3390/cells9091927.

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Growth factors are important regulators during organ development. For many vertebrates (but not humans) it is known how they contribute to the formation and expansion of PDX1-positive cells during pancreas organogenesis. Here, the effects of the fibroblast growth factors FGF2, FGF7, FGF10, and epidermal growth factor (EGF) on pancreas development in humans were assessed by using human pluripotent stem cells (hPSCs). During this, FGF2 was identified as a potent anti-pancreatic factor whereas FGF7, FGF10, and EGF increased the cell mass while retaining PDX1-positivity. FGF2 increased the express

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Shee, Kevin, Wei Yang, John W. Hinds, et al. "Therapeutically targeting tumor microenvironment–mediated drug resistance in estrogen receptor–positive breast cancer." Journal of Experimental Medicine 215, no. 3 (2018): 895–910. http://dx.doi.org/10.1084/jem.20171818.

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Drug resistance to approved systemic therapies in estrogen receptor–positive (ER+) breast cancer remains common. We hypothesized that factors present in the human tumor microenvironment (TME) drive drug resistance. Screening of a library of recombinant secreted microenvironmental proteins revealed fibroblast growth factor 2 (FGF2) as a potent mediator of resistance to anti-estrogens, mTORC1 inhibition, and phosphatidylinositol 3-kinase inhibition in ER+ breast cancer. Phosphoproteomic analyses identified ERK1/2 as a major output of FGF2 signaling via FGF receptors (FGFRs), with consequent up-r

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Rajendran, Ranjithkumar, Vinothkumar Rajendran, Mario Giraldo-Velasquez, et al. "Oligodendrocyte-Specific Deletion of FGFR1 Reduces Cerebellar Inflammation and Neurodegeneration in MOG35-55-Induced EAE." International Journal of Molecular Sciences 22, no. 17 (2021): 9495. http://dx.doi.org/10.3390/ijms22179495.

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Multiple sclerosis (MS) is a chronic inflammatory and degenerative disease of the central nervous system (CNS). MS commonly affects the cerebellum causing acute and chronic symptoms. Cerebellar signs significantly contribute to clinical disability, and symptoms such as tremor, ataxia, and dysarthria are difficult to treat. Fibroblast growth factors (FGFs) and their receptors (FGFRs) are involved in demyelinating pathologies such as MS. In autopsy tissue from patients with MS, increased expression of FGF1, FGF2, FGF9, and FGFR1 was found in lesion areas. Recent research using mouse models has f

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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 (2020): 4108. http://dx.doi.org/10.3390/ijms21114108.

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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

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Sun, Changye, Marco Marcello, Yong Li, David Mason, Raphaël Lévy, and David G. Fernig. "Selectivity in glycosaminoglycan binding dictates the distribution and diffusion of fibroblast growth factors in the pericellular matrix." Open Biology 6, no. 3 (2016): 150277. http://dx.doi.org/10.1098/rsob.150277.

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The range of biological outcomes generated by many signalling proteins in development and homeostasis is increased by their interactions with glycosaminoglycans, particularly heparan sulfate (HS). This interaction controls the localization and movement of these signalling proteins, but whether such control depends on the specificity of the interactions is not known. We used five fibroblast growth factors with an N-terminal HaloTag (Halo-FGFs) for fluorescent labelling, with well-characterized and distinct HS-binding properties, and measured their binding and diffusion in pericellular matrix of

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Han, Peng, Hilda Guerrero-Netro, Anthony Estienne, Binyun Cao, and Christopher A. Price. "Regulation and action of early growth response 1 in bovine granulosa cells." Reproduction 154, no. 4 (2017): 547–57. http://dx.doi.org/10.1530/rep-17-0243.

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Fibroblast growth factors (FGF) modify cell proliferation and differentiation through receptor tyrosine kinases, which stimulate the expression of transcription factors including members of the early growth response (EGR) family. In ovarian granulosa cells, most FGFs activate typical response genes, although the role of EGR proteins has not been described. In the present study, we determined the regulation of EGR mRNA by FGFs and explored the role of EGR1 in the regulation of FGF-response genes. Addition of FGF1, FGF2, FGF4 or FGF8b increased EGR1 and EGR3 mRNA levels, whereas FGF18 increased

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Rajendran, Ranjithkumar, Gregor Böttiger, Christine Stadelmann, Srikanth Karnati, and Martin Berghoff. "FGF/FGFR Pathways in Multiple Sclerosis and in Its Disease Models." Cells 10, no. 4 (2021): 884. http://dx.doi.org/10.3390/cells10040884.

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Multiple sclerosis (MS) is a chronic inflammatory and neurodegenerative disease of the central nervous system (CNS) affecting more than two million people worldwide. In MS, oligodendrocytes and myelin sheaths are destroyed by autoimmune-mediated inflammation, while remyelination is impaired. Recent investigations of post-mortem tissue suggest that Fibroblast growth factor (FGF) signaling may regulate inflammation and myelination in MS. FGF2 expression seems to correlate positively with macrophages/microglia and negatively with myelination; FGF1 was suggested to promote remyelination. In myelin

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Yang, Qi En, Mariana I. Giassetti, and Alan D. Ealy. "Fibroblast growth factors activate mitogen-activated protein kinase pathways to promote migration in ovine trophoblast cells." REPRODUCTION 141, no. 5 (2011): 707–14. http://dx.doi.org/10.1530/rep-10-0541.

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Fibroblast growth factors (FGFs) 2 and FGF10 are uterine- and conceptus-derived factors that mediate trophoblast activities in cattle and sheep. To extend our understanding of how FGFs may control peri-implantation development in ruminants, we determined whether FGF2 and FGF10 impact trophoblast cell migration. Transwell inserts containing 8 μm pores were used to examine whether FGF2 or FGF10 supplementation increased oTr1 cell migration. Supplementation with 0.5 ng/ml FGF2 or FGF10 did not affect oTr1 cell migration number, but exposure to 5 or 50 ng/ml FGF2 or FGF10 increased (P<0.05) oTr

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Boichuk, Sergei, Aigul Galembikova, Ekaterina Mikheeva, et al. "Inhibition of FGF2-Mediated Signaling in GIST—Promising Approach for Overcoming Resistance to Imatinib." Cancers 12, no. 6 (2020): 1674. http://dx.doi.org/10.3390/cancers12061674.

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Inhibition of KIT-signaling is a major molecular target for gastrointestinal stromal tumor (GIST) therapy, and imatinib mesylate (IM) is known as the most effective first-line treatment option for patients with advanced, unresectable, and/or metastatic GISTs. We show here for the first time that the inhibition of KIT-signaling in GISTs induces profound changes in the cellular secretome, leading to the release of multiple chemokines, including FGF-2. IM increased migration, invasion, and colony formation of IM-resistant GISTs in an FGF2-dependent manner, whereas the use of blocking anti-FGF2 an

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Takei, Yuichiro, Tomoko Minamizaki, and Yuji Yoshiko. "Functional Diversity of Fibroblast Growth Factors in Bone Formation." International Journal of Endocrinology 2015 (2015): 1–12. http://dx.doi.org/10.1155/2015/729352.

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The functional significance of fibroblast growth factor (FGF) signaling in bone formation has been demonstrated through genetic loss-of-function and gain-of-function approaches. FGFs, comprising 22 family members, are classified into three subfamilies: canonical, hormone-like, and intracellular. The former two subfamilies activate their signaling pathways through FGF receptors (FGFRs). Currently, intracellular FGFs appear to be primarily involved in the nervous system. Canonical FGFs such as FGF2 play significant roles in bone formation, and precise spatiotemporal control of FGFs and FGFRs at

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Martinez, Jacqueline, Nathalie Javidi-Sharifi, Isabel English, et al. "FGF2-Containing Exosomes Secreted from Bone Marrow Stromal Cells Protect Leukemia Cells from Tyrosine Kinase Inhibitors." Blood 126, no. 23 (2015): 2465. http://dx.doi.org/10.1182/blood.v126.23.2465.2465.

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Abstract Introduction. Mutational activation of kinases is a frequent event in leukemia, however resistance to kinase inhibitors remains a clinical dilemma. There is considerable evidence that proteins expressed by the bone marrow microenvironment protect leukemia cells from the effects of therapy. We previously reported that fibroblast growth factor 2 (FGF2) from bone marrow stroma protected chronic myeloid leukemia (CML) cells in a paracrine fashion. FGF2 expression was significantly increased in the marrow stroma of resistant CML patients without kinase domain mutations and resistance could

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Bates, Carlton M. "Role of fibroblast growth factor receptor signaling in kidney development." American Journal of Physiology-Renal Physiology 301, no. 2 (2011): F245—F251. http://dx.doi.org/10.1152/ajprenal.00186.2011.

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Fibroblast growth factor receptors (Fgfrs) consist of four signaling family members and one nonsignaling “decoy” receptor, Fgfr-like 1 (Fgfrl1), all of which are expressed in the developing kidney. Several studies have shown that exogenous fibroblast growth factors (Fgfs) affect growth and maturation of the metanephric mesenchyme (MM) and ureteric bud (UB) in cultured tissues. Transgenic and conditional knockout approaches in whole animals have shown that Fgfr1 and Fgfr2 (predominantly the IIIc isoform) in kidney mesenchyme are critical for early MM and UB formation. Conditional deletion of th

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House, Stacey L., Susan J. Melhorn, Gilbert Newman, Thomas Doetschman, and Jo El J. Schultz. "The protein kinase C pathway mediates cardioprotection induced by cardiac-specific overexpression of fibroblast growth factor-2." American Journal of Physiology-Heart and Circulatory Physiology 293, no. 1 (2007): H354—H365. http://dx.doi.org/10.1152/ajpheart.00804.2006.

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Elucidation of protective mechanisms against ischemia-reperfusion injury is vital to the advancement of therapeutics for ischemic heart disease. Our laboratory has previously shown that cardiac-specific overexpression of fibroblast growth factor-2 (FGF2) results in increased recovery of contractile function and decreased infarct size following ischemia-reperfusion injury and has established a role for the mitogen-activated protein kinase (MAPK) signaling cascade in the cardioprotective effect of FGF2. We now show an additional role for the protein kinase C (PKC) signaling cascade in the mediat

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Lonic, Ana, Emma F. Barry, Cindy Quach, Bostjan Kobe, Neil Saunders, and Mark A. Guthridge. "Fibroblast Growth Factor Receptor 2 Phosphorylation on Serine 779 Couples to 14-3-3 and Regulates Cell Survival and Proliferation." Molecular and Cellular Biology 28, no. 10 (2008): 3372–85. http://dx.doi.org/10.1128/mcb.01837-07.

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ABSTRACT The fibroblast growth factors (FGFs) exert their diverse (or pleiotropic) biological responses through the binding and activation of specific cell surface receptors (FGFRs). While FGFRs are known to initiate intracellular signaling through receptor tyrosine phosphorylation, the precise mechanisms by which the FGFRs regulate pleiotropic biological responses remain unclear. We now identify a new mechanism by which FGFR2 is able to regulate intracellular signaling and cellular responses. We show that FGFR2 is phosphorylated on serine 779 (S779) in response to FGF2. S779, which lies adjac

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Geng, Kang, Jing Wang, Pengfei Liu, et al. "Electrical stimulation facilitates the angiogenesis of human umbilical vein endothelial cells through MAPK/ERK signaling pathway by stimulating FGF2 secretion." American Journal of Physiology-Cell Physiology 317, no. 2 (2019): C277—C286. http://dx.doi.org/10.1152/ajpcell.00474.2018.

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Electrical stimulation (ES) is able to enhance angiogenesis by stimulating fibroblasts. Fibroblast growth factor 2 (FGF2) is an independent angiogenesis inducer. The present study aimed to evaluate the role of ES-induced FGF2 secretion in affecting angiogenesis during wound healing via the mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) signaling pathway. Fibroblasts and human umbilical vein endothelial cells (HUVECs) were exposed to ES, and the HUVECs were cocultured with ES-treated fibroblast culture solution. ES exposure showed no toxic effects on fibroblas

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Guillonneau, Xavier, Fabienne Régnier-Ricard, Olivier Laplace, et al. "Fibroblast Growth Factor (FGF) Soluble Receptor 1 Acts as a Natural Inhibitor of FGF2 Neurotrophic Activity during Retinal Degeneration." Molecular Biology of the Cell 9, no. 10 (1998): 2785–802. http://dx.doi.org/10.1091/mbc.9.10.2785.

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Fibroblast growth factors (FGF) 1 and 2 and their tyrosine kinase receptor (FGFR) are present throughout the adult retina. FGFs are potential mitogens, but adult retinal cells are maintained in a nonproliferative state unless the retina is damaged. Our work aims to find a modulator of FGF signaling in normal and pathological retina. We identified and sequenced a truncated FGFR1 form from rat retina generated by the use of selective polyadenylation sites. This 70-kDa form of soluble extracellular FGFR1 (SR1) was distributed mainly localized in the inner nuclear layer of the retina, whereas the

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Sosa, Liliana del V., Silvina Gutiérrez, Juan P. Petiti, Alicia M. Vaca, Ana L. De Paul, and Alicia I. Torres. "Cooperative effect of E2 and FGF2 on lactotroph proliferation triggered by signaling initiated at the plasma membrane." American Journal of Physiology-Endocrinology and Metabolism 305, no. 1 (2013): E41—E49. http://dx.doi.org/10.1152/ajpendo.00027.2013.

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In the present work, we investigated the effect of 17β-estradiol (E2) and basic fibroblast growth factor 2 (FGF2) on the lactotroph cell-proliferative response and the related membrane-initiated signaling pathway. Anterior pituitary mixed-cell cultures of random, cycling 3-mo-old female rats were treated with 10 nM E2, E2 membrane-impermeable conjugated BSA (E2-BSA), PPT (ERα agonist), and DPN (ERβ agonist) alone or combined with FGF2 (10 ng/ml) for 30 min or 4 h. Although our results showed that the uptake of BrdU into the nucleus of lactotrophs was not modified by E2 or FGF2 alone, a signifi

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Traer, Elie, Nathalie Javidi-Sharifi, Anupriya Agarwal, et al. "FGF2 Mediates Resistance In CML Patients In The Absence Of Kinase Domain Mutations, and Resistance Is Overcome By Ponatinib." Blood 122, no. 21 (2013): 3983. http://dx.doi.org/10.1182/blood.v122.21.3983.3983.

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Abstract Background Development of resistance to kinase inhibitors remains a challenge in chronic myeloid leukemia (CML). Kinase domain mutations are a common mechanism of resistance, yet the mechanism of resistance in the absence of mutations remains less clear. Recent evidence suggests that the bone marrow microenvironment provides a sanctuary for leukemia cells, and may be involved in mediating resistance to imatinib – particularly in the absence of BCR-ABL kinase domain mutations. We tested selected cytokines, growth factors, and extracellular matrix proteins expressed by cells in the bone

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Sabbieti, Maria Giovanna, Dimitrios Agas, Luigi Marchetti та ін. "Signaling pathways implicated in PGF2α effects on Fgf2+/+ and Fgf2−/− osteoblasts". Journal of Cellular Physiology 224, № 2 (2010): 465–74. http://dx.doi.org/10.1002/jcp.22143.

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Mansukhani, Alka, Paola Bellosta, Malika Sahni, and Claudio Basilico. "Signaling by Fibroblast Growth Factors (Fgf) and Fibroblast Growth Factor Receptor 2 (Fgfr2)–Activating Mutations Blocks Mineralization and Induces Apoptosis in Osteoblasts." Journal of Cell Biology 149, no. 6 (2000): 1297–308. http://dx.doi.org/10.1083/jcb.149.6.1297.

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Fibroblast growth factors (FGF) play a critical role in bone growth and development affecting both chondrogenesis and osteogenesis. During the process of intramembranous ossification, which leads to the formation of the flat bones of the skull, unregulated FGF signaling can produce premature suture closure or craniosynostosis and other craniofacial deformities. Indeed, many human craniosynostosis disorders have been linked to activating mutations in FGF receptors (FGFR) 1 and 2, but the precise effects of FGF on the proliferation, maturation and differentiation of the target osteoblastic cells

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Traer, Elie, Nathalie Javidi-Sharifi, Jacqueline Martinez, et al. "FGF2 from Bone Marrow Stroma Protects Acute Myeloid Leukemia Cells from the FLT3 Inhibitor Quizartinib and Facilitates Acquisition of Resistance Mutations." Blood 128, no. 22 (2016): 1080. http://dx.doi.org/10.1182/blood.v128.22.1080.1080.

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Abstract Background: Acute myeloid leukemia (AML) patients with internal tandem duplication of FLT3 (FLT3-ITD AML) routinely develop resistance to FLT3 inhibitor monotherapy. Resistance to inhibitors such as quizartinib can develop through mutation of the FLT3 kinase domain, but not all resistant patients have mutations indicating that additional mechanisms of resistance are important. Although quizartinib induces a rapid reduction of circulating leukemia blasts, residual blasts in the marrow persist, suggesting that the microenvironment protects blasts from quizartinib and may serve as a rese

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Forti, Fábio L., Érico T. Costa, Kátia M. Rocha, Miriam S. Moraes, and Hugo A. Armelin. "c-Ki-ras oncogene amplification and FGF2 signaling pathways in the mouse Y1 adrenocortical cell line." Anais da Academia Brasileira de Ciências 78, no. 2 (2006): 231–39. http://dx.doi.org/10.1590/s0001-37652006000200005.

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The mouse Y1 adrenocortical tumor cell line is highly responsive to FGF2-(Fibroblast Growth Factor 2) and possesses amplified and over-expressed c-Ki-ras proto-oncogene. We previously reported that this genetic lesion leads to high constitutive levels of activation of the c-Ki-Ras-GTP->PI3K->Akt signaling pathway (Forti et al. 2002). On the other hand, activation levels of another important pathway downstream of c-Ki-Ras-GTP, namely, Raf->MEK->ERK, remain strictly dependent on FGF2 stimulation (Rocha et al. 2003). Here we show that, first, FGF2 transiently up-regulates the c-Ki-Ras

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Zhang, Yufeng, Jianyi Li, Chohreh Partovian, Frank W. Sellke, and Michael Simons. "Syndecan-4 modulates basic fibroblast growth factor 2 signaling in vivo." American Journal of Physiology-Heart and Circulatory Physiology 284, no. 6 (2003): H2078—H2082. http://dx.doi.org/10.1152/ajpheart.00942.2001.

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Syndecan-4 is one of the principal heparan sulfate-carrying proteins on the cell surface. Unlike other members of syndecan family, syndecan-4 mediates phosphatidylinositol 4,5-bisphosphate 2 (PIP2)-dependent PKC-α activation, and overexpression of syndecan-4 in vitro results in enhanced FGF2 signaling. The present study was designed to test the functional effect of increased syndecan-4 expression in endothelial cells in transgenic mice. Several transgenic mice lines expressing syndecan-4 cDNA under control of human endothelial nitric oxide (NO) synthase (eNOS) promoter were generated. Exogenou

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Nadanaka, Satomi, and Hiroshi Kitagawa. "Exostosin-like 2 regulates FGF2 signaling by controlling the endocytosis of FGF2." Biochimica et Biophysica Acta (BBA) - General Subjects 1862, no. 4 (2018): 791–99. http://dx.doi.org/10.1016/j.bbagen.2018.01.002.

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Niger, Corinne, Atum M. Buo, Carla Hebert, Brian T. Duggan, Mark S. Williams та Joseph P. Stains. "ERK acts in parallel to PKCδ to mediate the connexin43-dependent potentiation of Runx2 activity by FGF2 in MC3T3 osteoblasts". American Journal of Physiology-Cell Physiology 302, № 7 (2012): C1035—C1044. http://dx.doi.org/10.1152/ajpcell.00262.2011.

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The gap junction protein, connexin43 (Cx43), plays an important role in skeletal biology. Previously, we have shown that Cx43 can enhance the signaling and transcriptional response to fibroblast growth factor 2 (FGF2) in osteoblasts by increasing protein kinase C-δ (PKCδ) activation to affect Runx2 activity. In the present study, we show by luciferase reporter assays that the ERK signaling cascade acts in parallel to PKCδ to modulate Runx2 activity downstream of the Cx43-dependent amplification of FGF2 signaling. The PKCδ-independent activation of ERK by FGF2 was confirmed by Western blotting,

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KREUGER, Johan, Per JEMTH, Emil SANDERS-LINDBERG, et al. "Fibroblast growth factors share binding sites in heparan sulphate." Biochemical Journal 389, no. 1 (2005): 145–50. http://dx.doi.org/10.1042/bj20042129.

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HS (heparan sulphate) proteoglycans bind secreted signalling proteins, including FGFs (fibroblast growth factors) through their HS side chains. Such chains contain a wealth of differentially sulphated saccharide epitopes. Whereas specific HS structures are commonly believed to modulate FGF-binding and activity, selective binding of defined HS epitopes to FGFs has generally not been demonstrated. In the present paper, we have identified a series of sulphated HS octasaccharide epitopes, derived from authentic HS or from biosynthetic libraries that bind with graded affinities to FGF4, FGF7 and FG

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Santolla, Maria Francesca, Adele Vivacqua, Rosamaria Lappano, et al. "GPER Mediates a Feedforward FGF2/FGFR1 Paracrine Activation Coupling CAFs to Cancer Cells Toward Breast Tumor Progression." Cells 8, no. 3 (2019): 223. http://dx.doi.org/10.3390/cells8030223.

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The FGF2/FGFR1 paracrine loop is involved in the cross-talk between breast cancer cells and components of the tumor stroma as cancer-associated fibroblasts (CAFs). By quantitative PCR (qPCR), western blot, immunofluorescence analysis, ELISA and ChIP assays, we demonstrated that 17β-estradiol (E2) and the G protein estrogen receptor (GPER) agonist G-1 induce the up-regulation and secretion of FGF2 via GPER together with the EGFR/ERK/c-fos/AP-1 signaling cascade in (ER)-negative primary CAFs. Evaluating the genetic alterations from METABRIC and TCGA datasets, we then assessed that FGFR1 is the m

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Sequeira, A., M. Gilling, T. Magalhães, C. Correia, G. Oliveira, and A. Vicente. "[P2.78]: FGF/FGFR signaling pathway in autism: Identification of a novel mutation in FGF2 gene and association of FGF2, FGFR1, FGFR2 and FGFR3 genetic variants in a Portuguese population sample." International Journal of Developmental Neuroscience 28, no. 8 (2010): 714. http://dx.doi.org/10.1016/j.ijdevneu.2010.07.208.

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Dell’Era, Patrizia, Moosa Mohammadi, and Marco Presta. "Different Tyrosine Autophosphorylation Requirements in Fibroblast Growth Factor Receptor-1 Mediate Urokinase-Type Plasminogen Activator Induction and Mitogenesis." Molecular Biology of the Cell 10, no. 1 (1999): 23–33. http://dx.doi.org/10.1091/mbc.10.1.23.

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Among the seven tyrosine autophosphorylation sites identified in the intracellular domain of tyrosine kinase fibroblast growth factor receptor-1 (FGFR1), five of them are dispensable for FGFR1-mediated mitogenic signaling. The possibility of dissociating the mitogenic activity of basic FGF (FGF2) from its urokinase-type plasminogen activator (uPA)-inducing capacity both at pharmacological and structural levels prompted us to evaluate the role of these autophosphorylation sites in transducing FGF2-mediated uPA upregulation. To this purpose, L6 myoblasts transfected with either wild-type (wt) or

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Wang, Kai, and Jing Zheng. "Signaling regulation of fetoplacental angiogenesis." Journal of Endocrinology 212, no. 3 (2011): 243–55. http://dx.doi.org/10.1530/joe-11-0296.

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During normal pregnancy, dramatically increased placental blood flow is critical for fetal growth and survival as well as neonatal birth weights and survivability. This increased blood flow results from angiogenesis, vasodilatation, and vascular remodeling. Locally produced growth factors including fibroblast growth factor 2 (FGF2) and vascular endothelial growth factor A (VEGFA) are key regulators of placental endothelial functions including cell proliferation, migration, and vasodilatation. However, the precise signaling mechanisms underlying such regulation in fetoplacental endothelium are

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Setiawan, Erif Maha Nugraha, Hyun Ju Oh, Min Jung Kim, et al. "The expression of growth factor signaling genes in co-culture IVM." Indonesian Journal of Biotechnology 22, no. 2 (2018): 98. http://dx.doi.org/10.22146/ijbiotech.27309.

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The objective of this study was to determine the expression of growth factor signaling genes in human adiposederived stem cells (ASCs), porcine oocytes, and cumulus during in vitro maturation (IVM). The human ASCs (from 2 young and 2 old donors) were used for the co-culture IVM system. The maturation rate was examined based on polar body extrusion. The expression of the growth factor signaling genes from ASCs, oocytes, and cumulus were measured using qPCR. All data were analyzed using ANOVA followed by Tukey’s test. The expression of the h-IGF1 signaling genes from human ASCs cells showed simi

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Hayashida, Maiko, Sadayuki Hashioka, Kenji Hayashida, et al. "Low Serum Levels of Fibroblast Growth Factor 2 in Gunn Rats: A Hyperbilirubinemia Animal Model of Schizophrenic Symptoms." CNS & Neurological Disorders - Drug Targets 19, no. 7 (2020): 503–8. http://dx.doi.org/10.2174/1871527319999200729153907.

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Background: Fibroblast growth factor (FGF) 2 (also referred to as basic FGF) is a multifunctional growth factor that plays a pivotal role in the pro-survival, pro-migration and pro-differentiation of neurons. Method: Because alterations in FGF2 levels are suggested to contribute to the pathogenesis schizophrenia, we investigated serum levels of FGF2 in the Gunn rat, a hyperbilirubinemia animal model of schizophrenic symptoms. Results: The enzyme-linked immunosorbent assay showed that the serum levels of FGF2 in Gunn rats were 5.09 ± 0.236 pg/mL, while those in the normal strain Wistar rats wer

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Sulpice, Eric, Marijke Bryckaert, Julie Lacour, Jean-Olivier Contreres, and Gerard Tobelem. "Platelet factor 4 inhibits FGF2-induced endothelial cell proliferation via the extracellular signal–regulated kinase pathway but not by the phosphatidylinositol 3–kinase pathway." Blood 100, no. 9 (2002): 3087–94. http://dx.doi.org/10.1182/blood.v100.9.3087.

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Abstract Platelet factor 4 (PF-4) is a member of the chemokine family with powerful antiangiogenic properties. The mechanism by which PF-4 inhibits endothelial cell proliferation is unclear. We investigated the effects of PF-4 on the intracellular signal transduction induced by basic fibroblast growth factor (FGF2). We found that PF-4 (10 μg/mL) inhibited the FGF2-induced proliferation of adrenal cortex capillary endothelial (ACE) cells. The inhibition of MEK1/2 (mitogen-activated protein kinase kinase) by PD98059 or of PI3K (phosphatidylinositol 3-kinase) by Ly294002 abolished the proliferati

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Stenhouse, Claire, Katherine M. Halloran, Makenzie G. Newton, Dana Gaddy, Larry J. Suva, and Fuller W. Bazer. "Novel mineral regulatory pathways in ovine pregnancy: I. phosphate, klotho signaling, and sodium-dependent phosphate transporters." Biology of Reproduction 104, no. 5 (2021): 1084–96. http://dx.doi.org/10.1093/biolre/ioab028.

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Abstract Appropriate mineralization of the fetal skeleton requires an excess of phosphate in the fetus compared to the mother. However, mechanisms for placental phosphate transport are poorly understood. This study aimed to identify phosphate regulatory pathways in ovine endometria and placentae throughout gestation. Suffolk ewes were bred with fertile rams upon visual detection of estrus (Day 0). On Days 9, 12, 17, 30, 70, 90, 110, and 125 of pregnancy (n = 3–14/Day), ewes were euthanized and hysterectomized. Phosphate abundance varied across gestational days in uterine flushings, allantoic f

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Manning, Janet R., Sarah O. Perkins, Elizabeth A. Sinclair, et al. "Low molecular weight fibroblast growth factor-2 signals via protein kinase C and myofibrillar proteins to protect against postischemic cardiac dysfunction." American Journal of Physiology-Heart and Circulatory Physiology 304, no. 10 (2013): H1382—H1396. http://dx.doi.org/10.1152/ajpheart.00613.2012.

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Among its many biological roles, fibroblast growth factor-2 (FGF2) acutely protects the heart from dysfunction associated with ischemia/reperfusion (I/R) injury. Our laboratory has demonstrated that this is due to the activity of the low molecular weight (LMW) isoform of FGF2 and that FGF2-mediated cardioprotection relies on the activity of protein kinase C (PKC); however, which PKC isoforms are responsible for LMW FGF2-mediated cardioprotection, and their downstream targets, remain to be elucidated. To identify the PKC pathway(s) that contributes to postischemic cardiac recovery by LMW FGF2,

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Zhou, Jian, Xiaotian Ni, Xiaojie Huang, et al. "Potential Role of Hyperglycemia in Fetoplacental Endothelial Dysfunction in Gestational Diabetes Mellitus." Cellular Physiology and Biochemistry 39, no. 4 (2016): 1317–28. http://dx.doi.org/10.1159/000447836.

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Background: Gestational diabetes mellitus (GDM) is associated with structural and functional alterations in various tissues including endothelial dysfunction. The aim of this study was to explore the effects of hyperglycemia on fibroblast growth factor 2 (FGF2)- and vascular endothelial growth factor (VEGF)-stimulated placental angiogenesis and the underlying molecular signaling mechanisms. Methods: The density of fetal placental capillaries was examined using immunohistochemistry. Human umbilical vein endothelial cells (HUVECs) derived from GDM (dHUVECs) and normal healthy patients (nHUVECs)

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Santolla, Maria Francesca, Marianna Talia, and Marcello Maggiolini. "S100A4 Is Involved in Stimulatory Effects Elicited by the FGF2/FGFR1 Signaling Pathway in Triple-Negative Breast Cancer (TNBC) Cells." International Journal of Molecular Sciences 22, no. 9 (2021): 4720. http://dx.doi.org/10.3390/ijms22094720.

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Triple-negative breast cancer (TNBC) is an aggressive breast tumor subtype characterized by poor clinical outcome. In recent years, numerous advancements have been made to better understand the biological landscape of TNBC, though appropriate targets still remain to be determined. In the present study, we have determined that the expression levels of FGF2 and S100A4 are higher in TNBC with respect to non-TNBC patients when analyzing “The Invasive Breast Cancer Cohort of The Cancer Genome Atlas” (TCGA) dataset. In addition, we have found that the gene expression of FGF2 is positively correlated

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Huh, Sung-Ho, Ligyeom Ha, and Hee-Seong Jang. "Nephron Progenitor Maintenance Is Controlled through Fibroblast Growth Factors and Sprouty1 Interaction." Journal of the American Society of Nephrology 31, no. 11 (2020): 2559–72. http://dx.doi.org/10.1681/asn.2020040401.

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BackgroundNephron progenitor cells (NPCs) give rise to all segments of functional nephrons and are of great interest due to their potential as a source for novel treatment strategies for kidney disease. Fibroblast growth factor (FGF) signaling plays pivotal roles in generating and maintaining NPCs during kidney development, but little is known about the molecule(s) regulating FGF signaling during nephron development. Sprouty 1 (SPRY1) is an antagonist of receptor tyrosine kinases. Although SPRY1 antagonizes Ret-GDNF signaling, which modulates renal branching, its role in NPCs is not known.Meth

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Tanimoto, Yukiho, Masahiko Yokozeki, Kenji Hiura, et al. "A Soluble Form of Fibroblast Growth Factor Receptor 2 (FGFR2) with S252W Mutation Acts as an Efficient Inhibitor for the Enhanced Osteoblastic Differentiation Caused by FGFR2 Activation in Apert Syndrome." Journal of Biological Chemistry 279, no. 44 (2004): 45926–34. http://dx.doi.org/10.1074/jbc.m404824200.

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Apert syndrome is an autosomal dominant disease characterized by craniosynostosis and bony syndactyly associated with point mutations (S252W and P253R) in the fibroblast growth factor receptor (FGFR) 2 that cause FGFR2 activation. Here we investigated the role of the S252W mutation of FGFR2 on osteoblastic differentiation. Osteoblastic cells derived from digital bone in two Apert patients with the S252W mutation showed more prominent alkaline phosphatase activity, osteocalcin and osteopontin mRNA expression, and mineralized nodule formation compared with the control osteoblastic cells derived

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Nishida, Takashi, Satoshi Kubota, Eriko Aoyama, Danilo Janune, Azusa Maeda, and Masaharu Takigawa. "Effect of CCN2 on FGF2-Induced Proliferation and MMP9 and MMP13 Productions by Chondrocytes." Endocrinology 152, no. 11 (2011): 4232–41. http://dx.doi.org/10.1210/en.2011-0234.

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CCN2 (also known as connective tissue growth factor) interacts with several growth factors involved in endochondral ossification via its characteristic four modules and modifies the effect of such growth factors. Presently we investigated whether CCN2 interacts with fibroblast growth factor 2 (FGF2). Solid-phase binding assay, immunoprecipitation-Western blot analysis, and surface plasmon resonance (SPR) spectroscopy revealed that the C-terminal module of CCN2 (CT) directly bound to FGF2 with a dissociation constant of 5.5 nm. Next, we examined the combinational effects of CCN2 and FGF2 on the

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Giuliani, R., M. Bastaki, D. Coltrini, and M. Presta. "Role of endothelial cell extracellular signal-regulated kinase1/2 in urokinase-type plasminogen activator upregulation and in vitro angiogenesis by fibroblast growth factor-2." Journal of Cell Science 112, no. 15 (1999): 2597–606. http://dx.doi.org/10.1242/jcs.112.15.2597.

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Downstream signaling triggered by the binding of fibroblast growth factor-2 (FGF2) to its tyrosine-kinase receptors involves the activation of mitogen-activated protein kinase kinase (MEK) with consequent phosphorylation of extracellular signal-regulated kinases (ERKs). Here we demonstrate that FGF2 induces ERK1/2 activation in bovine aortic endothelial (BAE) cells and that the continuous presence of the growth factor is required for sustained ERK1/2 phosphorylation. This is prevented by the MEK inhibitors PD 098059 and U0126, which also inhibit FGF2-mediated upregulation of urokinase-type pla

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