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Journal articles on the topic 'FGFBP1'

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

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1

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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2

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Taetzsch, Thomas, Milagros J. Tenga, and Gregorio Valdez. "Muscle Fibers Secrete FGFBP1 to Slow Degeneration of Neuromuscular Synapses during Aging and Progression of ALS." Journal of Neuroscience 37, no. 1 (November 14, 2016): 70–82. http://dx.doi.org/10.1523/jneurosci.2992-16.2016.

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12

Taetzsch, Thomas, Milagros J. Tenga, and Gregorio Valdez. "Muscle Fibers Secrete FGFBP1 to Slow Degeneration of Neuromuscular Synapses during Aging and Progression of ALS." Journal of Neuroscience 37, no. 1 (January 4, 2017): 70–82. http://dx.doi.org/10.1523/jneurosci.2992-16.2017.

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13

Huang, Wenjie, Zhangqian Chen, Xin Shang, Dean Tian, Daowen Wang, Kaichun Wu, Daiming Fan, and Limin Xia. "Sox12, a direct target of FoxQ1, promotes hepatocellular carcinoma metastasis through up-regulating Twist1 and FGFBP1." Hepatology 61, no. 6 (April 8, 2015): 1920–33. http://dx.doi.org/10.1002/hep.27756.

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14

Tomaszewski, M., F. Charchar, T. Barnes, C. Maric, E. Zukowska-Szczechowska, and N. J. Samani. "058 Fibroblast growth factor binding protein 1 gene (FGFBP1) and hypertension — from pathway analysis to renal glomerulus." Heart 96, Suppl 1 (June 2010): A35.1—A35. http://dx.doi.org/10.1136/hrt.2010.195966.6.

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15

Xia, Limin, Kaichun Wu, and Daiming Fan. "581 Sox12, a Direct Target of FoxQ1, Promotes Hepatocellular Carcinoma Metastasis Through up-Regulating TWIST1 and FGFBP1." Gastroenterology 148, no. 4 (April 2015): S—984—S—985. http://dx.doi.org/10.1016/s0016-5085(15)33366-7.

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16

Essa, Ayman Hashem, Abdul-Jabbar A. Al-Rawi, and Rehab Subhi Ramadhan. "The Relationship of the Genotype Effect to FGFBP1 Gene in Some Productive Traits in Broiler Type Ross 308." Indian Journal of Public Health Research & Development 10, no. 11 (2019): 2719. http://dx.doi.org/10.5958/0976-5506.2019.04029.4.

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17

Park, Yong-Sung, Ji-Hyun Kim, Jin-Hwa Cho, Hyo-Ihl Chang, Seung-Wook Kim, Hyun-Dong Paik, Chang-Won Kang, Tae-Hyoung Kim, Ha-Chin Sung, and Cheol-Won Yun. "Physical and functional interaction of FgFtr1–FgFet1 and FgFtr2–FgFet2 is required for iron uptake in Fusarium graminearum." Biochemical Journal 408, no. 1 (October 29, 2007): 97–104. http://dx.doi.org/10.1042/bj20070450.

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FgFtr1 and FgFtr2 are putative iron permeases, and FgFet1 and FgFet2 are putative ferroxidases of Fusarium graminearum. They have high homologies with iron permease ScFtr1 and ferroxidase ScFet3 of Saccharomyces cerevisiae at the amino acid level. The genes encoding iron permease and ferroxidase were localized to the same chromosome in the manner of FgFtr1/FgFet1 and FgFtr2/FgFet2. The GFP (green fluorescent protein)-fused versions of FgFtr1 and FgFtr2 showed normal functions when compared with FgFtr1 and FgFtr2 in an S. cerevisiae system, and the cellular localizations of FgFtr1 and FgFtr2 in S. cerevisiae depended on the expression of their putative ferroxidase partners FgFet1 and FgFet2 respectively. Although FgFtr1 was found on the plasma membrane when FgFet1 and FgFtr1 were co-transformed in S. cerevisiae, most of the FgFtr1 was found in the endoplasmic reticulum compartment when co-expressed with FgFet2. Furthermore, FgFtr2 was found on the vacuolar membrane when FgFet2 was co-expressed. From the two-hybrid analysis, we confirmed the interaction of FgFtr1 and FgFet1, and the same result was found between FgFtr2 and FgFet2. Iron-uptake activity also depended on the existence of the respective partner. Finally, the FgFtr1 and FgFtr2 were found on the plasma and vacuolar membrane respectively, in F. graminearum. Taken together, these results strongly suggest that FgFtr1 and FgFtr2 from F. graminearum encode the iron permeases of the plasma membrane and vacuolar membrane respectively, and require their specific ferroxidases to carry out normal function. Furthermore, the present study suggests that the reductive iron-uptake system is conserved from yeast to filamentous fungi.
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Al-Sharif, Mona, Hend Radwan, Basma Hendam, and Ahmed Ateya. "DNA polymorphisms of FGFBP1, leptin, κ-casein, and αs1-casein genes and their association with reproductive performance in dromedary she-camels." Theriogenology 178 (January 2022): 18–29. http://dx.doi.org/10.1016/j.theriogenology.2021.11.001.

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Yang, Zhulin, Zhi Yang, Qiong Zou, Yuan Yuan, Jinghe Li, Daiqiang Li, Lufeng Liang, Guixiang Zeng, and Senlin Chen. "A comparative study of clinicopathological significance, FGFBP1, and WISP-2 expression between squamous cell/adenosquamous carcinomas and adenocarcinoma of the gallbladder." International Journal of Clinical Oncology 19, no. 2 (April 17, 2013): 325–35. http://dx.doi.org/10.1007/s10147-013-0550-9.

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20

Hoppman, Nicole, John C. McLenithan, Daniel J. McBride, Haiqing Shen, Jan Bruder, Richard L. Bauer, John R. Shaffer, et al. "A common variant in fibroblast growth factor binding protein 1 (FGFBP1) is associated with bone mineral density and influences gene expression in vitro." Bone 47, no. 2 (August 2010): 272–80. http://dx.doi.org/10.1016/j.bone.2010.04.607.

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21

Or, Michelle, Jessica Lin, Johnson Lam, Eric Hau, and Puma Sundaresan. "What genes predict response to neoadjuvant chemoradiation in locally advanced rectal cancer? A systematic review based on gene expression profiling." Journal of Clinical Oncology 41, no. 4_suppl (February 1, 2023): 200. http://dx.doi.org/10.1200/jco.2023.41.4_suppl.200.

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200 Background: Curative management of locally advanced rectal cancer (LARC) involves neoadjuvant chemoradiation therapy (nCRT) followed by radical surgery. Pathological complete response (pCR) is seen in 15-27% of patients. The response to nCRT may be influenced by genetic variations. Gene signatures therefore may serve as biomarkers for predicting response or resistance to nCRT. We conducted a systematic review on genetic biomarkers for response prediction to nCRT in LARC and identify common genes or ontology pathways. Methods: A systematic search of electronic databases (MEDLINE, PubMed and EMBASE) was performed for relevant recent studies. Studies were screened as per the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines with search terms “rectal neoplasm”, “rectal cancer”, “gene”, “gene expression”, “gene expression profile”. The relevant studies were selected for full-text review. Studies that reported gene expression profile to predict response to nCRT were included. Results: Twelve of 367 studies screened were included. Most studies used microarray or real-time reverse transcription PCR. Six of these assessed for gene predictors of pCR with 2 studies reporting correlation between certain genes and pCR: thymidylate synthetase; gene set (including LMNB2, MLF2, DDX1, EIF4A1, FOXO3A, ILF3 and SEMA3C); 19 genes including (NPSR1, HYAL1, FGFBP1, PLLP and MALL). Common gene ontology pathways identified included DNA break repair via homologous recombination and apoptotic pathways. Conclusions: Multiple genes were identified as prospective biomarkers for nCRT in LARC patients. Further studies are required to validate these identified genes to personalize treatment for LARC patients.
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Katarzyna, Wójcik-Krowiranda. "The Role of The ?klotho Gene, Fgf21 and Fgfr1 in Cancerogenesis." Women Health Care and Issues 1, no. 1 (December 14, 2020): 01–07. http://dx.doi.org/10.31579/2642-9756/003.

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Klotho was discovered in 1997 as an anti-aging gene that, when overexpressed, may extend the life span, but when it is disrupted, it may be a factor responsible for premature aging syndrome. The structure and the role of αKlotho and βKlotho genes from Klotho family in malignant tumors is described. The expression profile of the βKlotho gene is significantly different from the expression of the αKlotho gene. Analysis of Klotho expression in breast cancer, cervical cancer as well as endometrial cancer are discussed. The available data indicate the involvement of βKlotho in the neoplastic transformation of the endometrium. More advanced disease is related to negative expression of βKlotho gene. Fibroblast growth factors (FGFs) are a large family of proteins characterized by different functions in the cell development and metabolism. The FGF signaling is also associated with cancerogenesis. The relation between some FGF subfamilies and endometrial cancer clinical data is reported. The interaction between FGF subfamilies and the Klotho subfamily proteins acting as a co-receptor is stressed. Disorders in signaling of the FGF / FGFR pathway have been confirmed in gynecology. It can be assumed that increased expression of FGF21 might be a suppressor factor in endometrial cancer. The FGF21 factor, like the βKlotho protein, achieves its biological effect via the FGFR1 receptor. High expression of the FGFR1 gene inhibits further tumor growth. FGFR1 has the potential to perform both a suppressor and promoter role in the oncogenesis process.
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Videla, Luis, Romina Vargas, Barbara Riquelme, Javier Fernández, and Virginia Fernández. "Thyroid Hormone-Induced Expression of the Hepatic Scaffold Proteins Sestrin2, β-Klotho, and FRS2α in Relation to FGF21-AMPK Signaling." Experimental and Clinical Endocrinology & Diabetes 126, no. 03 (September 11, 2017): 182–86. http://dx.doi.org/10.1055/s-0043-115533.

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AbstractThyroid hormone (3,3′,5-triiodothyronine, T3) accelerates energy metabolism in the liver through mechanisms involving upregulation of AMP-activated protein kinase (AMPK). This study aims to assess the influence of T3 on the expression of the scaffold proteins β-Klotho, fibroblast growth factor receptor substrate 2α (FRS2α), and Sestrin2 in relation to FGF21-AMPK signaling. Male Sprague-Dawley rats were given 0.1 mg T3/kg or hormone vehicle (controls) and studies were done 24 h after treatment. These include measurements of the mRNA expression (qPCR) of hepatic β-Klotho, FGF21, FGF21 receptor-1 (FGFR1), extracellular-signal-regulated kinase 1/2 (ERK1/2), FRS2α, ribosomal S6 kinase-1 (RSK1), liver kinase B1 (LKB1), AMPK, and Sestrin2. Also, protein levels of FGF21, FGFR1 (ELISA), and ERK1/2 (Western blot) were measured. T3 elicited a calorigenic response with higher hepatic mRNA expression of β-Klotho, FRS2α, and FGF21, increased serum FGF21, without changes in liver FGFR1 mRNA and its plasma levels. In addition, T3 enhanced ERK1/2 phosphorylation and the mRNA expression of ERK1/2, RSK1, LKB1, AMPK, and Sestrin2. T3 administration enhances liver FGF21-AMPK signaling involving upregulation of the scaffold proteins β-Klotho, FRS2α, and Sestrin2. β-Klotho and FRS2 induction favours the operation of the FGF21-FGFR1-β-Klotho complex as evidenced by the enhancement in ERK1/2 phosphorylation, whereas that of Sestrin2 recruits LKB1 to achieved AMPK activation, thus supporting a higher energy expenditure condition that may be desirable in some metabolic disorders
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Baruch, Amos, Chin Wong, Leslie W. Chinn, Anjali Vaze, Junichiro Sonoda, Thomas Gelzleichter, Shan Chen, et al. "Antibody-mediated activation of the FGFR1/Klothoβ complex corrects metabolic dysfunction and alters food preference in obese humans." Proceedings of the National Academy of Sciences 117, no. 46 (November 2, 2020): 28992–9000. http://dx.doi.org/10.1073/pnas.2012073117.

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Fibroblast growth factor 21 (FGF21) controls metabolic organ homeostasis and eating/drinking behavior via FGF receptor 1/Klothoβ (FGFR1/KLB) complexes expressed in adipocytes, pancreatic acinar cells, and the nervous system in mice. Chronic administration of recombinant FGF21 or engineered variants improves metabolic health in rodents, nonhuman primates, and humans; however, the rapid turnover of these molecules limits therapeutic utility. Here we show that the bispecific anti-FGFR1/KLB agonist antibody BFKB8488A induced marked weight loss in obese cynomolgus monkeys while elevating serum adiponectin and the adipose expression of FGFR1 target genes, demonstrating its action as an FGF21 mimetic. In a randomized, placebo-controlled, single ascending-dose study in overweight/obese human participants, subcutaneous BFKB8488A injection caused transient body weight reduction, sustained improvement in cardiometabolic parameters, and a trend toward reduction in preference for sweet taste and carbohydrate intake. These data suggest that specific activation of the FGFR1/KLB complex in humans can be used as therapy for obesity-related metabolic defects.
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Sørensen, Vigdis, Yan Zhen, Malgorzata Zakrzewska, Ellen Margrethe Haugsten, Sébastien Wälchli, Trine Nilsen, Sjur Olsnes, and Antoni Wiedlocha. "Phosphorylation of Fibroblast Growth Factor (FGF) Receptor 1 at Ser777 by p38 Mitogen-Activated Protein Kinase Regulates Translocation of Exogenous FGF1 to the Cytosol and Nucleus." Molecular and Cellular Biology 28, no. 12 (April 14, 2008): 4129–41. http://dx.doi.org/10.1128/mcb.02117-07.

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ABSTRACT Exogenous fibroblast growth factor 1 (FGF1) signals through activation of transmembrane FGF receptors (FGFRs) but may also regulate cellular processes after translocation to the cytosol and nucleus of target cells. Translocation of FGF1 occurs across the limiting membrane of intracellular vesicles and is a regulated process that depends on the C-terminal tail of the FGFR. Here, we report that translocation of FGF1 requires activity of the α isoform of p38 mitogen-activated protein kinase (MAPK). FGF1 translocation was inhibited after chemical inhibition of p38 MAPK or after small interfering RNA knockdown of p38α. Translocation was increased after stimulation of p38 MAPK with anisomycin, mannitol, or H2O2. The activity level of p38 MAPK was not found to affect endocytosis or intracellular sorting of FGF1/FGFR1. Instead, we found that p38 MAPK regulates FGF1 translocation by phosphorylation of FGFR1 at Ser777. The FGFR1 mutation S777A abolished FGF1 translocation, while phospho-mimetic mutations of Ser777 to Asp or Glu allowed translocation to take place and bypassed the requirement for active p38 MAPK. Ser777 in FGFR1 was directly phosphorylated by p38α in a cell-free system. These data demonstrate a crucial role for p38α MAPK in the regulated translocation of exogenous FGF1 into the cytosol/nucleus, and they reveal a specific role for p38α MAPK-mediated serine phosphorylation of FGFR1.
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Raja, Aroosha, Muhammad Faraz Arshad Malik, and Farhan Haq. "Genomic relevance of FGF14 and associated genes on the prognosis of pancreatic cancer." PLOS ONE 16, no. 6 (June 1, 2021): e0252344. http://dx.doi.org/10.1371/journal.pone.0252344.

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Background Fibroblast (FGFs) and insulin (IGF) growth factor pathways are among 10 most recurrently altered genomic pathways in pancreatic ductal adenocarcinoma (PDAC). However, the prognostic and therapeutic relevance of FGF and IGF pathways in PDAC is largely unknown. Methods We investigated the relationship between fibroblast and insulin pathway gene expression and clinicopathological features in three independent transcriptomic cohorts of 532 PDAC patients. Furthermore, we have examined the coexpressed genes specific to the prognostic marker identified from these cohorts. Statistical tests including Fisher-exact\Chi-square, Kaplan–Meier, Pearson Correlation and cox regression analyses were performed. Additionally, pathway analysis of gene-specific co-expressed genes was also performed. Results The dysregulation of six genes including FGF9, FGF14, FGFR1, FGFR4, IGF2BP2 and IGF2BP3 were significantly associated with different clinical characteristics (including grade, stage, recurrence and nodes) in PDAC cohorts. 11 genes (including FGF9, FGF13, FGF14, FGF17, FGFR1, FGFRL1, FGFBP3, IGFBP3, IGF2BP2, IGF2BP3 and IGFBPL1) showed association with overall survival in different PDAC cohorts. Interestingly, overexpression of FGF14 was found associated with better overall survival (OS) in all three cohorts. Of note, multivariate analysis also revealed FGF14 as an independent prognostic marker for better OS in all three cohorts. Furthermore, FMN2 and PGR were among the top genes that correlated with FGF14 in all 3 cohorts. Of note, overexpression of FMN2 and PGR was found significantly associated with good overall survival in PDAC patients, suggesting FMN2 and PGR can also act as potential markers for the prediction of prognosis in PDAC patients. Conclusion FGF14 may define a distinct subset of PDAC patients with better prognosis. Moreover, FGF14-based sub-classification of PDAC suggests that FMN2 and PGR can be employed as good prognostic markers in PDAC and this classification may lead to new therapeutic approaches.
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Gao, Yuan, Shuqin Zhao, Wangdong Zhang, Huaping Tang, Meilin Yan, Fang Yong, Xu Bai, Xiaochun Wu, Yong Zhang, and Quanwei Zhang. "Localization of FGF21 Protein and Lipid Metabolism-Related Genes in Camels." Life 13, no. 2 (February 3, 2023): 432. http://dx.doi.org/10.3390/life13020432.

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With the ability to survive under drought and chronic hunger, camels display a unique regulation characteristic of lipid metabolism. Fibroblast growth factor (FGF) 21 is a peptide hormone that regulates metabolic pathways, especially lipid metabolism, which was considered as a promising therapeutic target for metabolic diseases. To understand the FGF21 expression pattern and its potential relationship with lipid metabolism in camels, this study investigated the distribution and expression of FGF21, receptor FGFR1, and two lipid metabolism markers, leptin and hormone-sensitive lipase (HSL), using an immunohistochemistry (IHC) assay. The results showed that FGF21 was widely expressed in camel central nerve tissue and peripheral organs but absent in lung and gametogenic tissue, including the testis, epididymis, and ovary. In striated muscle, FGF21 is only present at the fiber junction. FGFR1 is expressed in almost all tissues and cells, indicating that all tissues are responsive to FGF21 and other FGF-mediated signals. Leptin and HSL are mainly located in metabolic and energy-consuming organs. In the CNS, leptin and HSL showed a similar expression pattern with FGFR1. In addition, leptin expression is extremely high in the bronchial epithelium, which may be due to its role in the immune responses of respiratory mucosa, in addition to fat stores and energy balance. This study found that FGF21 showed active expression in the nervous system of camels, which may be related to the adaptability of camels to arid environments and the specific regulation of lipid metabolism. This study showed a special FGF21-mediated fat conversion pattern in camels and provides a reference for developing a potential therapeutic method for fat metabolism disease.
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Poźniak, Marta, Weronika Zarzycka, Natalia Porębska, Agata Knapik, Paulina Marczakiewicz-Perera, Malgorzata Zakrzewska, Jacek Otlewski, and Łukasz Opaliński. "FGF1 Fusions with the Fc Fragment of IgG1 for the Assembly of GFPpolygons-Mediated Multivalent Complexes Recognizing FGFRs." Biomolecules 11, no. 8 (July 23, 2021): 1088. http://dx.doi.org/10.3390/biom11081088.

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FGFRs are cell surface receptors that, when activated by specific FGFs ligands, transmit signals through the plasma membrane, regulating key cellular processes such as differentiation, division, motility, metabolism and death. We have recently shown that the modulation of the spatial distribution of FGFR1 at the cell surface constitutes an additional mechanism for fine-tuning cellular signaling. Depending on the multivalent, engineered ligand used, the clustering of FGFR1 into diverse supramolecular complexes enhances the efficiency and modifies the mechanism of receptor endocytosis, alters FGFR1 lifetime and modifies receptor signaling, ultimately determining cell fate. Here, we present a novel approach to generate multivalent FGFR1 ligands. We functionalized FGF1 for controlled oligomerization by developing N- and C-terminal fusions of FGF1 with the Fc fragment of human IgG1 (FGF1-Fc and Fc-FGF1). As oligomerization scaffolds, we employed GFPpolygons, engineered GFP variants capable of well-ordered multivalent display, fused to protein G to ensure binding of Fc fragment. The presented strategy allows efficient assembly of oligomeric FGFR1 ligands with up to twelve receptor binding sites. We show that multivalent FGFR1 ligands are biologically active and trigger receptor clustering on the cell surface. Importantly, the approach described in this study can be easily adapted to oligomerize alternative growth factors to control the activity of other cell surface receptors.
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AMANN, RUTH, and BEAT TRUEB. "Evidence that the novel receptor FGFRL1 signals indirectly via FGFR1." International Journal of Molecular Medicine 32, no. 5 (September 10, 2013): 983–88. http://dx.doi.org/10.3892/ijmm.2013.1484.

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

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The oviduct presents the ideal conditions for fertilization and early embryonic development. In this study, (i) vascularization pattern; (ii) microvascular density; (iii) transcripts of angiogenic factors (FGF1, FGF2, VEGF) and their receptors—FGFR1, FGFR2, KDR, respectively, and (iv) the relative protein abundance of those receptors were assessed in cyclic mares’ oviducts. The oviductal artery, arterioles and their ramifications, viewed by means of vascular injection-corrosion, differed in the infundibulum, ampulla and isthmus. The isthmus, immunostained with CD31, presented the largest vascular area and the highest number of vascular structures in the follicular phase. Transcripts (qPCR) and relative protein abundance (Western blot) of angiogenic factors fibroblast growth factor 1 (FGF1) and 2 (FGF2) and vascular endothelial growth factor (VEGF), and their respective receptors (FGFR1, FGFR2, VEGFR2 = KDR), were present in all oviduct portions throughout the estrous cycle. Upregulation of the transcripts of angiogenic receptors FGF1 and FGFR1 in the ampulla and isthmus and of FGF2 and KDR in the isthmus were noted. Furthermore, in the isthmus, the relative protein abundance of FGFR1 and KDR was the highest. This study shows that the equine oviduct presents differences in microvascular density in its three portions. The angiogenic factors VEGF, FGF1, FGF2 and their respective receptors are expressed in all studied regions of the mare oviduct, in agreement with microvascular patterns.
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Okumu, L. A., N. Forde, S. Mamo, P. McGettigan, J. P. Mehta, J. F. Roche, and P. Lonergan. "Temporal regulation of fibroblast growth factors and their receptors in the endometrium and conceptus during the pre-implantation period of pregnancy in cattle." REPRODUCTION 147, no. 6 (June 2014): 825–34. http://dx.doi.org/10.1530/rep-13-0373.

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We hypothesised that the expression pattern of members of the fibroblast growth factor (FGF) family would be altered in the endometrium as the oestrous cycle/early pregnancy progressed associated with changes in the expression pattern of their receptors in the developing embryo/conceptus. Expression of FGF1 and FGF10 transcript variants 1 and 2 increased significantly as the oestrous cycle/early pregnancy progressed. Neither progesterone (P4) supplementation nor pregnancy status significantly affected the expression of any of the FGF ligands studied. However, there was a significant interaction between day, pregnancy and P4 status on FGF2 expression (P<0.05) and a significant interaction between P4 status and day on FGF10_tv2 expression. FGF10 protein was localised in the luminal and glandular epithelium as well as the stroma but was not detected in the myometrium. By RNA sequencing, the expression of FGF ligands in the developing embryo/conceptus was found to be minimal. The expression of FGF receptor 1 (FGFR1), FGFR2, FGFR3, FGFR4, FGFRL1 and FRS3 was significantly affected by the stage of conceptus development. Interestingly, the expression of FGFR1 and FGFR4 was higher during early embryo development (days 7–13, P<0.05) but decreased on day 16 (P<0.05) while FGFR2 (P<0.001) expression was similar from day 7 through to day 13, with a significant increase by day 16 (P<0.05) that was maintained until day 19 (P>0.05). In conclusion, these data demonstrate that FGF ligands are primarily expressed by the endometrium and their modulation throughout the luteal phase of the oestrous cycle/early pregnancy are associated with alterations in the expression of their receptors in the embryo/conceptus.
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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 (February 24, 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 fluid, and homogenized endometria and placentae (P &lt; 0.05). The expression of mRNAs for sodium-dependent phosphate transporters (SLC20A1 and SLC20A2) and klotho signaling mediators (FGF7, FGF21, FGF23, FGFR1–4, KL, KLB, ADAM10, and ADAM17) were quantified by qPCR. Day 17 conceptus tissue expressed SLC20A1, SLC20A2, KLB, FGF7, FGF21, FGF23, FGFR1, and FGFR2 mRNAs. Both sodium-dependent phosphate transporters and klotho signaling mediators were expressed in endometria and placentae throughout gestation. Gestational day influenced the expression of SLC20A1, ADAM10, ADAM17, FGF21, FGFR1, and FGFR3 mRNAs in both endometria and placentae (P &lt; 0.05). Gestational day influenced endometrial expression of FGF7 (P &lt; 0.001), and placental expression of FGF23 (P &lt; 0.05). Immunohistochemistry confirmed that both FGF23 and KL proteins were expressed in endometria and placentae throughout gestation. The observed spatiotemporal profile of KL-FGF signaling suggests a potential role in the establishment of pregnancy and regulation of fetal growth. This study provides a platform for further mechanistic investigation into the role for KL-FGF signaling in the regulation of phosphate transport at the ovine maternal–conceptus interface.
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Yu, Ying, Yingjie Shen, Siyi Zhang, Nan Wang, Lan Luo, Xinyi Zhu, Xiejun Xu, Weitao Cong, Litai Jin, and Zhongxin Zhu. "Suppression of Cutibacterium acnes-Mediated Inflammatory Reactions by Fibroblast Growth Factor 21 in Skin." International Journal of Molecular Sciences 23, no. 7 (March 25, 2022): 3589. http://dx.doi.org/10.3390/ijms23073589.

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Cutibacterium acnes (C. acnes) is a common commensal bacterium that is closely associated with the pathogenesis of acne. Fibroblast growth factor 21 (FGF21), as a favorable regulator of glucose and lipid metabolism and insulin sensitivity, was recently shown to exert anti-inflammatory effects. The role and mechanism of FGF21 in the inflammatory reactions induced by C. acnes, however, have not been determined. The present study shows that FGF21 in the dermis inhibits epidermal C. acnes-induced inflammation in a paracrine manner while it functions on the epidermal layer through a receptor complex consisting of FGF receptor 1 (FGFR1) and β-Klotho (KLB). The effects of FGF21 in heat-killed C. acnes-induced HaCaT cells and living C. acnes-injected mouse ears were examined. In the presence of C. acnes, FGF21 largely counteracted the activation of Toll-like receptor 2 (TLR2), the downstream nuclear factor-κB (NF-κB), and mitogen-activated protein kinase (MAPK) signaling pathways induced by C. acnes. FGF21 also significantly reduced the expression of proinflammatory cytokines, including interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor (TNF)-α. Taken together, these findings indicate that FGF21 suppresses C. acnes-induced inflammation and might be used clinically in the management and treatment of acne.
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Yang, Wenqi, Ling Liu, Yuan Wei, Chunlu Fang, Fu Zhou, Jinbao Chen, Qinghua Han, et al. "Exercise ameliorates the FGF21–adiponectin axis impairment in diet-induced obese mice." Endocrine Connections 8, no. 5 (May 2019): 596–604. http://dx.doi.org/10.1530/ec-19-0034.

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Objective The protective effects of exercise against glucose dysmetabolism have been generally reported. However, the mechanism by which exercise improves glucose homeostasis remains poorly understood. The FGF21–adiponectin axis participates in the regulation of glucose metabolism. Elevated levels of FGF21 and decreased levels of adiponectin in obesity indicate FGF21–adiponectin axis dysfunction. Hence, we investigated whether exercise could improve the FGF21–adiponectin axis impairment and ameliorate disturbed glucose metabolism in diet-induced obese mice. Methods Eight-week-old C57BL/6J mice were randomly assigned to three groups: low-fat diet control group, high-fat diet group and high-fat diet plus exercise group. Glucose metabolic parameters, the ability of FGF21 to induce adiponectin, FGF21 receptors and co-receptor levels and adipose tissue inflammation were evaluated after 12 weeks of intervention. Results Exercise training led to reduced levels of fasting blood glucose and insulin, improved glucose tolerance and better insulin sensitivity in high-fat diet-induced obese mice. Although serum FGF21 levels were not significantly changed, both total and high-molecular-weight adiponectin concentrations were markedly enhanced by exercise. Importantly, exercise protected against high-fat diet-induced impaired ability of FGF21 to stimulate adiponectin secretion. FGF21 co-receptor, β-klotho, as well as receptors, FGFR1 and FGFR2, were upregulated by exercise. We also found that exercise inhibited adipose tissue inflammation, which may contribute to the improvement in the FGF21–adiponectin axis impairment. Conclusions Our data indicate exercise protects against high-fat diet-induced FGF21–adiponectin axis impairment, and may thereby exert beneficial effects on glucose metabolism.
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Alieva, Amina M., Irina E. Baikova, Elena V. Reznik, Ramiz K. Valiev, Islam Z. Akhmatov, Roza A. Arakelyan, Mukhammetsakhet N. Saryev, and Igor G. Nikitin. "Fibroblast growth factor 21 as a new tool in the multicomponent assessment of cardiovascular diseases." Medical Journal of the Russian Federation 28, no. 1 (July 26, 2022): 75–88. http://dx.doi.org/10.17816/medjrf108900.

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Currently, the search and study of new biological markers that can assist in the early diagnosis of cardiovascular diseases, serving as a laboratory tool for assessing the efficiency of ongoing therapy and being a prognostic criterion of possible clinical outcomes and a significant indicator in risk stratification, remain relevant. Two decades have passed since fibroblast growth factor 21 (FGF21), the 21st member of the FGF family, was identified and cloned. FGF21 is a secreted protein that acts as a metabolic regulator and participates in glucose homeostasis, ketogenesis, and regulation of insulin sensitivity. FGF21 expression is controlled by PPAR alpha receptor, which activates peroxisome proliferation. The liver is the main site of FGF21 production. Extrahepatic tissues such as white adipose tissue, brown adipose tissue, and skeletal muscle also express FGF21. Human FGF21 contains 209 amino acids, whereas the mouse counterpart has 210. Mouse and human FGF21 have 75% homology. Endocrine actions of FGF21 include enhancing glucose uptake by adipocytes of white adipose tissue via a unidirectional glucose transporter protein and activating the thermogenic function of brown adipose tissue. Furthermore, FGF21 has autocrine/paracrine effects, such as the induction of hepatic ketogenesis. FGF21 affects target cells with the participation of FGFR1 and FGFR4 receptors and beta-Klotho, a single-pass transmembrane protein that functions as an obligate cofactor of FGF21 signaling. Animal studies have clearly demonstrated that FGF21 acts directly on cardiac tissue, preventing the development of cardiac hypertrophy and reducing post-infarction damage and diabetic cardiomyopathy. Accumulating data emphasize the value of FGF21 as a new biological marker for diagnosis and prognosis assessment in patients with cardiac issues. Moreover, the role of FGF21 in heart diseases is very interesting because of its cardioprotective effects. Future large-scale prospective studies are necessary to confirm of the diagnostic, predictive, and possibly therapeutic role of this marker.
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Hu, Ying, Hui-Xin Liu, Prasant Kuma Jena, Lili Sheng, Mohamed R. Ali, and Yu-Jui Yvonne Wan. "miR-22 inhibition reduces hepatic steatosis via FGF21 and FGFR1 induction." JHEP Reports 2, no. 2 (April 2020): 100093. http://dx.doi.org/10.1016/j.jhepr.2020.100093.

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Justesen, Sarah, Kirsten V. Haugegaard, Jacob B. Hansen, Harald S. Hansen, and Birgitte Andersen. "The autocrine role of FGF21 in cultured adipocytes." Biochemical Journal 477, no. 13 (July 10, 2020): 2477–87. http://dx.doi.org/10.1042/bcj20200220.

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Exposure to cold alters glucose and lipid metabolism of white and brown adipose tissue via activation of β-adrenergic receptor (ADRB). Fibroblast growth factor 21 (FGF21) has been shown to be locally released from adipose tissue upon activation of ADRBs and FGF21 increases glucose uptake in adipocytes. Therefore, FGF21 may play an autocrine role in inducing glucose uptake after β-adrenergic stimulation. To determine the putative autocrine role of FGF21, we stimulated three different types of adipocytes in vitro with Isoprenaline (Iso), an ADRB agonist, in the presence or absence of the FGF receptor (FGFR) inhibitor PD 173074. The three cell lines represent white (3T3-L1), beige (ME3) and brown (WT-1) adipocyte phenotypes, respectively. All three cells systems expressed β-klotho (KLB) and FGFR1 after differentiation and treatment with recombinant FGF21 increased glucose uptake in 3T3-L1 and WT-1 adipocytes, while no significant effect was observed in ME3. Oppositely, all three cell lines responded to Iso treatment and an increase in glucose uptake and lipolysis were observed. Interestingly, in response to the Iso treatment only the WT-1 adipocytes showed an increase in FGF21 in the medium. This was consistent with the observation that PD 173074 decreased Iso-induced glucose uptake in the WT-1 adipocytes. This suggests that FGF21 plays an autocrine role and increases glucose uptake after β-adrenergic stimulation of cultured brown WT-1 adipocytes.
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Xerri, L., Z. Battyani, J.-J. Grob, P. Parc, J. Hassoun, J. J. Bonerandi, and D. Birnbaum. "Expression of FGF1 and FGFR1 in human melanoma tissues." Melanoma Research 6, no. 3 (June 1996): 223–30. http://dx.doi.org/10.1097/00008390-199606000-00005.

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Taliyan, Rajeev, Sarathlal K. Chandran, and Violina Kakoty. "Therapeutic Approaches to Alzheimer’s Type of Dementia: A Focus on FGF21 Mediated Neuroprotection." Current Pharmaceutical Design 25, no. 23 (September 30, 2019): 2555–68. http://dx.doi.org/10.2174/1381612825666190716101411.

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Neurodegenerative disorders are the most devastating disorder of the nervous system. The pathological basis of neurodegeneration is linked with dysfunctional protein trafficking, mitochondrial stress, environmental factors and aging. With the identification of insulin and insulin receptors in some parts of the brain, it has become evident that certain metabolic conditions associated with insulin dysfunction like Type 2 diabetes mellitus (T2DM), dyslipidemia, obesity etc., are also known to contribute to neurodegeneration mainly Alzheimer’s Disease (AD). Recently, a member of the fibroblast growth factor (FGF) superfamily, FGF21 has proved tremendous efficacy in diseases like diabetes mellitus, obesity and insulin resistance (IR). Increased levels of FGF21 have been reported to exert multiple beneficial effects in metabolic syndrome. FGF21 receptors are present in certain areas of the brain involved in learning and memory. However, despite extensive research, its function as a neuroprotectant in AD remains elusive. FGF21 is a circulating endocrine hormone which is mainly secreted by the liver primarily in fasting conditions. FGF21 exerts its effects after binding to FGFR1 and co-receptor, β-klotho (KLB). It is involved in regulating energy via glucose and lipid metabolism. It is believed that aberrant FGF21 signalling might account for various anomalies like neurodegeneration, cancer, metabolic dysfunction etc. Hence, this review will majorly focus on FGF21 role as a neuroprotectant and potential metabolic regulator. Moreover, we will also review its potential as an emerging candidate for combating metabolic stress induced neurodegenerative abnormalities.
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Bo, Wenyan, Yixuan Ma, Yue Xi, Qiaoqin Liang, Mengxin Cai, and Zhenjun Tian. "The Roles of FGF21 and ALCAT1 in Aerobic Exercise-Induced Cardioprotection of Postmyocardial Infarction Mice." Oxidative Medicine and Cellular Longevity 2021 (November 5, 2021): 1–17. http://dx.doi.org/10.1155/2021/8996482.

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Aerobic exercise mitigates oxidative stress and apoptosis caused by myocardial infarction (MI) even though the precise mechanisms remain completely elusive. In this study, we investigated the potential mechanisms of aerobic exercise in ameliorating the cardiac function of mice with MI. In vivo, MI was induced by left anterior descending (LAD) coronary artery ligation in wild-type mice, alcat1 knockout, and fgf21 knockout mice. The mice were exercised under a moderate-intensity protocol for 6 weeks at one week later post-MI. In vitro, H9C2 cells were treated with lentiviral vector carrying alcat1 gene, recombinant human FGF21 (rhFGF21), PI3K inhibitor, and H2O2 to explore the potential mechanisms. Our results showed that aerobic exercise significantly increased the FGF21 expression and decreased the ALCAT1 expression in the hearts of mice with MI. fgf21 knockout weakened the inhibitory effects of aerobic exercise on oxidative stress, endoplasmic reticulum (ER) stress, and apoptosis in mice with MI. Both/either alcat1 knockout and/or aerobic exercise improved cardiac function by inhibiting oxidative stress and apoptosis in the MI heart. rhFGF21 inhibited both H2O2 and overexpression of ALCAT1-induced oxidative stress and apoptosis by activating the PI3K/AKT pathway in H9C2 cells. In conclusion, our results showed that aerobic exercise alleviated oxidative stress and apoptosis by activating the FGF21/FGFR1/PI3K/AKT pathway or inhibiting the hyperexpression of ALCAT1, which ultimately improved the cardiac function in MI mice.
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Tian, Haoyu, Shuairan Zhang, Ying Liu, Yifan Wu, and Dianbao Zhang. "Fibroblast Growth Factors for Nonalcoholic Fatty Liver Disease: Opportunities and Challenges." International Journal of Molecular Sciences 24, no. 5 (February 26, 2023): 4583. http://dx.doi.org/10.3390/ijms24054583.

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Nonalcoholic fatty liver disease (NAFLD), a chronic condition associated with metabolic dysfunction and obesity, has reached epidemic proportions worldwide. Although early NAFLD can be treated with lifestyle changes, the treatment of advanced liver pathology, such as nonalcoholic steatohepatitis (NASH), remains a challenge. There are currently no FDA-approved drugs for NAFLD. Fibroblast growth factors (FGFs) play essential roles in lipid and carbohydrate metabolism and have recently emerged as promising therapeutic agents for metabolic diseases. Among them, endocrine members (FGF19 and FGF21) and classical members (FGF1 and FGF4) are key regulators of energy metabolism. FGF-based therapies have shown therapeutic benefits in patients with NAFLD, and substantial progress has recently been made in clinical trials. These FGF analogs are effective in alleviating steatosis, liver inflammation, and fibrosis. In this review, we describe the biology of four metabolism-related FGFs (FGF19, FGF21, FGF1, and FGF4) and their basic action mechanisms, and then summarize recent advances in the biopharmaceutical development of FGF-based therapies for patients with NAFLD.
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Koinis, Filippos, Paul Corn, Nila Parikh, Jian Song, Ioulia Vardaki, Ioanna Mourkioti, Sue-Hwa Lin, Christopher Logothetis, Theocharis Panaretakis, and Gary Gallick. "Resistance to MET/VEGFR2 Inhibition by Cabozantinib Is Mediated by YAP/TBX5-Dependent Induction of FGFR1 in Castration-Resistant Prostate Cancer." Cancers 12, no. 1 (January 19, 2020): 244. http://dx.doi.org/10.3390/cancers12010244.

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The overall goal of this study was to elucidate the role of FGFR1 induction in acquired resistance to MET and VEGFR2 inhibition by cabozantinib in prostate cancer (PCa) and leverage this understanding to improve therapy outcomes. The response to cabozantinib was examined in mice bearing patient-derived xenografts in which FGFR1 was overexpressed. Using a variety of cell models that reflect different PCa disease states, the mechanism underpinning FGFR1 signaling activation by cabozantinib was investigated. We performed parallel investigations in specimens from cabozantinib-treated patients to confirm our in vitro and in vivo data. FGFR1 overexpression was sufficient to confer resistance to cabozantinib. Our results demonstrate transcriptional activation of FGF/FGFR1 expression in cabozantinib-resistant models. Further analysis of molecular pathways identified a YAP/TBX5-driven mechanism of FGFR1 and FGF overexpression induced by MET inhibition. Importantly, knockdown of YAP and TBX5 led to decreased FGFR1 protein expression and decreased mRNA levels of FGFR1, FGF1, and FGF2. This association was confirmed in a cohort of hormone-naïve patients with PCa receiving androgen deprivation therapy and cabozantinib, further validating our findings. These findings reveal that the molecular basis of resistance to MET inhibition in PCa is FGFR1 activation through a YAP/TBX5-dependent mechanism. YAP and its downstream target TBX5 represent a crucial mediator in acquired resistance to MET inhibitors. Thus, our studies provide insight into the mechanism of acquired resistance and will guide future development of clinical trials with MET inhibitors.
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Wu, Shufang, Tal Grunwald, Alexei Kharitonenkov, Julie Dam, Ralf Jockers, and Francesco De Luca. "Increased Expression of Fibroblast Growth Factor 21 (FGF21) during Chronic Undernutrition Causes Growth Hormone Insensitivity in Chondrocytes by Inducing Leptin Receptor Overlapping Transcript (LEPROT) and Leptin Receptor Overlapping Transcript-like 1 (LEPROTL1) Expression." Journal of Biological Chemistry 288, no. 38 (August 12, 2013): 27375–83. http://dx.doi.org/10.1074/jbc.m113.462218.

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During calorie restriction in mice, increased expression of FGF21 causes growth attenuation and growth hormone (GH) insensitivity. Previous evidence also indicates that fasting-associated increased expression of leptin receptor overlapping transcript (LEPROT) and LEPROT-like 1 (LEPROTL1) (two proteins that regulate intracellular protein trafficking) reduces GH receptor cell-surface expression in the liver. Thus, we hypothesized that FGF21 causes GH insensitivity through regulation of LEPROT and/or LEPROTL1 expression. After 4 weeks of food restriction, LEPROT and LEPROTL1 mRNA expression in the liver and in the tibial growth plate of wild-type (WT) mice was increased compared with WT mice fed ad libitum. In Fgf21 knock-out (KO) mice, LEPROT and LEPROTL1 mRNA expression in food-restricted and fed ad libitum was similar, with the exception of a subgroup of food-restricted Fgf21 KO mice treated with recombinant human (rh) FGF21 that experienced increased LEPROT and LEPROTL1 mRNA expression compared with untreated food-restricted Fgf21 KO mice. In cultured growth plate chondrocytes, FGF21 stimulated LEPROT and LEPROTL1 mRNA expression, with such effect being prevented in chondrocytes transfected with FGFR1 siRNA or ERK1 siRNA. In cells transfected with control siRNA, GH increased [3H]thymidine incorporation, collagen X, and IGF-1 mRNA expression, with all effects being prevented by rhFGF21. In addition, rhFGF21 decreased 125I-GH binding. In LEPROT siRNA- and/or LEPROTL1 siRNA-transfected cells, rhFGF21 did not prevent the GH stimulatory effects on thymidine incorporation, collagen X, and IGF-1 expression; furthermore, rhFGF21 did not prevent 125I-GH binding. Consistent with the effects of rhFGF21, LEPROT overexpression in chondrocytes resulted in the inhibition of GH action. Our findings indicate that the increased expression of FGF21 during chronic undernutrition inhibits GH action on chondrocytes by activating LEPROT and LEPROTL1.
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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 (August 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 the ligand, Fgf8, in nephron precursors or global deletion of Fgfrl1 interrupts nephron formation. Fgfr2 (likely the IIIb isoform signaling downstream of Fgf7 and Fgf10) is critical for ureteric morphogenesis. Moreover, Fgfr2 appears to act independently of Frs2α (the major signaling adapter for Fgfrs) in regulating UB branching. Loss of Fgfr2 in the MM leads to many kidney and urinary tract anomalies, including vesicoureteral reflux. Thus Fgfr signaling is critical for patterning of virtually all renal lineages at early and later stages of development.
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Ye, Min, Weiqin Lu, Xiaojie Wang, Cong Wang, James L. Abbruzzese, Guang Liang, Xiaokun Li, and Yongde Luo. "FGF21-FGFR1 Coordinates Phospholipid Homeostasis, Lipid Droplet Function, and ER Stress in Obesity." Endocrinology 157, no. 12 (December 2016): 4754–69. http://dx.doi.org/10.1210/en.2016-1710.

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Chiumia, Daniel, Katy Schulke, Anna E. Groebner, Nadine Waldschmitt, Horst-Dieter Reichenbach, Valeri Zakhartchenko, Stefan Bauersachs, and Susanne E. Ulbrich. "Initiation of Conceptus Elongation Coincides with an Endometrium Basic Fibroblast Growth Factor (FGF2) Protein Increase in Heifers." International Journal of Molecular Sciences 21, no. 5 (February 26, 2020): 1584. http://dx.doi.org/10.3390/ijms21051584.

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Fibroblast growth factors (FGF) play an important role during embryo development. To date, the role of FGF and the respective receptors (FGFR) during the preimplantation phase in cattle are not fully characterized. We examined FGF1, FGF2, FGFR1, FGFR2, and FGFR3 in cyclic and early pregnant heifers at Days 12, 15, and 18 after insemination (Day 0). Endometrial FGF1 mRNA transcript abundance in heifers varied significantly with respect to the day after insemination, the pregnancy status, and their interaction. The expression was higher in nonpregnant than in pregnant heifers at Day 18. The conceptus transcripts abundance of FGFR2 and FGFR3 were significantly lower at Day 15 than 18. In the endometrium, FGF1 protein abundance significantly decreased from Day 12 onwards and FGF2 protein abundance showed a minor, but a significant increase at Day 15 in comparison to Days 12 and 18. We concluded that the decrease in FGF1 mRNA expression in pregnant heifers at Day 18 points towards a potential contribution of FGF1 in the preimplantation process. Additionally, successful embryo elongation might require a spatiotemporal FGF2 protein increase in the endometrium.
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47

Adams, Andrew C., Chaofeng Yang, Tamer Coskun, Christine C. Cheng, Ruth E. Gimeno, Yongde Luo, and Alexei Kharitonenkov. "The breadth of FGF21's metabolic actions are governed by FGFR1 in adipose tissue." Molecular Metabolism 2, no. 1 (February 2013): 31–37. http://dx.doi.org/10.1016/j.molmet.2012.08.007.

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48

Christidis, Grigorios, Ersin Karatayli, Rabea A. Hall, Susanne N. Weber, Matthias C. Reichert, Mathias Hohl, Sen Qiao, et al. "Fibroblast Growth Factor 21 Response in a Preclinical Alcohol Model of Acute-on-Chronic Liver Injury." International Journal of Molecular Sciences 22, no. 15 (July 23, 2021): 7898. http://dx.doi.org/10.3390/ijms22157898.

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Background and Aims: Fibroblast growth factor (FGF) 21 has recently been shown to play a potential role in bile acid metabolism. We aimed to investigate the FGF21 response in an ethanol-induced acute-on-chronic liver injury (ACLI) model in Abcb4−/− mice with deficiency of the hepatobiliary phospholipid transporter. Methods: Total RNA was extracted from wild-type (WT, C57BL/6J) and Abcb4−/− (KO) mice, which were either fed a control diet (WT-Cont and KO-Cont groups; n = 28/group) or ethanol diet, followed by an acute ethanol binge (WT-EtOH and KO-EtOH groups; n = 28/group). A total of 58 human subjects were recruited into the study, including patients with alcohol-associated liver disease (AALD; n = 31) and healthy controls (n = 27). The hepatic and ileal expressions of genes involved in bile acid metabolism, plasma FGF levels, and bile acid and its precursors 7α- and 27-hydroxycholesterol (7α- and 27-OHC) concentrations were determined. Primary mouse hepatocytes were isolated for cell culture experiments. Results: Alcohol feeding significantly induced plasma FGF21 and decreased hepatic Cyp7a1 levels. Hepatic expression levels of Fibroblast growth factor receptor 1 (Fgfr1), Fgfr4, Farnesoid X-activated receptor (Fxr), and Small heterodimer partner (Shp) and plasma FGF15/FGF19 levels did not differ with alcohol challenge. Exogenous FGF21 treatment suppressed Cyp7a1 in a dose-dependent manner in vitro. AALD patients showed markedly higher FGF21 and lower 7α-OHC plasma levels while FGF19 did not differ. Conclusions: The simultaneous upregulation of FGF21 and downregulation of Cyp7a1 expressions upon chronic plus binge alcohol feeding together with the invariant plasma FGF15 and hepatic Shp and Fxr levels suggest the presence of a direct regulatory mechanism of FGF21 on bile acid homeostasis through inhibition of CYP7A1 by an FGF15-independent pathway in this ACLI model. Lay Summary: Alcohol challenge results in the upregulation of FGF21 and repression of Cyp7a1 expressions while circulating FGF15 and hepatic Shp and Fxr levels remain constant both in healthy and pre-injured livers, suggesting the presence of an alternative FGF15-independent regulatory mechanism of FGF21 on bile acid homeostasis through the inhibition of Cyp7a1.
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49

Wu, Zhengliang L., Lijuan Zhang, Tomio Yabe, B. Kuberan, David L. Beeler, Andre Love, and Robert D. Rosenberg. "The Involvement of Heparan Sulfate (HS) in FGF1/HS/FGFR1 Signaling Complex." Journal of Biological Chemistry 278, no. 19 (February 25, 2003): 17121–29. http://dx.doi.org/10.1074/jbc.m212590200.

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50

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

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