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1. Full Text Development of covalent inhibitors that can overcome resistance to first-generation FGFR kinase inhibitors
by Li Tan and Jun Wang and Junko Tanizaki and Zhifeng Huang and Amir R. Aref and Maria Rusan and Su-Jie Zhu and Yiyun Zhang and Dalia Ercan and Rachel G. Liao and Marzia Capelletti and Wenjun Zhou and Wooyoung Hur and NamDoo Kim and Taebo Sim and Suzanne Gaudet and David A. Barbie and Jing-Ruey Joanna Yeh and Cai-Hong Yun and Peter S. Hammerman and Moosa Mohammadi and Pasi A. Jänne and Nathanael S. Gray
Proceedings of the National Academy of Sciences, ISSN 0027-8424, 11/2014, Volume 111, Issue 45, pp. E4869 - E4877
The human FGF receptors (FGFRs) play critical roles in various human cancers, and several FGFR inhibitors are currently under clinical investigation.... 
Structure-based drug design | Drug discovery | Cancer drug resistance | Kinase inhibitor | structure-based drug design | WILD-TYPE | MULTIDISCIPLINARY SCIENCES | BCR-ABL | GROWTH-FACTOR RECEPTORS | DRUG-RESISTANCE | kinase inhibitor | LUNG-CANCER | GENE FUSIONS | cancer drug resistance | SELECTIVE INHIBITOR | drug discovery | THERAPEUTIC TARGET | FACTOR RECEPTOR 4 | REGULATES PROLIFERATION | Receptor, Fibroblast Growth Factor, Type 4 - chemistry | Receptor, Epidermal Growth Factor - genetics | Receptor, Fibroblast Growth Factor, Type 4 - metabolism | Receptor, Fibroblast Growth Factor, Type 2 - chemistry | Receptor, Fibroblast Growth Factor, Type 2 - metabolism | Humans | Receptor, Fibroblast Growth Factor, Type 1 - metabolism | Crystallography, X-Ray | Structure-Activity Relationship | Mutation, Missense | Receptor, Fibroblast Growth Factor, Type 1 - genetics | Protein Kinase Inhibitors - chemistry | Receptor, Epidermal Growth Factor - metabolism | Neoplasms - genetics | Receptor, Fibroblast Growth Factor, Type 2 - antagonists & inhibitors | Antineoplastic Agents - pharmacology | Receptor, Fibroblast Growth Factor, Type 4 - genetics | Binding Sites | Neoplasms - enzymology | Antineoplastic Agents - chemistry | Receptor, Fibroblast Growth Factor, Type 1 - antagonists & inhibitors | Receptor, Epidermal Growth Factor - chemistry | Neoplasms - drug therapy | Drug Resistance, Neoplasm - genetics | Cell Line, Tumor | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Protein Kinase Inhibitors - pharmacology | Receptor, Fibroblast Growth Factor, Type 1 - chemistry | Neoplasms - pathology | Receptor, Fibroblast Growth Factor, Type 4 - antagonists & inhibitors | Receptor, Fibroblast Growth Factor, Type 2 - genetics | Amino Acid Substitution | Drug Resistance, Neoplasm - drug effects | Amino acids | T cell receptors | Mutation | Kinases | Binding sites | Adenosine triphosphatase | Index Medicus | Biological Sciences | PNAS Plus
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2. Full Text Activation of Cardiac Fibroblast Growth Factor Receptor 4 Causes Left Ventricular Hypertrophy
by Grabner, Alexander and Amaral, Ansel P and Schramm, Karla and Singh, Saurav and Sloan, Alexis and Yanucil, Christopher and Li, Jihe and Shehadeh, Lina A and Hare, Joshua M and David, Valentin and Martin, Aline and Fornoni, Alessia and Di Marco, Giovana Seno and Kentrup, Dominik and Reuter, Stefan and Mayer, Anna B and Pavenstädt, Hermann and Stypmann, Jörg and Kuhn, Christian and Hille, Susanne and Frey, Norbert and Leifheit-Nestler, Maren and Richter, Beatrice and Haffner, Dieter and Abraham, Reimar and Bange, Johannes and Sperl, Bianca and Ullrich, Axel and Brand, Marcus and Wolf, Myles and Faul, Christian
Cell Metabolism, ISSN 1550-4131, 12/2015, Volume 22, Issue 6, pp. 1020 - 1032
Chronic kidney disease (CKD) is a worldwide public health threat that increases risk of death due to cardiovascular complications, including left ventricular... 
SIGNAL-TRANSDUCTION | MORTALITY | FACTOR FAMILY | KLOTHO | POINT MUTATION | TYROSINE KINASE | ENDOCRINOLOGY & METABOLISM | CHRONIC KIDNEY-DISEASE | CANCER PROGRESSION | EXPRESSION | FGF RECEPTOR | CELL BIOLOGY | Receptor, Fibroblast Growth Factor, Type 4 - metabolism | Humans | Glucuronidase - metabolism | Fibroblast Growth Factors - genetics | Male | Renal Insufficiency, Chronic - metabolism | Fibroblast Growth Factors - metabolism | Hypertrophy, Left Ventricular - pathology | HEK293 Cells | Receptor, Fibroblast Growth Factor, Type 4 - deficiency | Female | Receptor, Fibroblast Growth Factor, Type 4 - genetics | Disease Models, Animal | Phospholipase C gamma - metabolism | Mutagenesis, Site-Directed | Myocytes, Cardiac - cytology | Signal Transduction | Hypertrophy, Left Ventricular - metabolism | Mice, Inbred C57BL | NFATC Transcription Factors - metabolism | Cells, Cultured | Rats | Rats, Sprague-Dawley | Gene Knock-In Techniques | Mice, Knockout | Renal Insufficiency, Chronic - pathology | Animals | Glucuronidase - genetics | Myocytes, Cardiac - metabolism | Mice | Calcineurin - metabolism | Hypertension | Medical colleges | Chronic kidney failure | Heart enlargement | Stem cells | Physiological aspects | Fibroblast growth factors | Phospholipases | Drug discovery | T cells | Health aspects | Heart | Resveratrol | Development and progression | Kidney diseases | Cells | Index Medicus
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3. Full Text Differential specificity of endocrine FGF19 and FGF21 to FGFR1 and FGFR4 in complex with KLB
by Yang, Chaofeng and Jin, Chengliu and Li, Xiaokun and Wang, Fen and McKeehan, Wallace L and Luo, Yongde
PLoS ONE, ISSN 1932-6203, 03/2012, Volume 7, Issue 3, pp. e33870 - e33870
Background: Recent studies suggest that betaKlotho (KLB) and endocrine FGF19 and FGF21 redirect FGFR signaling to regulation of metabolic homeostasis and... 
BETA-KLOTHO | PPAR-ALPHA | TRANSCRIPTS ENCODING MEMBRANE | METABOLIC REGULATOR | MULTIDISCIPLINARY SCIENCES | INCREASES ENERGY-EXPENDITURE | ACTIVATED-RECEPTOR-GAMMA | FIBROBLAST-GROWTH-FACTOR | BILE-ACID SYNTHESIS | MOUSE KLOTHO GENE | INSULIN SENSITIVITY | Receptor, Fibroblast Growth Factor, Type 4 - metabolism | Diabetes Mellitus - genetics | Membrane Proteins - genetics | Humans | Receptor, Fibroblast Growth Factor, Type 1 - metabolism | Diabetes Mellitus - metabolism | Fibroblast Growth Factors - genetics | Multiprotein Complexes - genetics | Receptor, Fibroblast Growth Factor, Type 1 - genetics | Obesity - genetics | Mice, Knockout | Obesity - metabolism | Fibroblast Growth Factors - metabolism | Multiprotein Complexes - metabolism | Animals | Cell Line, Tumor | Protein Binding | Membrane Proteins - metabolism | Mice | Adipose Tissue | Receptor, Fibroblast Growth Factor, Type 4 - genetics | Type 2 diabetes | Physiological aspects | Obesity | Cellular signal transduction | Fibroblast growth factors | Liver | Adipose tissue | Body fat | Laboratories | Dietary minerals | Science | Homeostasis | Biology | Adipocytes | Metabolic syndrome | Angiogenesis | Signal transduction | Rodents | Animal tissues | Fibroblast growth factor receptor 4 | Fibroblasts | Physiology | Fibroblast growth factor receptor 1 | Vascular endothelial growth factor | Binding | Heparan sulfate | Fibroblast growth factor 1 | Fasting | Diabetes mellitus | Melanoma | Gene expression | Metabolism | Ablation | Musculoskeletal system | Signaling | Proteomics | Stem cells | Affinity | Insulin resistance | Transduction | Diabetes | Kinetics | Nanotechnology | Cancer | Fibroblast growth factor receptors | Index Medicus
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4. Full Text Amplification of FRS2 and activation of FGFR/FRS2 signaling pathway in high-grade liposarcoma
by Zhang, Keqiang and Chu, Kevin and Wu, Xiwei and Gao, Hanlin and Wang, Jinhui and Yuan, Yate-Ching and Loera, Sofia and Ho, Kimberley and Wang, Yafan and Chow, Warren and Un, Frank and Chu, Peiguo and Yen, Yun
Cancer Research, ISSN 0008-5472, 01/2013, Volume 73, Issue 4, pp. 1298 - 1307
Fibroblast growth factor (FGF) receptor (FGFR) substrate 2 (FRS2) is an adaptor protein that plays a critical role in FGFR signaling. FRS2 is located on... 
DEDIFFERENTIATED LIPOSARCOMA | GENE | ONCOLOGY | COPY-NUMBER | GROWTH | MDM2 | CLASSIFICATION | PLEOMORPHIC SARCOMA | EXPRESSION | CANCER | CELL-LINE | Immunohistochemistry | Receptor, Fibroblast Growth Factor, Type 4 - metabolism | Proto-Oncogene Proteins c-mdm2 - genetics | Receptor, Fibroblast Growth Factor, Type 2 - metabolism | Cyclin-Dependent Kinase 4 - genetics | Humans | Middle Aged | Gene Expression Regulation, Neoplastic | Male | Receptor, Fibroblast Growth Factor, Type 3 - antagonists & inhibitors | Extracellular Signal-Regulated MAP Kinases - metabolism | Receptor, Fibroblast Growth Factor, Type 3 - metabolism | Arginine - analogs & derivatives | Liposarcoma - metabolism | Neoplasm Grading | RNA Interference | Receptors, Fibroblast Growth Factor - genetics | Female | Receptor, Fibroblast Growth Factor, Type 2 - antagonists & inhibitors | Membrane Proteins - metabolism | Proto-Oncogene Proteins c-akt - metabolism | Receptor, Fibroblast Growth Factor, Type 4 - genetics | Proto-Oncogene Proteins c-mdm2 - metabolism | Receptor, Fibroblast Growth Factor, Type 3 - genetics | Signal Transduction | Membrane Proteins - genetics | Liposarcoma - pathology | Receptors, Fibroblast Growth Factor - antagonists & inhibitors | Liposarcoma - genetics | Pyrimidines - pharmacology | Cyclin-Dependent Kinase 4 - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | Gene Amplification | Receptors, Fibroblast Growth Factor - metabolism | Adaptor Proteins, Signal Transducing - genetics | Cell Line, Tumor | Cell Proliferation - drug effects | Phenylurea Compounds - pharmacology | Adaptor Proteins, Signal Transducing - metabolism | Receptor, Fibroblast Growth Factor, Type 4 - antagonists & inhibitors | Receptor, Fibroblast Growth Factor, Type 2 - genetics | Index Medicus
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5. Full Text Selective over‐expression of fibroblast growth factor receptors 1 and 4 in clinical prostate cancer
by Sahadevan, K and Darby, S and Leung, HY and Mathers, ME and Robson, CN and Gnanapragasam, VJ
The Journal of Pathology, ISSN 0022-3417, 09/2007, Volume 213, Issue 1, pp. 82 - 90
Fibroblast growth factor receptors (FGFRs) mediate the tumourigenic effects of FGFs in prostate cancer. These receptors are therefore potential therapeutic... 
prostate cancer | tissue microarray | laser capture microdissection | fibroblast growth factor receptors | Laser capture microdissection | Tissue microarray | Prostate cancer | Fibroblast growth factor receptors | FACTOR FAMILY | ISOFORMS | FGF | SPECIFICITY | RESTORATION | PATHOLOGY | TUMORIGENICITY | ARG ALLELE | EPITHELIAL-CELLS | GENES | PROGRESSION | Immunohistochemistry | Prostatic Neoplasms - metabolism | Receptor, Fibroblast Growth Factor, Type 4 - metabolism | Cell Proliferation | Microdissection | Oligonucleotide Array Sequence Analysis | Receptor, Fibroblast Growth Factor, Type 2 - metabolism | Humans | Gene Expression Regulation, Neoplastic | Receptor, Fibroblast Growth Factor, Type 1 - metabolism | Male | Gene Expression Profiling | Receptor, Fibroblast Growth Factor, Type 1 - genetics | Receptor, Fibroblast Growth Factor, Type 3 - metabolism | Case-Control Studies | Receptors, Fibroblast Growth Factor - analysis | Prostatic Neoplasms - genetics | RNA Interference | Receptor, Fibroblast Growth Factor, Type 2 - analysis | Receptors, Fibroblast Growth Factor - genetics | Transcription, Genetic | Receptor, Fibroblast Growth Factor, Type 4 - genetics | Receptor, Fibroblast Growth Factor, Type 1 - analysis | Receptor, Fibroblast Growth Factor, Type 3 - genetics | RNA, Small Interfering - pharmacology | Receptor, Fibroblast Growth Factor, Type 4 - analysis | Microscopy, Confocal | Receptors, Fibroblast Growth Factor - metabolism | Cell Line, Tumor | Polymorphism, Single Nucleotide | Receptor, Fibroblast Growth Factor, Type 3 - analysis | Receptor, Fibroblast Growth Factor, Type 2 - genetics | Protein Isoforms - genetics | Index Medicus
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6. Full Text FGF signalling regulates bone growth through autophagy
by Cinque, Laura and Forrester, Alison and Bartolomeo, Rosa and Svelto, Maria and Venditti, Rossella and Montefusco, Sandro and Polishchuk, Elena and Nusco, Edoardo and Rossi, Antonio and Medina, Diego L and Polishchuk, Roman and De Matteis, Maria Antonietta and Settembre, Carmine
Nature, ISSN 0028-0836, 12/2015, Volume 528, Issue 7581, pp. 272 - 275
Skeletal growth relies on both biosynthetic and catabolic processes(1,2). While the role of the former is clearly established, how the latter contributes to... 
CELLS | MULTIDISCIPLINARY SCIENCES | CRE RECOMBINASE | ENDOPLASMIC-RETICULUM | TISSUES | PROCOLLAGEN | EXPRESSION | LC3 | CHONDROGENESIS | TRANSGENIC MICE | Receptor, Fibroblast Growth Factor, Type 4 - metabolism | Chondrocytes - cytology | Cell Proliferation | Microtubule-Associated Proteins - genetics | Embryo, Mammalian | Microtubule-Associated Proteins - metabolism | Bone Development - physiology | Fibroblast Growth Factors - genetics | Autophagy - physiology | MAP Kinase Signaling System | Extracellular Matrix - genetics | Fibroblast Growth Factors - metabolism | Growth Plate - cytology | Collagen Type II - secretion | Cell Differentiation | Autophagy - genetics | Receptor, Fibroblast Growth Factor, Type 4 - genetics | Chondrocytes - metabolism | Signal Transduction | Cells, Cultured | Growth Plate - metabolism | Autophagy-Related Protein 7 | Animals | Mice | Bone Development - genetics | Physiological aspects | Autophagy (Cytology) | Bones | Fibroblast growth factors | Growth | Signal transduction | Autophagy | Growth factors | Index Medicus
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7. Full Text Expression profile and overexpression outcome indicate a role for βKlotho in skeletal muscle fibro/adipogenesis
by Phelps, Michael and Stuelsatz, Pascal and Yablonka‐Reuveni, Zipora
FEBS Journal, ISSN 1742-464X, 05/2016, Volume 283, Issue 9, pp. 1653 - 1668
Regeneration of skeletal muscles is required throughout life to ensure optimal performance. Therefore, a better understanding of the resident cells involved in... 
fibro/adipocytes | adipogenesis | FAP | FGF | fibroblast growth factor receptor | adipogenic differentiation | βKlotho | αKlotho | PiggyBac transposon | satellite cells | FAPs | FGF21 | PROGENITORS | CONNECTIVE-TISSUE FIBROBLASTS | BIOCHEMISTRY & MOLECULAR BIOLOGY | FIBROBLAST-GROWTH-FACTOR | MYOGENIC CELLS | GENE | METABOLIC-ACTIVITY | alpha Klotho | DIFFERENTIATION | beta Klotho | ADIPOSE-TISSUE | Receptor, Fibroblast Growth Factor, Type 4 - metabolism | Receptor, Fibroblast Growth Factor, Type 2 - metabolism | Receptor, Fibroblast Growth Factor, Type 1 - metabolism | Fibroblast Growth Factors - genetics | Adipocytes - cytology | Male | Muscle, Skeletal - metabolism | Muscle, Skeletal - cytology | RNA, Messenger - metabolism | Receptor, Fibroblast Growth Factor, Type 1 - genetics | Receptor, Fibroblast Growth Factor, Type 3 - metabolism | Fibroblast Growth Factors - metabolism | Cell Differentiation | Membrane Proteins - metabolism | Receptor, Fibroblast Growth Factor, Type 4 - genetics | Adipogenesis - genetics | Fibroblasts - metabolism | Cell Line | Receptor, Fibroblast Growth Factor, Type 3 - genetics | Signal Transduction | Membrane Proteins - genetics | Mice, Inbred C57BL | RNA, Messenger - genetics | Satellite Cells, Skeletal Muscle - cytology | Gene Expression Regulation | Mice, Transgenic | Satellite Cells, Skeletal Muscle - metabolism | Lipid Droplets | Animals | Adipocytes - metabolism | Fibroblasts - cytology | Mice | Receptor, Fibroblast Growth Factor, Type 2 - genetics | Index Medicus | Piggybac transposon | Fibro | Adipogenic differentiation | Satellite cells | adipocytes | Fibroblast growth factor receptors | Adipogenesis
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8. Full Text Selective Activation of FGFR4 by an FGF19 Variant Does Not Improve Glucose Metabolism in ob/ob Mice
by Xinle Wu and Hongfei Ge and Bryan Lemon and Jennifer Weiszmann and Jamila Gupte and Nessa Hawkins and Xiaofan Li and Jie Tang and Richard Lindberg and Yang Li and Steven L. McKnight
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 8/2009, Volume 106, Issue 34, pp. 14379 - 14384
FGF19 is a hormone that regulates bile acid and glucose homeostasis. Progress has been made in identifying cofactors for receptor activation. However, several... 
Adipose tissues | Molecules | Receptors | Phosphorylation | Bile acids | Liver | Homeostasis | Fibroblast growth factors | Heparin | Adipocytes | Diabetes | FGF21 | BETA-KLOTHO | SIGNAL | HOMEOSTASIS | SPECIFICITY | liver | MULTIDISCIPLINARY SCIENCES | RECEPTOR | FIBROBLAST-GROWTH-FACTOR | SUPPRESSION | DETERMINES | diabetes | FGF23 | Receptor, Fibroblast Growth Factor, Type 4 - metabolism | Receptor, Fibroblast Growth Factor, Type 2 - metabolism | Transcriptional Activation | Receptor, Fibroblast Growth Factor, Type 1 - metabolism | Fibroblast Growth Factors - genetics | Receptor, Fibroblast Growth Factor, Type 1 - genetics | Obesity - genetics | Receptor, Fibroblast Growth Factor, Type 3 - metabolism | Tissue Distribution | Adipose Tissue - metabolism | Fibroblast Growth Factors - metabolism | Membrane Proteins - metabolism | Receptor, Fibroblast Growth Factor, Type 4 - genetics | Cell Line | Receptor, Fibroblast Growth Factor, Type 3 - genetics | Glucose Tolerance Test | Membrane Proteins - genetics | Liver - metabolism | Mice, Inbred C57BL | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | Obesity - metabolism | Animals | Fibroblast Growth Factors - pharmacokinetics | Glucose - pharmacokinetics | Glucose - metabolism | Protein Binding | Mice, Obese | Mice | Receptor, Fibroblast Growth Factor, Type 2 - genetics | Glucose metabolism | Hormone receptors | Research | Chemical properties | Signal transduction | Rodents | Glucose | Gene expression | Metabolism | Index Medicus | Biological Sciences
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9. Full Text Targeting FGF19 inhibits tumor growth in colon cancer xenograft and FGF19 transgenic hepatocellular carcinoma models
by Desnoyers, L.R and Pai, R and Ferrando, R.E and Hötzel, K and Le, T and Ross, J and Carano, R and D'Souza, A and Qing, J and Mohtashemi, I and Ashkenazi, A and French, D.M
Oncogene, ISSN 0950-9232, 01/2008, Volume 27, Issue 1, pp. 85 - 97
Although fibroblast growth factor 19 (FGF19) can promote liver carcinogenesis in mice its involvement in human cancer is not well characterized. Here we report... 
β-catenin | Fibroblast growth factor | Hepatocellular carcinoma | Colon adenocarcinoma | FGFR4 | FGF19 | beta-catenin | MULTIPLE-MYELOMA | colon adenocarcinoma | INCREASED EXPRESSION | FIBROBLAST | BIOCHEMISTRY & MOLECULAR BIOLOGY | FACTOR RECEPTOR-3 | HUMAN BREAST-CANCER | ARG ALLELE | CELL BIOLOGY | fibroblast growth factor | GENE | ONCOLOGY | PROSTATE-CANCER | GENETICS & HEREDITY | hepatocellular carcinoma | ACTIVATING MUTATIONS | Gene Targeting - methods | Lung Neoplasms - drug therapy | Neoplasm Transplantation | Receptor, Fibroblast Growth Factor, Type 4 - metabolism | Colonic Neoplasms - genetics | Carcinoma, Squamous Cell - metabolism | Colonic Neoplasms - drug therapy | Humans | Fibroblast Growth Factors - genetics | Antibodies, Monoclonal - therapeutic use | Transplantation, Heterologous | Fibroblast Growth Factors - biosynthesis | Liver Neoplasms, Experimental - immunology | Receptor, Fibroblast Growth Factor, Type 4 - biosynthesis | Fibroblast Growth Factors - immunology | Carcinoma, Hepatocellular - drug therapy | Colonic Neoplasms - immunology | Carcinoma, Hepatocellular - genetics | Antineoplastic Agents - pharmacology | Carcinoma, Hepatocellular - immunology | Receptor, Fibroblast Growth Factor, Type 4 - genetics | Lung Neoplasms - genetics | HCT116 Cells | Mice, Transgenic | Xenograft Model Antitumor Assays - methods | Carcinoma, Squamous Cell - immunology | HT29 Cells | Lung Neoplasms - immunology | Animals | Carcinoma, Squamous Cell - drug therapy | Liver Neoplasms, Experimental - drug therapy | Mice, Nude | Antibodies, Blocking - therapeutic use | Mice | Mice, Inbred BALB C | Fibroblast Growth Factors - antagonists & inhibitors | Care and treatment | Colon cancer | Xenotransplantation | Physiological aspects | Fibroblast growth factors | Research | Health aspects | Risk factors | Genetics | Gene expression | Transgenic animals | Rodents | Colorectal cancer | Tumors | Index Medicus
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10. Full Text Convergent signaling pathways regulate parathyroid hormone and fibroblast growth factor-23 action on NPT2A-mediated phosphate transport
by Sneddon, W. Bruce and Ruiz, Giovanni W and Gallo, Luciana I and Xiao, Kunhong and Zhang, Qiangmin and Rbaibi, Youssef and Weisz, Ora A and Apodaca, Gerard L and Friedman, Peter A
Journal of Biological Chemistry, ISSN 0021-9258, 09/2016, Volume 291, Issue 36, pp. 18632 - 18642
Parathyroid hormone (PTH) and FGF23 are the primary hormones regulating acute phosphate homeostasis. Human renal proximal tubule cells (RPTECs) were used to... 
RENAL PROXIMAL TUBULE | PROTEIN-KINASE-A | MDCK CELLS | ACTIVATION | PTH | FGF-RECEPTOR | BIOCHEMISTRY & MOLECULAR BIOLOGY | DOWN-REGULATION | I COTRANSPORTERS | FACTOR RECEPTOR GENES | CALCIUM-TRANSPORT | Receptor, Fibroblast Growth Factor, Type 3 - genetics | Receptor, Parathyroid Hormone, Type 1 - metabolism | Humans | Receptor, Fibroblast Growth Factor, Type 1 - metabolism | Fibroblast Growth Factors - genetics | Phosphoproteins - genetics | Phosphoproteins - metabolism | Receptor, Fibroblast Growth Factor, Type 1 - genetics | Receptor, Fibroblast Growth Factor, Type 4 - biosynthesis | Parathyroid Hormone - genetics | Sodium-Hydrogen Exchangers - metabolism | Sodium-Phosphate Cotransporter Proteins, Type IIa - metabolism | Sodium-Phosphate Cotransporter Proteins, Type IIa - genetics | Fibroblast Growth Factors - metabolism | Phosphates - metabolism | Glucuronidase - biosynthesis | Glucuronidase - genetics | Parathyroid Hormone - metabolism | Receptor, Parathyroid Hormone, Type 1 - genetics | Signal Transduction - physiology | Sodium-Hydrogen Exchangers - genetics | Receptor, Fibroblast Growth Factor, Type 3 - biosynthesis | Receptor, Fibroblast Growth Factor, Type 4 - genetics | Cell Line, Transformed | Index Medicus | parathyroid hormone | NPT2A | klotho | PDZ Protein | fibroblast growth factor receptor (FGFR) | NHERF1 | alternative splicing | G protein-coupled receptor (GPCR) | transport | Cell Biology
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