Autosomal dominant hypophosphataemic rickets is associated with mutations in FGF23

[1]  James S. Dyer,et al.  Too Much of a Good Thing? , 1999, Oper. Res..

[2]  Y. Kihara,et al.  Development of enzyme-linked immunosorbent assay for acidic fibroblast growth factor and its clinical application. , 1999, Clinica chimica acta; international journal of clinical chemistry.

[3]  D. Danilenko,et al.  Fgf-10 is required for both limb and lung development and exhibits striking functional similarity to Drosophila branchless. , 1998, Genes & development.

[4]  G. Martin,et al.  An Fgf8 mutant allelic series generated by Cre- and Flp-mediated recombination , 1998, Nature Genetics.

[5]  M. Speer,et al.  Autosomal dominant hypophosphatemic rickets is linked to chromosome 12p13. , 1997, The Journal of clinical investigation.

[6]  T. Meitinger,et al.  Genomic organization of the human PEX gene mutated in X-linked dominant hypophosphatemic rickets. , 1997, Genome research.

[7]  D. Donoghue,et al.  FGFR activation in skeletal disorders: too much of a good thing. , 1997, Trends in genetics : TIG.

[8]  S. Karlin,et al.  Prediction of complete gene structures in human genomic DNA. , 1997, Journal of molecular biology.

[9]  M. Econs,et al.  Autosomal dominant hypophosphatemic rickets/osteomalacia: clinical characterization of a novel renal phosphate-wasting disorder. , 1997, The Journal of clinical endocrinology and metabolism.

[10]  Michael Ruogu Zhang,et al.  Identification of protein coding regions in the human genome by quadratic discriminant analysis. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[11]  P. Leder,et al.  Fibroblast Growth Factor Receptor 3 Is a Negative Regulator of Bone Growth , 1996, Cell.

[12]  G. Dorn,et al.  Abnormal bone growth and selective translational regulation in basic fibroblast growth factor (FGF-2) transgenic mice. , 1995, Molecular biology of the cell.

[13]  A. Poustka,et al.  A gene (PEX) with homologies to endopeptidases is mutated in patients with X–linked hypophosphatemic rickets , 1995, Nature Genetics.

[14]  Sue Malcolm,et al.  Mutations in the fibroblast growth factor receptor 2 gene cause Crouzon syndrome , 1994, Nature Genetics.

[15]  D. Church,et al.  Mutations in the transmembrane domain of FGFR3 cause the most common genetic form of dwarfism, achondroplasia , 1994, Cell.

[16]  M. Econs,et al.  Tumor-induced osteomalacia--unveiling a new hormone. , 1994, The New England journal of medicine.

[17]  P. Kao,et al.  Brief report: inhibition of renal phosphate transport by a tumor product in a patient with oncogenic osteomalacia. , 1994, The New England journal of medicine.

[18]  J. Bonaventure,et al.  Reexpression of cartilage-specific genes by dedifferentiated human articular chondrocytes cultured in alginate beads. , 1994, Experimental cell research.

[19]  E. Uberbacher,et al.  Locating protein-coding regions in human DNA sequences by a multiple sensor-neural network approach. , 1991, Proceedings of the National Academy of Sciences of the United States of America.

[20]  U. Liberman,et al.  Hereditary hypophosphatemic rickets with hypercalciuria. , 1985, The New England journal of medicine.

[21]  Harrison He,et al.  Familial hypophosphatemic rickets showing autosomal dominant inheritance. , 1971 .

[22]  R. Winters,et al.  A GENETIC STUDY OF FAMILIAL HYPOPHOSPHATEMIA AND VITAMIN D RESISTANT RICKETS WITH A REVIEW OF THE LITERATURE , 1958, Medicine.

[23]  I. Kaitila,et al.  A recurrent mutation in the tyrosine kinase domain of fibroblast growth factor receptor 3 causes hypochondroplasia , 1995, Nature Genetics.

[24]  J. Opitz,et al.  Hypophosphatemic nonrachitic bone disease: an entity distinct from X-linked hypophosphatemia in the renal defect, bone involvement, and inheritance. , 1977, American journal of medical genetics.

[25]  J. Bianchine,et al.  Familial hypophosphatemic rickets showing autosomal dominant inheritance. , 1971, Birth defects original article series.