Relevant bibliographies by topics / FGFBP1

Academic literature on the topic 'FGFBP1'

Author: Grafiati
Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "FGFBP1"

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Zhang, Zheng, Yi Qin, Shunrong Ji, Wenyan Xu, Mengqi Liu, Qiangsheng Hu, Zeng Ye, et al. "FGFBP1-mediated crosstalk between fibroblasts and pancreatic cancer cells via FGF22/FGFR2 promotes invasion and metastasis of pancreatic cancer." Acta Biochimica et Biophysica Sinica 53, no. 8 (June 12, 2021): 997–1008. http://dx.doi.org/10.1093/abbs/gmab074.

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Abstract Fibroblast growth factor-binding protein 1 (FGFBP1) promotes fibroblast growth factor (FGF) activity by releasing FGFs from extracellular matrix storage. We previously reported that the tumor suppressor F-box and WD repeat domain-containing 7 suppresses FGFBP1 by reducing expression of c-Myc, which inhibits the proliferation and migration of pancreatic cancer cells. However, the potential mechanism by which FGFBP1 facilitates pancreatic ductal adenocarcinoma (PDAC) remains unexplored. In this study, we focused on the function of FGFBP1 in the interplay between cancer-associated fibroblasts (CAFs) and pancreatic cancer cells (PCCs). Decreased FGF22 expression was detected in CAFs co-cultured with PCCs with FGFBP1 abrogation, which was verified in the cell culture medium by enzyme-linked immunosorbent assay. Active cytokine FGF22 significantly facilitated the migration and invasion of PANC-1 and Mia PaCa-2 cells. The number of penetrating PCCs cocultured with CAFs with FGF22 abrogation was significantly less than that of the control group. Interestingly, higher expressions of FGF22 and fibroblast growth factor receptor 2 (FGFR2) were associated with worse prognosis of patients with PDAC and FGFR2, an independent prognostic marker of PDAC. The PANC-1 and Mia PaCa-2 cells with silenced FGFR2 showed weaker invasion and metastasis, even if these cells were simultaneously treated with cytokine FGF22. These results revealed that FGFBP1-mediated interaction between CAFs and PCCs via FGF22/FGFR2 facilitates the migration and invasion of PCCs. FGFR2 could act as a prognostic marker for patients with PDAC.
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Cottarelli, Azzurra, Monica Corada, Galina V. Beznoussenko, Alexander A. Mironov, Maria A. Globisch, Saptarshi Biswas, Hua Huang, et al. "Fgfbp1 promotes blood-brain barrier development by regulating collagen IV deposition and maintaining Wnt/β-catenin signaling." Development 147, no. 16 (August 3, 2020): dev185140. http://dx.doi.org/10.1242/dev.185140.

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ABSTRACTCentral nervous system (CNS) blood vessels contain a functional blood-brain barrier (BBB) that is necessary for neuronal survival and activity. Although Wnt/β-catenin signaling is essential for BBB development, its downstream targets within the neurovasculature remain poorly understood. To identify targets of Wnt/β-catenin signaling underlying BBB maturation, we performed a microarray analysis that identified Fgfbp1 as a novel Wnt/β-catenin-regulated gene in mouse brain endothelial cells (mBECs). Fgfbp1 is expressed in the CNS endothelium and secreted into the vascular basement membrane during BBB formation. Endothelial genetic ablation of Fgfbp1 results in transient hypervascularization but delays BBB maturation in specific CNS regions, as evidenced by both upregulation of Plvap and increased tracer leakage across the neurovasculature due to reduced Wnt/β-catenin activity. In addition, collagen IV deposition in the vascular basement membrane is reduced in mutant mice, leading to defective endothelial cell-pericyte interactions. Fgfbp1 is required cell-autonomously in mBECs to concentrate Wnt ligands near cell junctions and promote maturation of their barrier properties in vitro. Thus, Fgfbp1 is a crucial extracellular matrix protein during BBB maturation that regulates cell-cell interactions and Wnt/β-catenin activity.
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Zhao, Liang, Xiaoyun Cao, Lingli Li, Xiaohua Wang, Qin Wang, Shan Jiang, Chun Tang, et al. "Acute Kidney Injury Sensitizes the Brain Vasculature to Ang II (Angiotensin II) Constriction via FGFBP1 (Fibroblast Growth Factor Binding Protein 1)." Hypertension 76, no. 6 (December 2020): 1924–34. http://dx.doi.org/10.1161/hypertensionaha.120.15582.

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Acute kidney injury (AKI) causes multiple organ dysfunction. Here, we identify a possible mechanism that can drive brain vessel injury after AKI. We induced 30-minute bilateral renal ischemia-reperfusion injury in C57Bl/6 mice and isolated brain microvessels and macrovessels 24 hours or 1 week later to test their responses to vasoconstrictors and found that after AKI brain vessels were sensitized to Ang II (angiotensin II). Upregulation of FGF2 (fibroblast growth factor 2) and FGFBP1 (FGF binding protein 1) expression in both serum and kidney tissue after AKI suggested a potential contribution to the vascular sensitization. Administration of FGF2 and FGFBP1 proteins to isolated healthy brain vessels mimicked the sensitization to Ang II after AKI. Brain vessels in Fgfbp1 −/− AKI mice failed to induce Ang II sensitization. Complementary to this, systemic treatment with the clinically used FGF receptor kinase inhibitor BGJ398 (Infigratinib) reversed the AKI-induced brain vascular sensitization to Ang II. All these findings lead to the conclusion that FGFBP1 is especially necessary for AKI-mediated brain vascular sensitization to Ang II and inhibitors of FGFR pathway may be beneficial in preventing AKI-induced brain vessel injury.
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Gardela, Jaume, Mateo Ruiz-Conca, Dominic Wright, Manel López-Béjar, Cristina A. Martínez, Heriberto Rodríguez-Martínez, and Manuel Álvarez-Rodríguez. "Semen Modulates Cell Proliferation and Differentiation-Related Transcripts in the Pig Peri-Ovulatory Endometrium." Biology 11, no. 4 (April 18, 2022): 616. http://dx.doi.org/10.3390/biology11040616.

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Uterine homeostasis is maintained after mating by eliminating pathogens, foreign cells, and proteins by a transient inflammation of the uterus. Such inflammation does not occur in the oviductal sperm reservoir (utero-tubal junction, UTJ), colonized by a population of potentially fertile spermatozoa before the inflammatory changes are triggered. Semen entry (spermatozoa and/or seminal plasma) modifies the expression of regulatory genes, including cell proliferation and differentiation-related transcripts. Considering pigs display a fractionated ejaculation, this study aims to determine whether different ejaculate fractions differentially modulate cell proliferation and differentiation-related transcripts in the sow reproductive tract during the peri-ovulatory stage. Using species-specific microarray analyses, the differential expression of 144 cell proliferation and differentiation-related transcripts was studied in specific segments: cervix (Cvx), distal and proximal uterus (DistUt, ProxUt), UTJ, isthmus (Isth), ampulla (Amp), and infundibulum (Inf) of the peri-ovulatory sow reproductive tract in response to semen and/or seminal plasma cervical deposition. Most mRNA expression changes were induced by mating. In addition, while mating upregulates the fibroblast growth factor 1 (FGF1, p-value DistUt = 0.0007; ProxUt = 0.0253) transcript in the endometrium, both its receptor, the fibroblast growth factor receptor 1 (FGFR1, p-value DistUt = 2.14 e−06; ProxUt = 0.0027; UTJ = 0.0458) transcript, and a potentiator of its biological effect, the fibroblast growth factor binding protein 1 (FGFBP1), were downregulated in the endometrium (p-value DistUt = 0.0068; ProxUt = 0.0011) and the UTJ (p-value UTJ = 0.0191). The FGFBP1 was downregulated in the whole oviduct after seminal depositions (p-value Isth = 0.0007; Amp = 0.0007; Inf = 6.87 e−05) and, interestingly, FGFR1 was downregulated in the endometrium in the absence of semen (p-value DistUt = 0.0097; ProxUt = 0.0456). In conclusion, the findings suggest that spermatozoa, seminal components, and the act of mating trigger, besides inflammation, differential mechanisms in the peri-ovulatory female reproductive tract, relevant for tissue repair.
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Zhang, Wenjing, Yaxing Zhou, Chao Li, Shanshan Xu, Mengyan Li, Wenying Liu, Yuqing Ma, and Hui Wang. "The Expression and Prognostic Value of FGF2, FGFR3, and FGFBP1 in Esophageal Squamous Cell Carcinoma." Analytical Cellular Pathology 2020 (December 11, 2020): 1–17. http://dx.doi.org/10.1155/2020/2872479.

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Background. Esophageal squamous cell carcinoma was treated by operation and chemoradiotherapy. However, the prognosis of most patients is poor after treatment, and most studies have shown that FGF2 and its receptor (FGFR) are involved in the development of various malignant tumors. FGF2 plays an important role in tumor progression and malignancy. In this study, the immunohistochemistry of FGF2, FGFR3, and FGFBP1 was used to further verify the expression of the three proteins in 172 patients with esophageal squamous cell carcinoma (ESCC) who had not received preoperative chemoradiotherapy and its effect on the prognosis of ESCC. Methods. (1) χ 2 test was used to analyze the relationship between proteins and clinicopathological parameters. Survival analysis was used to investigate the effect of three proteins on prognosis. (2) Paired sample t -test was used to analyze the mRNA expression of the three proteins in fresh ESCC tissues and adjacent normal tissues. Results. FGF2 was correlated with tumor size ( p = 0.026 ), gender ( p = 0.047 ), and lymph metastasis ( p = 0.007 ) in ESCC tissues. The high expression of FGFR3 was associated with tumor differentiation ( p = 0.043 and p < 0.05 ), lymph node metastasis ( p = 0.078 and p < 0.1 ), and race ( p = 0.033 and p < 0.05 ). The high expression of FGFBP1 was significantly associated with the degree of tumor differentiation ( p = 0.012 ), age ( p = 0.045 ), and lymph node metastasis ( p = 0.032 ) of ESCC patients. The expression of FGF2, FGFR3, and FGFBP1-mRNA in ESCC tissues was significantly higher than that in adjacent tissues ( p < 0.001 , p < 0.001 , and p = 0.001 ). Patients with high expression of FGF2, FGFBP1, and FGFR3 had poor prognosis. There was a weak positive correlation between FGF2 and FGFBP1, as well as FGFR. Conclusion. The FGF2-FGFR3 axis may promote the progression of esophageal squamous cell carcinoma. The FGF2-FGFR3 axis may be a new direction of targeted therapy for esophageal squamous cell carcinoma. FGF2 and FGFR3 may be used as prognostic markers of esophageal squamous cell carcinoma.
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Felício, A. M., C. Boschiero, J. C. C. Balieiro, M. C. Ledur, J. B. S. Ferraz, A. S. A. M. T. Moura, and L. L. Coutinho. "Polymorphisms in FGFBP1 and FGFBP2 genes associated with carcass and meat quality traits in chickens." Genetics and Molecular Research 12, no. 1 (2013): 208–22. http://dx.doi.org/10.4238/2013.january.24.13.

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Tomaszewski, Maciej, Fadi J. Charchar, Christopher P. Nelson, Timothy Barnes, Matthew Denniff, Michael Kaiser, Radoslaw Debiec, et al. "Pathway Analysis Shows Association between FGFBP1 and Hypertension." Journal of the American Society of Nephrology 22, no. 5 (March 24, 2011): 947–55. http://dx.doi.org/10.1681/asn.2010080829.

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CHUNCHOB, SUPATRA, RUDI GRAMS, VITHOON VIYANANT, PETER M. SMOOKER, and SUKSIRI VICHASRI-GRAMS. "Comparative analysis of two fatty acid binding proteins fromFasciola gigantica." Parasitology 137, no. 12 (June 16, 2010): 1805–17. http://dx.doi.org/10.1017/s003118201000079x.

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SUMMARYFatty acid binding proteins are considered to be promising vaccine candidates against trematodiasis. In order to provide additional information about their function inFasciola giganticawe performed a comparative analysis of FgFABP1 and FgFABP3, two isoforms with quite different isoelectric points of 4·9 and 9·9 and 67% sequence identity. Both are expressed in the juvenile and adult parasite but differ in their tissue-specific distribution. In addition, the sequence of FABP3 is identical inF. hepaticaandF. giganticaindicating the protein's functional importance in this genus. Immune sera produced against soluble recombinant FgFABPs reacted with 14 kDa antigens in crude worm, soluble egg, cirrus sac extracts, and excretion/secretion product. Both FgFABPs were located in the parenchyma of the parasite but in addition, FgFABP1 was abundant in testes and spermatozoa while FgFABP3 was abundant in vitelline cells, eggs, and caecal epithelium. Mass spectrometry identified FgFABP1 and FgFABP3 in the ES product whereas only FgFABP3 was identified in egg extract. Serum samples of an experimentally infected rabbit reacted from week 6 post-infection with FgFABP3 and from week 12 with FgFABP1 while sera of infected sheep were not reactive. The results suggest differences in the biological functions of these 2 isoforms and differences in the host/parasite interaction that should be considered for their potential as vaccines against fascioliasis.
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Lee, Hae-ock, Hyerim Choe, Kyungwoon Seo, Hyunsook Lee, Jinseon Lee, and Jhingook Kim. "Fgfbp1 is essential for the cellular survival during zebrafish embryogenesis." Molecules and Cells 29, no. 5 (April 12, 2010): 501–7. http://dx.doi.org/10.1007/s10059-010-0062-7.

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Tassi, Elena, En Yin Lai, Lingli Li, Glenn Solis, Yifan Chen, William E. Kietzman, Patricio E. Ray, et al. "Blood Pressure Control by a Secreted FGFBP1 (Fibroblast Growth Factor–Binding Protein)." Hypertension 71, no. 1 (January 2018): 160–67. http://dx.doi.org/10.1161/hypertensionaha.117.10268.

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Dissertations / Theses on the topic "FGFBP1"

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Cottarelli, A. "FIBROBLAST GROWTH FACTOR BINDING PROTEIN 1 (FGFBP1) CONTRIBUTES IN THE ESTABLISHMENT AND MAINTENANCE OF THE BLOOD BRAIN BARRIER." Doctoral thesis, Università degli Studi di Milano, 2015. http://hdl.handle.net/2434/262620.

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The Blood Brain Barrier (BBB) is a highly specialized vascular structure whose aim is to tightly regulate the permeability between the blood flow and the Central Nervous System (CNS). To this purpose, the ECs in the brain need to present some peculiar features: the presence of high-resistance tight junctions (TJs) to block paracellular permeability, the lack of fenestrations, and the expression of some specific transmembrane transporters to selectively allow the entrance of nutrients and the exit of toxic metabolites. The high level of specialization of the brain microvasculature is obtained as a result of the interaction of the endothelial compartment with the other components of the so-called NeuroVascular Unit (NVU), such as the Basement Membrane (BM), pericytes and astrocyte end-feet. The canonical Wnt/β-catenin pathway, that is specifically activated in CNS vessels during development, regulates BBB initiation and maintenance. Moreover, inactivation of this pathway in vivo leads to angiogenic defects in the CNS and not in other vascular regions. Affymetrix analysis previously performed in our group provided a list of genes whose transcription is selectively regulated upon Wnt3a stimulation in murine primary ECs isolated from brain (bMEC). One of the most upregulated transcripts is that of Fibroblast Growth Factor Binding Protein 1 (FGFBP1) gene. FGFBP1 is a cargo protein that, after being secreted in the extracellular matrix (ECM), is able to non-covalently bind the FGF immobilized in the ECM and to mobilize it, protecting it from degradation and presenting it to FGF tyrosine-kinase receptor on the cell membrane. Given the capability of Wnt3a stimulation to selectively induce FGFBP1 expression in brain ECs, we hypothesized that this protein could be involved in the process of initiation and/or maturation of the BBB. In this work, we demonstrate in vivo in the zebrafish model that FGFBP1 knock down by morpholino presents vascular abnormalities in the brain and in the trunk, together with cerebral hemorrhages and impaired permeability. Taking advantage of the endothelial-specific FGFBP1 knock out murine model, we further demonstrate that inhibition of endothelial FGFBP1 expression affects brain vascular development, causing vascular defects and increased BBB permeability and also influencing the number of pericytes and the composition of the BM. Finally, we show in vitro that FGFBP1 absence promotes a “tip-like” phenotype and an increase in the expression of Plvap in bMECs. In conclusion, our work proposes a novel role for FGFBP1 in the maintenance of the properties of the BBB and in the regulation of the complex interactions of the endothelial compartment with the other components of the NVU.
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BonDurant, Lucas Donald. "Regulation of glucose homeostasis by FGF21." Diss., University of Iowa, 2018. https://ir.uiowa.edu/etd/6060.

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Fibroblast Growth Factor 21 (FGF21) is an endocrine hormone derived from the liver that exerts pleiotropic effects on the body to maintain overall metabolic homeostasis. During the past decade, there has been an enormous effort to understand the physiological roles of FGF21 in regulating metabolism and to identify the mechanism for its potent pharmacological effects to reverse diabetes and obesity. Through both human and rodent studies, it is now evident that FGF21 is dynamically regulated by nutrient sensing and consequently functions as a critical regulator of nutrient homeostasis. In addition, recent studies with new genetic and molecular tools have provided critical insight into the actions of this exciting endocrine factor. Dissection of these FGF21-regulated pathways has tremendous potential for new targeted therapies to treat metabolic disease. The goals of this thesis are 1) to identify FGF21’s physiological role as a carbohydrate-regulated signal of macronutrient-specific satiety and 2) to determine the mechanism and tissues responsible for mediating the pharmacological effects of FGF21. To address the first goal, we used different FGF21 genetic knockout mouse models to determine if loss of FGF21 would affect macronutrient preference. We found that loss of FGF21 led to an increase in simple sugar intake whereas this had no effect on other macronutrients such as lipid or protein. To further characterize the relationship between carbohydrates and FGF21, in vitro and in vivo techniques revealed that FGF21 transcription in the liver increased in response to carbohydrate intake and this was dependent on the presence of a transcription factor activated by carbohydrates, ChREBP. We next addressed whether or not increased FGF21 levels would affect preference for simple sugars. We found that in response to increased circulating levels of FGF21, either through genetic overexpression or pharmacological administration, FGF21 would lead to a significant decrease in caloric and non-caloric sweeteners. Finally, we were able to determine that FGF21 was signaling to the hypothalamus to mediate this suppression of simple sugar intake through region specific knockout of the co-receptor beta-klotho. To address the pharmacological actions of FGF21, we generated an adipose-specific KLB KO mouse using mice that express Cre-recombinase under the adiponectin promoter. These mice lack the co-receptor for FGF21 in adipose tissue and are a more reliable adipose knockout model than previous studies that have used aP2-Cre mice. We were able to determine that the acute glucose lowering effects of FGF21 are mediated through direct signaling to adipose tissue and that FGF21 enhances insulin sensitivity by increasing glucose uptake in brown adipose tissue. However, FGF21 mediates its chronic effects, including lowering body weight and triglycerides, by signaling to some other non-adipose tissue. Overall our work has shown that FGF21 can significantly regulate glucose metabolism through multiple mechanisms.
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Ribas, Aulinas Francesc. "Regulació de FGF21 en la cèl·lula muscular." Doctoral thesis, Universitat de Barcelona, 2014. http://hdl.handle.net/10803/284546.

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Tot i que el fetge és considerat com el principal lloc de producció del FGF21 sistèmic, sobretot en condicions de dejuni i sota control de PPARα, darrerament s’han acumulat diverses evidències que indiquen que FGF21 també pot actuar com a mioquina, un factor hormonal que pot ser produït i alliberat a la circulació pel múscul esquelètic. Concretament, s’ha observat que pacients que pateixen malalties neuromusculars causades per alteracions en la funció mitocondrial, com ara mutacions i deplecions al DNA mitocondrial, presenten valors d’expressió d’FGF21 incrementats, així com també els de la seva secreció a la circulació. Per tant, alguns indicis mostren que el múscul pot ser un lloc de producció i secreció d’FGF21 associat a l’estrès mitocondrial muscular. Durant la realització d’aquesta tesi, hem trobat que l’expressió i la secreció d’FGF21 en un context de cèl•lula muscular estan íntimament associades amb la diferenciació miogènica tant en rosegadors com en models humans. Per contra, els nivells dels seus receptors es mantenen bastant estables, mentre que pel que fa al cofactor β-Klotho, necessari pel seu procés de senyalització, no es detecta expressió del transcrit. Aquest fet suggereix, que la cèl•lula muscular podria ser una font d’expressió i secreció d’FGF21, però no un teixit diana d’aquesta. A part, s’ha identificat el factor miogènic MyoD com a un regulador molt potent de la transcripció del gen FGF21, així com també se n’ha mapat la regió del promotor responsable de vehicular aquest efecte. D’altra banda, s’han intentat descriure altres factors de transcripció i coreguladors que poden actuar com a activadors o inhibidors, els quals poden estar involucrats en el control de la transcripció gènica d’FGF21, com ara els PPARs, PGC-1α o Sirt1, així com també esbrinar els efectes de diversos activadors naturals i sintètics. En aquest sentit, val la pena destacar que dins d’un context en presència del factor miogènic MyoD s’ha identificat a PPARα, juntament amb el seu activador, com a un clar activador de l’activitat transcripcional d’aquest promotor. PGC-1α, sembla actuar de la mateixa manera, potenciant-ne l’efecte en presència de MyoD. Per contra, Sirt1 s’ha revelat com a un inactivador de l’activitat transcripcional del gen FGF21 en presència del factor MyoD. Altres experiments indiquen que el tractament amb diferents àcids grassos no sorgeixen cap efecte sobre l’expressió ni la secreció del gen en el context muscular, sinó més aviat el contrari, malgrat que la cèl•lula muscular es mostrava sensible a l’acció dels àcids grassos sobre altres gens. De la mateixa manera que ja indicaven determinats indicis bibliogràfics, vam poder comprovar que pacients de patologia MNGIE (miopatia associada a alteracions del DNA mitocondrial), mostraven la presència d’alts nivells d’FGF21 circulants. Així doncs, intentant mimetitzar una disfunció mitocondrial experimentalment, utilitzant inhibidors de la cadena respiratòria/fosforilació oxidativa, es van poder confirmar aquests increments d’expressió i secreció d’FGF21 per part de les cèl•lules musculars. Investigant una mica més a fons la mecanística de tot el procés, es va veure que l’increment de la producció d’espècies reactives d’oxigen derivades d’aquesta disfunció, provocava una inducció de la p38-MAP cinasa i conseqüentment l’activació ATF2, el qual és capaç d’interaccionar amb el seu lloc d’unió en la regió proximal del promotor del gen FGF21, provocant així aquest efecte sobre el gen FGF21 a les cèl•lules miogèniques. Alhora, s’ha descrit que la presència de MyoD és imprescindible per tal que es doni la resposta de la transcripció del gen FGF21 a la disfunció mitocondrial induïda experimentalment, justificant la resposta d’increment de la secreció d’FGF21 per part de les cèl•lules musculars en resposta a aquesta disfunció. Aquests canvis en la secreció d’FGF21 per part de les cèl•lules miogèniques en resposta a les afectacions a nivell mitocondrial, també poden ser un reflex del mecanisme fisiològic pel qual es detecten canvis a nivell d’estatus energètic a nivell muscular. D’aquesta manera, un increment de l’alliberació d’FGF21 podria desencadenar diferents respostes metabòliques adaptatives a nivell sistèmic. Aquest procés posa de manifest la gran capacitat que té la funció mitocondrial, per tal d’influenciar en el metabolisme sistèmic a través de la senyalització mitocondrial retrògrada. Així doncs, aquest mecanisme de senyalització permet l’expressió i alliberació de molècules d’acció endocrina com ara FGF21 i reforça la idea de considerar el múscul esquelètic com a una important font d’FGF21, la qual podem considerar com a una mioquina.
Although the liver is generally considered the main production site for fibroblast growth factor-21 (FGF21), high FGF21 levels have been found to be associated with neuromuscular mitochondrial genetic diseases, and there are indications that shows muscle as a source of FGF21 production under conditions of muscular mitochondrial stress. In this thesis we describe that FGF21 expression and release is associated with myogenic differentiation in different muscular cell lines. However, FGFRs transcription levels don’t change across differentiation and β-Klotho is undetectable, suggesting that muscle cells as a source but not as a target of FGF21. Furthermore we have identified MyoD as a major controller of FGF21 gene transcription, as well as we have mapped the most important region in the promoter responsible for MyoD-dependent regulation. Moreover, we determined the role of some transcription factors and co-regulators potentially involved in the control of FGF21 gene transcription, such as PPARs, PGC-1α or Sirt1, as well as several natural and synthetic agents (e.g. fatty acids) On the other hand, mimicking mitochondrial dysfunction by the use of respiratory chain/oxidative phosphorylation inhibitors resulted in enhanced expression and release of FGF21 by muscle cells. Increased production of reactive oxygen species, subsequent induction of p38-MAP kinase and activation of an ATF2-binding site at the proximal promoter region of the FGF21 gene were found to comprise the major mechanism connecting mitochondrial dysfunction and enhanced FGF21 gene transcription in myogenic cells. Furthermore, we show that MyoD is required for the responsiveness of FGF21 gene transcription to experimentally induced mitochondrial dysfunction, which explains the preferential response of muscle cells to enhanced FGF21 secretion in response to mitochondrial alterations. FGF21 release by muscle cells in response to mitochondrial alterations may reflect a physiological mechanism by which the sensing of internal energetic status by muscle tissue results in the release of FGF21 to favor systemic metabolic adaptations. This process highlights the capacity of mitochondrial function to influence systemic metabolism by retrograde signaling, which leads to the expression and release of molecules with endocrine action, such as FGF2,1 and reinforces the concept of considering the skeletal muscle as an important source of the FGF21, as well as to consider FGF21 as a myokine.
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Ribas, Aulinas Francesc. "Regulació de FGF21 en la cèl.lula muscular." Doctoral thesis, Universitat de Barcelona, 2014. http://hdl.handle.net/10803/284546.

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Tot i que el fetge és considerat com el principal lloc de producció del FGF21 sistèmic, sobretot en condicions de dejuni i sota control de PPARα, darrerament s’han acumulat diverses evidències que indiquen que FGF21 també pot actuar com a mioquina, un factor hormonal que pot ser produït i alliberat a la circulació pel múscul esquelètic. Concretament, s’ha observat que pacients que pateixen malalties neuromusculars causades per alteracions en la funció mitocondrial, com ara mutacions i deplecions al DNA mitocondrial, presenten valors d’expressió d’FGF21 incrementats, així com també els de la seva secreció a la circulació. Per tant, alguns indicis mostren que el múscul pot ser un lloc de producció i secreció d’FGF21 associat a l’estrès mitocondrial muscular. Durant la realització d’aquesta tesi, hem trobat que l’expressió i la secreció d’FGF21 en un context de cèl•lula muscular estan íntimament associades amb la diferenciació miogènica tant en rosegadors com en models humans. Per contra, els nivells dels seus receptors es mantenen bastant estables, mentre que pel que fa al cofactor β-Klotho, necessari pel seu procés de senyalització, no es detecta expressió del transcrit. Aquest fet suggereix, que la cèl•lula muscular podria ser una font d’expressió i secreció d’FGF21, però no un teixit diana d’aquesta. A part, s’ha identificat el factor miogènic MyoD com a un regulador molt potent de la transcripció del gen FGF21, així com també se n’ha mapat la regió del promotor responsable de vehicular aquest efecte. D’altra banda, s’han intentat descriure altres factors de transcripció i coreguladors que poden actuar com a activadors o inhibidors, els quals poden estar involucrats en el control de la transcripció gènica d’FGF21, com ara els PPARs, PGC-1α o Sirt1, així com també esbrinar els efectes de diversos activadors naturals i sintètics. En aquest sentit, val la pena destacar que dins d’un context en presència del factor miogènic MyoD s’ha identificat a PPARα, juntament amb el seu activador, com a un clar activador de l’activitat transcripcional d’aquest promotor. PGC-1α, sembla actuar de la mateixa manera, potenciant-ne l’efecte en presència de MyoD. Per contra, Sirt1 s’ha revelat com a un inactivador de l’activitat transcripcional del gen FGF21 en presència del factor MyoD. Altres experiments indiquen que el tractament amb diferents àcids grassos no sorgeixen cap efecte sobre l’expressió ni la secreció del gen en el context muscular, sinó més aviat el contrari, malgrat que la cèl•lula muscular es mostrava sensible a l’acció dels àcids grassos sobre altres gens. De la mateixa manera que ja indicaven determinats indicis bibliogràfics, vam poder comprovar que pacients de patologia MNGIE (miopatia associada a alteracions del DNA mitocondrial), mostraven la presència d’alts nivells d’FGF21 circulants. Així doncs, intentant mimetitzar una disfunció mitocondrial experimentalment, utilitzant inhibidors de la cadena respiratòria/fosforilació oxidativa, es van poder confirmar aquests increments d’expressió i secreció d’FGF21 per part de les cèl•lules musculars. Investigant una mica més a fons la mecanística de tot el procés, es va veure que l’increment de la producció d’espècies reactives d’oxigen derivades d’aquesta disfunció, provocava una inducció de la p38-MAP cinasa i conseqüentment l’activació ATF2, el qual és capaç d’interaccionar amb el seu lloc d’unió en la regió proximal del promotor del gen FGF21, provocant així aquest efecte sobre el gen FGF21 a les cèl•lules miogèniques. Alhora, s’ha descrit que la presència de MyoD és imprescindible per tal que es doni la resposta de la transcripció del gen FGF21 a la disfunció mitocondrial induïda experimentalment, justificant la resposta d’increment de la secreció d’FGF21 per part de les cèl•lules musculars en resposta a aquesta disfunció. Aquests canvis en la secreció d’FGF21 per part de les cèl•lules miogèniques en resposta a les afectacions a nivell mitocondrial, també poden ser un reflex del mecanisme fisiològic pel qual es detecten canvis a nivell d’estatus energètic a nivell muscular. D’aquesta manera, un increment de l’alliberació d’FGF21 podria desencadenar diferents respostes metabòliques adaptatives a nivell sistèmic. Aquest procés posa de manifest la gran capacitat que té la funció mitocondrial, per tal d’influenciar en el metabolisme sistèmic a través de la senyalització mitocondrial retrògrada. Així doncs, aquest mecanisme de senyalització permet l’expressió i alliberació de molècules d’acció endocrina com ara FGF21 i reforça la idea de considerar el múscul esquelètic com a una important font d’FGF21, la qual podem considerar com a una mioquina.
Although the liver is generally considered the main production site for fibroblast growth factor-21 (FGF21), high FGF21 levels have been found to be associated with neuromuscular mitochondrial genetic diseases, and there are indications that shows muscle as a source of FGF21 production under conditions of muscular mitochondrial stress. In this thesis we describe that FGF21 expression and release is associated with myogenic differentiation in different muscular cell lines. However, FGFRs transcription levels don’t change across differentiation and β-Klotho is undetectable, suggesting that muscle cells as a source but not as a target of FGF21. Furthermore we have identified MyoD as a major controller of FGF21 gene transcription, as well as we have mapped the most important region in the promoter responsible for MyoD-dependent regulation. Moreover, we determined the role of some transcription factors and co-regulators potentially involved in the control of FGF21 gene transcription, such as PPARs, PGC-1α or Sirt1, as well as several natural and synthetic agents (e.g. fatty acids) On the other hand, mimicking mitochondrial dysfunction by the use of respiratory chain/oxidative phosphorylation inhibitors resulted in enhanced expression and release of FGF21 by muscle cells. Increased production of reactive oxygen species, subsequent induction of p38-MAP kinase and activation of an ATF2-binding site at the proximal promoter region of the FGF21 gene were found to comprise the major mechanism connecting mitochondrial dysfunction and enhanced FGF21 gene transcription in myogenic cells. Furthermore, we show that MyoD is required for the responsiveness of FGF21 gene transcription to experimentally induced mitochondrial dysfunction, which explains the preferential response of muscle cells to enhanced FGF21 secretion in response to mitochondrial alterations. FGF21 release by muscle cells in response to mitochondrial alterations may reflect a physiological mechanism by which the sensing of internal energetic status by muscle tissue results in the release of FGF21 to favor systemic metabolic adaptations. This process highlights the capacity of mitochondrial function to influence systemic metabolism by retrograde signaling, which leads to the expression and release of molecules with endocrine action, such as FGF2,1 and reinforces the concept of considering the skeletal muscle as an important source of the FGF21, as well as to consider FGF21 as a myokine.
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Brooks, Nicole E. "Fibroblast Growth Factor 21 Expression in Mice with Altered Growth Hormone Action: Links to Obesity, Type 2 Diabetes Mellitus, and Increased Longevity." Ohio University Honors Tutorial College / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=ouhonors1461161246.

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Ameka, Magdalene Khang'ai. "The role of FGF21 in regulating energy homeostasis." Diss., University of Iowa, 2017. https://ir.uiowa.edu/etd/5908.

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Fibroblast Growth Factor 21 (FGF21) is a hormone that is produced from the liver which has pleiotropic effects. Physiologically, FGF21 increases energy expenditure, increases glucose uptake, enhances glucose tolerance, and increases peripheral insulin sensitivity. Pharmacologically, FGF21 reverses obesity and diabetes in animal models and significantly improves metabolic profiles in humans through unknown mechanisms. We hypothesized that the physiological actions of FGF21 may provide insights to explain FGF21’s beneficial pharmacological effects. The overall theme of this work was to identify the elusive mechanism by which FGF21 regulates energy homeostasis. In chapter 1, I review some adipokines and hepatokines that regulate energy homeostasis. In chapter 2, I provide background on fibroblast growth factors (FGFs), metabolic FGFs, and the tissue-specific effects of FGF21. In chapter 3, I will review the role of growth factors in thermoregulation. In chapter 4, we use tissue-specific loss of function models to investigate the trajectory of FGF21’s thermogenic effects during prolonged cold. In chapter 5, we specifically address the necessity and sufficiency of FGF21 signaling directly to adipose tissue, and the contribution of the adipokine adiponectin in mediating FGF21’s metabolic effects. In chapter 6, I summarize our results, reflect upon the ramifications of these results, and briefly address potential future experiments given our results on the physiological and pharmacological actions of FGF21 in adipose tissues.
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Coleman, Stacey J. "The role of nuclear FGFR1 and FGF2 in pancreatic cancer." Thesis, Queen Mary, University of London, 2013. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8403.

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Patients who are diagnosed with pancreatic ductal adenocarcinoma (PDAC) face a dismal prognosis. One reason for this is the dense stroma that is a characteristic of PDAC, which may preclude drugs from accessing the tumour cells. Pancreatic stellate cells (PSCs) are the key cell responsible for desmoplasia in PDAC and it is becoming clear that they are a promising target for therapy. Over-expression of FGFs and their receptors is a feature of PDAC and correlates with poor prognosis, but whether their expression impacts on PSCs is unclear. The aim of my research was 1) to understand the role and function of nuclear FGFR1 and FGF using 2D based assays; 2) to use a physiologically relevant 3D organotypic model to study the effects of blocking nuclear FGFR1 and FGF2 in PSCs; 3) to assess whether this target could provide a novel therapeutic strategy in PDAC. At the invasive front of human pancreatic cancer, FGF2 and FGFR1 localised to the nucleus in activated PSCs but not cancer cells. Inhibiting FGFR1 and FGF2 in PSCs, using RNAi or chemical inhibition in vitro, resulted in significantly reduced cell proliferation, which was not seen in cancer cells. Cancer cells co-cultured on top of collagen/Matrigel gels together with PSCs showed marked invasion of both cancer cells and PSCs. However, FGFR inhibition blocked invasion of both PSCs and cancer cells. FGFR inhibition resulted in cytoplasmic localisation of FGFR1 and FGF2, in contrast to vehicle-treated conditions where PSCs with nuclear FGFR1 and FGF2 led cancer cells to invade the underlying extra-cellular matrix. Strikingly, abrogation of nuclear FGFR1 and FGF2 in PSCs abolished cancer cell invasion. These findings suggest a novel therapeutic approach, where preventing nuclear FGF/FGFR mediated proliferation and invasion in PSCs leads to disruption of the tumour microenvironment, preventing pancreatic cancer cell invasion. Thus, for 6 patients with PDAC which is resistant to conventional chemotherapy, targeting the stroma by blocking nuclear FGFR1 and FGF2 in PSCs identifies a novel therapeutic approach.
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Kristofersdottir, Isidora Anna. "Effect of FGF21 on short-term white adipocyte adiponectin secretion." Thesis, Högskolan i Skövde, Institutionen för biovetenskap, 2020. http://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-18682.

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Reduced levels of white adipocyte hormone adiponectin have been observed in obese individuals with type 2 diabetes (T2D). Higher adiponectin levels are monotonically associated with a lower risk of T2D and hence increasing circulating adiponectin levels is of great interest in diabetic research. A novel compound, called fibroblast growth factor 21 (FGF21), is showing great potential in treatment of obesity and T2D. In animal models with obesity and T2D FGF21 increases glucose uptake, improves lipid homeostasis, decreases fat mass and increases circulating adiponectin levels. In this study, theaim is to explore the acute effect of FGF21 on white adipocyte adiponectin secretion. Adiponectinsecretion experiments were performed on primary murine adipocytes incubated with FGF21 for 30minutes and adiponectin levels were measured with ELISA and normalised to total protein content.To study the signalling pathway of FGF21, a separate batch of murine adipocytes were pretreated with an Epac and PI3K inhibitor prior to addition of FGF21. Results from this thesis show that FGF21potently stimulates short-term adiponectin release via PI3K-dependent pathways with no effect on adiponectin synthesis.
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Guash, Géraldine. "Caractérisation moléculaire du symdrome myéloprolifératif 8p12 impliquant le gène FGFR1." Aix-Marseille 2, 2001. http://www.theses.fr/2002AIX22013.

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Elsayed, Asmaa. "A Polymorphism in the FGF21 Gene is a Novel Risk Variant for Metabolic-Associated Steatohepatitis." Thesis, The University of Sydney, 2020. https://hdl.handle.net/2123/22453.

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Background: Metabolic associated fatty liver disease (MAFLD) afflicts about a quarter of the global population. A proportion of these patients develop chronic inflammation which can progress to cirrhosis and cancer. Sugar consumption is a major risk factor of MAFLD progression and a human FGF21 variant (rs838133) was recently found to be a risk variant for increased sugar consumption. Whether this variant is a novel risk factor for MAFLD is unknown. Methods: We studied the association of FGF21 rs838133 with liver disease severity and the metabolic profile of patients with MAFLD. Functional investigations were undertaken using allele-specific expression of FGF21 in liver, by measurement of serum FGF21 by ELIZA, bioinformatics analysis and by complementary mouse studies. Results: FGF21 rs838133 was associated with an increased risk of metabolic associated steatohepatitis (MASH), but not simple steatosis. The variant did not affect hepatic FGF21 expression or splicing, but likely affects FGF21 mRNA structure. Compared to healthy controls, patients with MAFLD have higher serum FGF21 levels (p < 0.05). This difference was more profound in patients with MASH (162 ± 47.26, p < 0.01) compared to those with simple steatosis (155.2 ± 51.98, p < 0.01). Similarly, FGF21 levels increased with progression of the NAS score and with fibrosis (p <0.05, for both). Consistently, there was a positive correlation between FGF21 levels and blood glucose, HOMA-IR, AST, GGT, triglycerides, total bile acids and primary bile acids (p < 0.05, for all). In mouse models of liver injury, Fgf21 expression was increased by a high sucrose diet, and in two liver injury models, namely bile duct ligation (p < 0.05, for both) and a methionine and choline deficient diet (p < 0.0001). There was no correlation between serum levels of FGF21 and other FGF family proteins (FGF19, FGF23). Conclusion: FGF21 rs838133 is a novel risk variant for MASH, likely via a change in mRNA folding and subsequently, stability. FGF21 serum levels are likely increased in MASH due to hepatic resistance and correlates with markers of glycaemic profile and bile acids in these patients. Different members of the FGF family of proteins are likely regulated by different mechanisms.
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Books on the topic "FGFBP1"

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D, Marcus. FGF21 - Diet. Notion Press, 2021.

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Ciruna, Brian Garrett. The role of FGFR1 signalling in the specification and morphogenesis of mesoderm during mouse gastrulation. 2001.

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Book chapters on the topic "FGFBP1"

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Cheng, Tsz Wai, and Po Sing Leung. "FGF21." In Encyclopedia of Signaling Molecules, 1703–8. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101992.

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Cheng, Tsz Wai, and Po Sing Leung. "FGF21." In Encyclopedia of Signaling Molecules, 1–6. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4614-6438-9_101992-1.

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Katoh, Masaru, Giorgio Berton, Anna Baruzzi, Jennifer Boylston, Charles Brenner, Yong-Hun Lee, William Schiemann, et al. "FGF11." In Encyclopedia of Signaling Molecules, 607. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100429.

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Katoh, Masaru, Giorgio Berton, Anna Baruzzi, Jennifer Boylston, Charles Brenner, Yong-Hun Lee, William Schiemann, et al. "FGF21." In Encyclopedia of Signaling Molecules, 608. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100440.

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Katoh, Masaru, Giorgio Berton, Anna Baruzzi, Jennifer Boylston, Charles Brenner, Yong-Hun Lee, William Schiemann, et al. "FGF1." In Encyclopedia of Signaling Molecules, 607. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100427.

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Zhao, Yang, James D. Dunbar, and Alexei Kharitonenkov. "FGF21 as a Therapeutic Reagent." In Advances in Experimental Medicine and Biology, 214–28. New York, NY: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-0887-1_14.

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Miranda, Roberto N., Joseph D. Khoury, and L. Jeffrey Medeiros. "Lymphomas Associated with FGFR1 Abnormalities." In Atlas of Lymph Node Pathology, 179–83. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7959-8_41.

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Villanueva, C., and N. de Roux. "FGFR1 Mutations in Kallmann Syndrome." In Frontiers of Hormone Research, 51–61. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000312693.

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Pérez-Martí, Albert, Pedro F. Marrero, Diego Haro, and Joana Relat. "Lipid Response to Amino Acid Starvation in Fat Cells: Role of FGF21." In Handbook of Famine, Starvation, and Nutrient Deprivation, 1–17. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-40007-5_15-1.

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Pérez-Martí, Albert, Pedro F. Marrero, Diego Haro, and Joana Relat. "Lipid Response to Amino Acid Starvation in Fat Cells: Role of FGF21." In Handbook of Famine, Starvation, and Nutrient Deprivation, 2185–201. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-55387-0_15.

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Conference papers on the topic "FGFBP1"

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Sos, Martin L., and Roman K. Thomas. "Abstract A20: FGFR1-amplified squamous cell lung cancers depend on FGFR1." In Abstracts: AACR International Conference on Translational Cancer Medicine-- Jul 11-14, 2010; San Francisco, CA. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1078-0432.tcmusa10-a20.

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Yu, Lan, Andrew Erickson, Mervi Toriseva, Teresa Elo, Johanna Tuomela, Heikki Seikkula, Martti Nurmi, et al. "Abstract 4951: FGFRL1 in prostate cancer progression." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-4951.

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Ghanem, M., A. Justet, M. Hachem, T. Boghanim, A. Vadel, M. Jaillet, A. Mailleux, and B. Crestani. "Involvement of FGF21 in pulmonary fibrosis." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.1094.

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Ghanem, M., A. Justet, M. Hachem, T. Boghanim, A. Vadel, M. Jaillet, A. Mailleux, and B. Crestani. "Involvement of FGF21 in Pulmonary Fibrosis." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a1942.

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Ghanem, Mada, Aurelien Justet, Mouna Hachem, Tiara Boghanim, Aurelie Vadel, Madeleine Jaillet, Arnaud Mailleux, and Bruno Crestani. "Involvement of FGF21 in pulmonary fibrosis." In ERS Lung Science Conference 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/23120541.lsc-2022.108.

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Moes-Sosnowska, Joanna, Adriana Rozy, Monika Skupińska, Urszula Lechowicz, Ewa Szczepulska-Wojcik, Renata Langfort, Piotr Rudzinski, et al. "FGFR1 gene aberrations and FGFR1 protein expression in squamous non-small cell lung cancer (Sq-NSCLC)." In ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.pa1126.

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Servetto, Alberto, Luigi Formisano, Rahul Kollipara, Dhivya R. Sudhan, Kyung-min Lee, Sumanta Chatterjee, Ariella B. Hanker, Saurabh Mendiratta, Ralf Kittler, and Carlos L. Arteaga. "Abstract 4402: FGFR1 signaling modulates estrogen-independent ER transcriptional activity in ER+/FGFR1-amplified breast cancer cells." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-4402.

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Servetto, Alberto, Luigi Formisano, Rahul Kollipara, Dhivya R. Sudhan, Kyung-min Lee, Sumanta Chatterjee, Ariella B. Hanker, Saurabh Mendiratta, Ralf Kittler, and Carlos L. Arteaga. "Abstract 4402: FGFR1 signaling modulates estrogen-independent ER transcriptional activity in ER+/FGFR1-amplified breast cancer cells." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-4402.

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Albiges, L., L. Albiges, V. Quidville, A. Valent, M. Mathieu, F. Drusch, B. Job, et al. "FGFR1 and FGF Coamplification in Breast Cancer." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-4170.

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Wang, Y., L. Guo, L. Cao, M. Jia, L. Wen, C. Ren, G. Zhang, and N. Liao. "Abstract P5-04-25: Characterization of FGFR1/2 genetic alterations reveals novel fusions of FGFR1 in Chinese breast cancer." In Abstracts: 2018 San Antonio Breast Cancer Symposium; December 4-8, 2018; San Antonio, Texas. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-p5-04-25.

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Reports on the topic "FGFBP1"

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Liu, Chuannan, Yanan He, Yue Zong, yue Xiao, Guan Yang, and Songtao Wang. The Relationship Between Exercise and FGF21 in Adults−Meta Analysis and system review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2022. http://dx.doi.org/10.37766/inplasy2022.9.0080.

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