Klotho converts canonical FGF receptor into a specific receptor for FGF23

[1]  K. White,et al.  Analysis of the biochemical mechanisms for the endocrine actions of fibroblast growth factor-23. , 2005, Endocrinology.

[2]  Y. Nabeshima,et al.  Impaired negative feedback suppression of bile acid synthesis in mice lacking betaKlotho. , 2005, The Journal of clinical investigation.

[3]  J. Gromada,et al.  FGF-21 as a novel metabolic regulator. , 2005, The Journal of clinical investigation.

[4]  N. Itoh,et al.  Evolution of the Fgf and Fgfr gene families. , 2004, Trends in genetics : TIG.

[5]  M. Razzaque,et al.  Homozygous ablation of fibroblast growth factor-23 results in hyperphosphatemia and impaired skeletogenesis, and reverses hypophosphatemia in Phex-deficient mice. , 2004, Matrix biology : journal of the International Society for Matrix Biology.

[6]  K. Nozaki,et al.  Secreted Klotho protein in sera and CSF: implication for post‐translational cleavage in release of Klotho protein from cell membrane , 2004, FEBS letters.

[7]  Y. Takeuchi,et al.  Targeted ablation of Fgf23 demonstrates an essential physiological role of FGF23 in phosphate and vitamin D metabolism. , 2004, The Journal of clinical investigation.

[8]  Y. Takeuchi,et al.  FGF‐23 Is a Potent Regulator of Vitamin D Metabolism and Phosphate Homeostasis , 2003, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.

[9]  K. Fukuda,et al.  Klotho, a gene related to a syndrome resembling human premature aging, functions in a negative regulatory circuit of vitamin D endocrine system. , 2003, Molecular endocrinology.

[10]  H. Jüppner,et al.  Circulating concentration of FGF-23 increases as renal function declines in patients with chronic kidney disease, but does not change in response to variation in phosphate intake in healthy volunteers. , 2003, Kidney international.

[11]  K. White,et al.  FGF-23 in fibrous dysplasia of bone and its relationship to renal phosphate wasting. , 2003, The Journal of clinical investigation.

[12]  S. Kliewer,et al.  Definition of a novel growth factor-dependent signal cascade for the suppression of bile acid biosynthesis. , 2003, Genes & development.

[13]  K. White,et al.  Fibroblast growth factor 23 in oncogenic osteomalacia and X-linked hypophosphatemia. , 2003, The New England journal of medicine.

[14]  Y. Takeuchi,et al.  Increased circulatory level of biologically active full-length FGF-23 in patients with hypophosphatemic rickets/osteomalacia. , 2002, The Journal of clinical endocrinology and metabolism.

[15]  Y. Nabeshima.  Klotho: a fundamental regulator of aging , 2002, Ageing Research Reviews.

[16]  Nobuyuki Itoh,et al.  Fibroblast Growth Factor (FGF)-23 Inhibits Renal Phosphate Reabsorption by Activation of the Mitogen-activated Protein Kinase Pathway* , 2002, The Journal of Biological Chemistry.

[17]  T. Yoneya,et al.  Mutant FGF-23 responsible for autosomal dominant hypophosphatemic rickets is resistant to proteolytic cleavage and causes hypophosphatemia in vivo. , 2002, Endocrinology.

[18]  Y. Hayashizaki,et al.  Identification of a novel mouse membrane-bound family 1 glycosidase-like protein, which carries an atypical active site structure. , 2002, Biochimica et biophysica acta.

[19]  Y. Nabeshima,et al.  Mediation of Unusually High Concentrations of 1,25-Dihydroxyvitamin D in Homozygous klotho Mutant Mice by Increased Expression of Renal 1α-Hydroxylase Gene. , 2002, Endocrinology.

[20]  A. Turjanski,et al.  Structure, solvation, and bonding in pentacyano(L)ferrate(II) ions (L=aliphatic amine): a density functional study , 2001 .

[21]  S. Takeda,et al.  Cloning and characterization of FGF23 as a causative factor of tumor-induced osteomalacia , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[22]  Nobuyuki Itoh,et al.  Fibroblast growth factors , 2001, Genome Biology.

[23]  K. Wikvall.  Cytochrome P450 enzymes in the bioactivation of vitamin D to its hormonal form (review). , 2001, International journal of molecular medicine.

[24]  T. Meitinger,et al.  Autosomal dominant hypophosphataemic rickets is associated with mutations in FGF23 , 2000, Nature Genetics.

[25]  Y. Nabeshima,et al.  Molecular cloning and expression analyses of mouse βklotho, which encodes a novel Klotho family protein , 2000, Mechanisms of Development.

[26]  W. Aird,et al.  Egr-1 gene is induced by the systemic administration of the vascular endothelial growth factor and the epidermal growth factor. , 2000, Blood.

[27]  H. Murer,et al.  Proximal tubular phosphate reabsorption: molecular mechanisms. , 2000, Physiological reviews.

[28]  Tadashi Kaname,et al.  Mutation of the mouse klotho gene leads to a syndrome resembling ageing , 1997, Nature.

[29]  K. Alitalo,et al.  Signal transduction by fibroblast growth factor receptor-4 (FGFR-4). Comparison with FGFR-1. , 1994, The Journal of biological chemistry.

[30]  L. Lau,et al.  A gene activated in mouse 3T3 cells by serum growth factors encodes a protein with "zinc finger" sequences. , 1988, Proceedings of the National Academy of Sciences of the United States of America.

[31]  V. Sukhatme,et al.  Early growth response protein 1 (Egr-1): prototype of a zinc-finger family of transcription factors. , 1995, Progress in nucleic acid research and molecular biology.