Fibroblast Growth Factor 13 (FGF13) Monoclonal Antibody

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Fibroblast Growth Factor 13 (FGF13) Monoclonal Antibody ORDERING INFORMATION Catalog no.: 30109 (clone S235-22) Format: 100ug (1mg/ml) Protein G-purified antibody in PBS, pH 7.4, 0.1% sodium azide, 50% glycerol. BACKGROUND FGF13 (also known as FGF2 and FHF2) is a member of the fibroblast growth factor family. FGF family members possess broad mitogenic and cell survival activities, and are involved in a variety of biological processes including embryonic development, cell growth, morphogenesis, tissue repair, tumor growth, and invasion. The FGF13 gene is located in a region on chromosome X that is associated with Borjeson-Forssman-Lehmann syndrome (BFLS), making it a candidate gene for familial cases of BFLS and other syndromal and nonspecific forms of X-linked mental retardation mapping to this region. Alternative splicing of this gene at the 5' end results in several transcript variants encoding different isoforms with different N-termini. SPECIFICATION SUMMARY Antigen: Fusion protein corresponding to aa 2-18 (AAAIASSLIRQKRQARE) of human FGF13. This sequence is 100% identical in rat, 94% identical in mouse, and >80% identical in FGF11, FGF12, and FGF14. Accession nos: AAH34340, Q92913 Gene ID: 2258 Host Species: Mouse Antibody Class: IgG2b Specificity: This antibody recognizes human, mouse, and rat FGF13. APPLICATIONS Immunoblotting: use at 1-5ug/ml. A band of Immunofluorescence: use at 10ug/ml. ~30kDa is detected. Detection of FGF13 in neuroblastoma cell line Detection of FGF13 in rat brain lysate with SK-N-BE with #30109 at 10ug/ml: DAPI (blue) #30109 at 5ug/ml. nuclear stain, Texas Red F actin stain, ATTO 488 (green) FGF13 stain. These are recommended concentrations. Endusers should determine optimal concentrations for their application. Fibroblast Growth Factor 13 (FGF13) Monoclonal Antibody DILUTION INSTRUCTIONS Dilute in PBS or medium that is identical to that used in the assay system. STORAGE AND STABILITY This product is stable for at least one (1) year at -20oC. For in vitro investigational use only. Not intended for therapeutic or diagnostic procedures. .

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ARTICLES Fibroblast Growth Factors 1, 2, 17, and 19 Are The
0031-3998/07/6103-0267 PEDIATRIC RESEARCH Vol. 61, No. 3, 2007 Copyright © 2007 International Pediatric Research Foundation, Inc. Printed in U.S.A. ARTICLES Fibroblast Growth Factors 1, 2, 17, and 19 Are the Predominant FGF Ligands Expressed in Human Fetal Growth Plate Cartilage PAVEL KREJCI, DEBORAH KRAKOW, PERTCHOUI B. MEKIKIAN, AND WILLIAM R. WILCOX Medical Genetics Institute [P.K., D.K., P.B.M., W.R.W.], Cedars-Sinai Medical Center, Los Angeles, California 90048; Department of Obstetrics and Gynecology [D.K.] and Department of Pediatrics [W.R.W.], UCLA School of Medicine, Los Angeles, California 90095 ABSTRACT: Fibroblast growth factors (FGF) regulate bone growth, (G380R) or TD (K650E) mutations (4–6). When expressed at but their expression in human cartilage is unclear. Here, we deter- physiologic levels, FGFR3-G380R required, like its wild-type mined the expression of entire FGF family in human fetal growth counterpart, ligand for activation (7). Similarly, in vitro cul- plate cartilage. Using reverse transcriptase PCR, the transcripts for tivated human TD chondrocytes as well as chondrocytes FGF1, 2, 5, 8–14, 16–19, and 21 were found. However, only FGF1, isolated from Fgfr3-K644M mice had an identical time course 2, 17, and 19 were detectable at the protein level. By immunohisto- of Fgfr3 activation compared with wild-type chondrocytes and chemistry, FGF17 and 19 were uniformly expressed within the showed no receptor activation in the absence of ligand (8,9). growth plate. In contrast, FGF1 was found only in proliferating and hypertrophic chondrocytes whereas FGF2 localized predominantly to Despite the importance of the FGF ligand for activation of the resting and proliferating cartilage.
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FGF Signaling Network in the Gastrointestinal Tract (Review)
163-168 1/6/06 16:12 Page 163 INTERNATIONAL JOURNAL OF ONCOLOGY 29: 163-168, 2006 163 FGF signaling network in the gastrointestinal tract (Review) MASUKO KATOH1 and MASARU KATOH2 1M&M Medical BioInformatics, Hongo 113-0033; 2Genetics and Cell Biology Section, National Cancer Center Research Institute, Tokyo 104-0045, Japan Received March 29, 2006; Accepted May 2, 2006 Abstract. Fibroblast growth factor (FGF) signals are trans- Contents duced through FGF receptors (FGFRs) and FRS2/FRS3- SHP2 (PTPN11)-GRB2 docking protein complex to SOS- 1. Introduction RAS-RAF-MAPKK-MAPK signaling cascade and GAB1/ 2. FGF family GAB2-PI3K-PDK-AKT/aPKC signaling cascade. The RAS~ 3. Regulation of FGF signaling by WNT MAPK signaling cascade is implicated in cell growth and 4. FGF signaling network in the stomach differentiation, the PI3K~AKT signaling cascade in cell 5. FGF signaling network in the colon survival and cell fate determination, and the PI3K~aPKC 6. Clinical application of FGF signaling cascade in cell polarity control. FGF18, FGF20 and 7. Clinical application of FGF signaling inhibitors SPRY4 are potent targets of the canonical WNT signaling 8. Perspectives pathway in the gastrointestinal tract. SPRY4 is the FGF signaling inhibitor functioning as negative feedback apparatus for the WNT/FGF-dependent epithelial proliferation. 1. Introduction Recombinant FGF7 and FGF20 proteins are applicable for treatment of chemotherapy/radiation-induced mucosal injury, Fibroblast growth factor (FGF) family proteins play key roles while recombinant FGF2 protein and FGF4 expression vector in growth and survival of stem cells during embryogenesis, are applicable for therapeutic angiogenesis. Helicobacter tissues regeneration, and carcinogenesis (1-4).
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FGF-13 (H-40): Sc-50293
SAN TA C RUZ BI OTEC HNOL OG Y, INC . FGF-13 (H-40): sc-50293 BACKGROUND PRODUCT Fibroblast growth factor-1 (FGF-1), also designated acidic FGF, and fibroblast Each vial contains 200 µg IgG in 1.0 ml of PBS with < 0.1% sodium azide growth factor-2 (FGF-2), also designated basic FGF, are members of a family and 0.1% gelatin. of growth factors that stimulate proliferation of cells of mesenchymal, epithe-lial and neuroectodermal origin. Additional members of the FGF fami ly APPLICATIONS include the oncogenes FGF-3 (Int2) and FGF-4 (hst/Kaposi), FGF-5, FGF-6, FGF-13 (H-40) is recommended for detection of FGF-13 of mouse, rat and FGF-7 (KGF), FGF-8 (AIGF), FGF-9 (GAF) and FGF-10–FGF-23. Members of the human origin by Western Blotting (starting dilution 1:200, dilution range FGF family share 30-55% amino acid sequence identity and similar gene 1:100-1:1000), immunoprecipitation [1-2 µg per 100-500 µg of total protein structure, and are capable of transforming cultured cells when overex - (1 ml of cell lysate)], immunofluorescence (starting dilution 1:50, dilution pressed in transfected cells. Cellular receptors for FGFs are members of a range 1:50-1:500) and solid phase ELISA (starting dilution 1:30, dilution second multigene family including four tyrosine kinases, designated Flg range 1:30-1:3000). (FGFR-1), Bek (FGFR-L), TKF and FGFR-3. FGF-13 (H-40) is also recommended for detection of FGF-13 in additional REFERENCES species, including bovine and porcine.
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A Novel Fibroblast Growth Factor 1 Variant Reverses Nonalcoholic Fatty Liver Disease in Type 2 Diabetes
University of Louisville ThinkIR: The University of Louisville's Institutional Repository Electronic Theses and Dissertations 8-2018 A novel fibroblast growth factor 1 variant reverses nonalcoholic fatty liver disease in type 2 diabetes. Qian Lin University of Louisville Follow this and additional works at: https://ir.library.louisville.edu/etd Part of the Endocrine System Diseases Commons, and the Pharmacology Commons Recommended Citation Lin, Qian, "A novel fibroblast growth factor 1 variant reverses nonalcoholic fatty liver disease in type 2 diabetes." (2018). Electronic Theses and Dissertations. Paper 3016. https://doi.org/10.18297/etd/3016 This Doctoral Dissertation is brought to you for free and open access by ThinkIR: The University of Louisville's Institutional Repository. It has been accepted for inclusion in Electronic Theses and Dissertations by an authorized administrator of ThinkIR: The University of Louisville's Institutional Repository. This title appears here courtesy of the author, who has retained all other copyrights. For more information, please contact [email protected]. A NOVEL FIBROBLAST GROWTH FACTOR 1 VARIANT REVERSES NONALCOHOLIC FATTY LIVER DISEASE IN TYPE 2 DIABETES BY Qian Lin M.S. at Wenzhou Medical University, 2016 A Dissertation Submitted to the Faculty of the School of Medicine of the University of Louisville for the Degree of Doctor of Philosophy in Pharmacology and Toxicology Department of Pharmacology and Toxicology University of Louisville Louisville, Kentucky August 2018 A NOVEL FIBROBLAST GROWTH FACTOR 1 VARIANT REVERSES NONALCOHOLIC FATTY LIVER DISEASE IN TYPE 2 DIABETES BY Qian Lin Dissertation Approved on August 2, 2018 Dissertation Committee: Dr. Yi Tan Dr. Paul Epstein Dr.
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Upregulated Expression of FGF13/FHF2 Mediates Resistance To
OPEN Upregulated expression of FGF13/FHF2 SUBJECT AREAS: mediates resistance to platinum drugs in CANCER THERAPEUTIC RESISTANCE cervical cancer cells CANCER PREVENTION Tomoko Okada1, Kazuhiro Murata1,2, Ryoma Hirose1,3, Chie Matsuda1, Tsunehiko Komatsu2, STRESS SIGNALLING Masahiko Ikekita3, Miyako Nakawatari4, Fumiaki Nakayama4, Masaru Wakatsuki5, Tatsuya Ohno5,6, CHEMOTHERAPY Shingo Kato5,7, Takashi Imai4 & Toru Imamura1,3 Received 1Signaling Molecules Research Group, Biomedical Research Institute, National Institute of Advanced Industrial Science and 27 June 2013 2 Technology (AIST), Tsukuba, Ibaraki 305-8566, Japan, Division of Hematology, 3rd Department of Internal Medicine, Teikyo 3 Accepted University Chiba Medical Center, Ichihara, Chiba 299-0111, Japan, Department of Applied Biological Science, Faculty of Science 4 18 September 2013 and Technology, Tokyo University of Science, Noda, Chiba 278-8510, Japan, Advanced Radiation Biology Research Program, National Institute of Radiological Sciences, Chiba, Chiba 263-8555, Japan, 5Research Center Hospital for Charged Particle Published Therapy, National Institute of Radiological Sciences, Chiba, Chiba 263-8555, Japan, 6Gunma University Graduate School of 11 October 2013 Medicine, Maebashi, Gunma 371-8511, Japan, 7Saitama Medical University International Medical Center, Hidaka, Saitama 350- 1298, Japan. Correspondence and Cancer cells often develop drug resistance. In cisplatin-resistant HeLa cisR cells, fibroblast growth factor 13 requests for materials (FGF13/FHF2) gene and protein expression was strongly upregulated, and intracellular platinum should be addressed to concentrations were kept low. When the FGF13 expression was suppressed, both the cells’ resistance to T.Imamura (imamura- platinum drugs and their ability to keep intracellular platinum low were abolished. Overexpression of [email protected]) FGF13 in parent cells led to greater resistance to cisplatin and reductions in the intracellular platinum concentration.
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Disruption Offgf13causes Synaptic Excitatory–Inhibitory Imbalance and Genetic Epilepsy and Febrile Seizures Plus
8866 • The Journal of Neuroscience, June 10, 2015 • 35(23):8866–8881 Neurobiology of Disease Disruption of Fgf13 Causes Synaptic Excitatory–Inhibitory Imbalance and Genetic Epilepsy and Febrile Seizures Plus X Ram S. Puranam,1,2 Xiao Ping He,1,2 Lijun Yao,1 Tri Le,3 Wonjo Jang,1 Catherine W. Rehder,4 XDarrell V. Lewis,5 and James O. McNamara1,2,6 1Department of Neurobiology, 2Department of Neurology, 3Duke University School of Medicine, 4Department of Pathology, 5Department of Pediatrics (Neurology), and 6Center for Translational Neuroscience, Duke University Medical Center, Durham, North Carolina 27710 We identified a family in which a translocation between chromosomes X and 14 was associated with cognitive impairment and a complex genetic disorder termed “Genetic Epilepsy and Febrile Seizures Plus” (GEFS ϩ). We demonstrate that the breakpoint on the X chromo- some disrupted a gene that encodes an auxiliary protein of voltage-gated Na ϩ channels, fibroblast growth factor 13 (Fgf13). Female mice in which one Fgf13 allele was deleted exhibited hyperthermia-induced seizures and epilepsy. Anatomic studies revealed expression of Fgf13 mRNA in both excitatory and inhibitory neurons of hippocampus. Electrophysiological recordings revealed decreased inhibitory and increased excitatory synaptic inputs in hippocampal neurons of Fgf13 mutants. We speculate that reduced expression of Fgf13 impairs excitability of inhibitory interneurons, resulting in enhanced excitability within local circuits of hippocampus and the clinical phenotype of epilepsy. These findings reveal a novel cause of this syndrome and underscore the powerful role of FGF13 in control of neuronal excitability. Key words: animal model; epilepsy; excitatory inhibitory imbalance; Fgf13; GEFS ϩ; translocation Introduction ilepsies, such as temporal lobe epilepsy and frontal lobe epilepsy, occur but less commonly in GEFS ϩ families (Scheffer and Berk- Epilepsy is a common, serious neurological disorder affecting 1% ϩ of the population worldwide (Banerjee and Hauser, 2008).
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Expression of Fgfs During Early Mouse Tongue Development
Gene Expression Patterns 20 (2016) 81e87 Contents lists available at ScienceDirect Gene Expression Patterns journal homepage: http://www.elsevier.com/locate/gep Expression of FGFs during early mouse tongue development * Wen Du a, b, Jan Prochazka b, c, Michaela Prochazkova b, c, Ophir D. Klein b, d, a State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan, 610041, China b Department of Orofacial Sciences and Program in Craniofacial Biology, University of California San Francisco, San Francisco, CA 94143, USA c Laboratory of Transgenic Models of Diseases, Institute of Molecular Genetics of the ASCR, v.v.i., Prague, Czech Republic d Department of Pediatrics and Institute for Human Genetics, University of California San Francisco, San Francisco, CA 94143, USA article info abstract Article history: The ﬁbroblast growth factors (FGFs) constitute one of the largest growth factor families, and several Received 29 September 2015 ligands and receptors in this family are known to play critical roles during tongue development. In order Received in revised form to provide a comprehensive foundation for research into the role of FGFs during the process of tongue 13 December 2015 formation, we measured the transcript levels by quantitative PCR and mapped the expression patterns by Accepted 29 December 2015 in situ hybridization of all 22 Fgfs during mouse tongue development between embryonic days (E) 11.5 Available online 31 December 2015 and E14.5. During this period, Fgf5, Fgf6, Fgf7, Fgf9, Fgf10, Fgf13, Fgf15, Fgf16 and Fgf18 could all be detected with various intensities in the mesenchyme, whereas Fgf1 and Fgf2 were expressed in both the Keywords: Tongue epithelium and the mesenchyme.
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Fibroblasts from the Human Skin Dermo-Hypodermal Junction Are
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Downloaded and Amplified
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Journal of Cancer 2020, Vol. 11 2000 Ivyspring International Publisher Journal of Cancer 2020; 11(8): 2000-2007. doi: 10.7150/jca.40531 Review FGF/FGFR signaling pathway involved resistance in various cancer types Yangyang Zhou1*, Chengyu Wu1*, Guangrong Lu2, Zijing Hu3, Qiuxiang Chen4, Xiaojing Du5 1. Department of Rheumatology and Immunology, the Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, China 2. Department of Gastroenterology, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical, Wenzhou, Zhejiang 325000, China) 3. College of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang 325000, China 4. Department of Ultrasonic Imaging, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325035, China 5. Department of Gastroenterology, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325035, China *Yangyang Zhou and Chengyu Wu contributed equally to this work Corresponding authors: Qiuxiang Chen, Department of Ultrasonic Imaging, the First Affiliated Hospital of Wenzhou Medical University, South Baixiang, Ouhai district, Wenzhou, Zhejiang 325035, China; Tel/Tex: +86 0577 55579122; E-mail: [email protected] and Xiaojing Du, Department of Gastroenterology, the First Affiliated Hospital of Wenzhou Medical University, South Baixiang, Ouhai district, Wenzhou, Zhejiang 325035, China; Tel/Tex: +86 0577 55579125; E-mail: [email protected] © The author(s). This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions. Received: 2019.09.22; Accepted: 2020.01.04; Published: 2020.02.03 Abstract Resistance becomes major clinical issue in cancer treatment, which strongly limits patients to benefit from oncotherapy.
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