A novel human homologue of the Drosophila frizzled wnt receptor gene binds wingless protein and is in the Williams syndrome deletion at 7q11.23.
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R. Nusse | U. Francke | R. Peoples | Y. Wang | L. Pérez-Jurado | C. H. Samos | Yu-Ker Wang | Luis A. Pérez-Jurado
[1] U. Francke,et al. Molecular definition of the chromosome 7 deletion in Williams syndrome and parent-of-origin effects on growth. , 1996, American journal of human genetics.
[2] S. Scherer,et al. Identification of genes from a 500-kb region at 7q11.23 that is commonly deleted in Williams syndrome patients. , 1996, Genomics.
[3] Jeremy Nathans,et al. A new member of the frizzled family from Drosophila functions as a Wingless receptor , 1996, Nature.
[4] Mark Noble,et al. LIM-kinase1 Hemizygosity Implicated in Impaired Visuospatial Constructive Cognition , 1996, Cell.
[5] M. Tassabehji,et al. LIM–kinase deleted in Williams syndrome , 1996, Nature Genetics.
[6] U. Francke,et al. The gene for replication factor C subunit 2 (RFC2) is within the 7q11.23 Williams syndrome deletion. , 1996, American journal of human genetics.
[7] A. Wessel,et al. Incidence and spectrum of renal abnormalities in Williams-Beuren syndrome. , 1996, American journal of medical genetics.
[8] J. Nathans,et al. A Large Family of Putative Transmembrane Receptors Homologous to the Product of the Drosophila Tissue Polarity Gene frizzled(*) , 1996, The Journal of Biological Chemistry.
[9] C. Morris,et al. Strong correlation of elastin deletions, detected by FISH, with Williams syndrome: evaluation of 235 patients. , 1995, American journal of human genetics.
[10] A. Baldini,et al. A human homologue of the Drosophila polarity gene frizzled has been identified and mapped to 17q21.1. , 1995, Genomics.
[11] L. Shaffer,et al. Deletions of the elastin gene at 7q11.23 occur in approximately 90% of patients with Williams syndrome. , 1995, American journal of human genetics.
[12] J. Klingensmith,et al. Signaling by wingless in Drosophila. , 1994, Developmental biology.
[13] R. John,et al. Identification of genes within CpG-enriched DNA from human chromosome 4p16.3. , 1994, Human molecular genetics.
[14] P. Adler,et al. A single frizzled protein has a dual function in tissue polarity. , 1994, Development.
[15] R. Nusse,et al. Biological activity of soluble wingless protein in cultured Drosophila imaginal disc cells , 1994, Nature.
[16] Norbert Perrimon,et al. The genetic basis of patterned baldness in Drosophila , 1994, Cell.
[17] C. Strader,et al. Structure and function of G protein-coupled receptors. , 1994, Annual review of biochemistry.
[18] C. Morris,et al. Williams syndrome: autosomal dominant inheritance. , 1993, American journal of medical genetics.
[19] L. Sadler,et al. The Williams syndrome: evidence for possible autosomal dominant inheritance. , 1993, American journal of medical genetics.
[20] Patricia Spallone,et al. Hemizygosity at the elastin locus in a developmental disorder, Williams syndrome , 1993, Nature Genetics.
[21] M. Krasnow,et al. Intercellular signalling in Drosophila segment formation reconstructed in vitro , 1993, Nature.
[22] Colleen A. Morris,et al. The elastin gene is disrupted by a translocation associated with supravalvular aortic stenosis , 1993, Cell.
[23] P. Adler. The genetic control of tissue polarity in Drosophila , 1992, BioEssays : news and reviews in molecular, cellular and developmental biology.
[24] M. Capecchi,et al. Swaying is a mutant allele of the proto-oncogene Wnt-1 , 1991, Cell.
[25] W. Talbot,et al. The drosophila EcR gene encodes an ecdysone receptor, a new member of the steroid receptor superfamily , 1991, Cell.
[26] A. Monaco,et al. Mapping irradiation hybrids to cosmid and yeast artificial chromosome libraries by direct hybridization of Alu-PCR products. , 1991, Nucleic acids research.
[27] U. Bellugi,et al. Neuropsychological, neurological, and neuroanatomical profile of Williams syndrome. , 2005, American journal of medical genetics. Supplement.
[28] Andrew P. McMahon,et al. The Wnt-1 (int-1) proto-oncogene is required for development of a large region of the mouse brain , 1990, Cell.
[29] Mario R. Capecchi,et al. Targeted disruption of the murine int-1 proto-oncogene resulting in severe abnormalities in midbrain and cerebellar development , 1990, Nature.
[30] M. Caron,et al. Role of extracellular disulfide-bonded cysteines in the ligand binding function of the beta 2-adrenergic receptor. , 1990, Biochemistry.
[31] M. Caron,et al. Palmitoylation of the human beta 2-adrenergic receptor. Mutation of Cys341 in the carboxyl tail leads to an uncoupled nonpalmitoylated form of the receptor. , 1989, The Journal of biological chemistry.
[32] C A Morris,et al. Natural history of Williams syndrome: physical characteristics. , 1988, The Journal of pediatrics.
[33] H. Varmus,et al. Expression of the proto-oncogene int-1 is restricted to postmeiotic male germ cells and the neural tube of mid-gestational embryos , 1987, Cell.
[34] A. McMahon,et al. Expression of the proto-oncogene int-1 is restricted to specific neural cells in the developing mouse embryo , 1987, Cell.
[35] J. Charlton,et al. Allelic variation at the frizzled locus of Drosophila , 1987 .
[36] K. Suzuki,et al. Gene organization of the small subunit of human calcium-activated neutral protease. , 1986, Nucleic acids research.
[37] U. Francke,et al. Chromosomal mapping of genes involved in growth control. , 1986, Cold Spring Harbor symposia on quantitative biology.
[38] R. Doolittle,et al. A simple method for displaying the hydropathic character of a protein. , 1982, Journal of molecular biology.
[39] H. Wesselhoeft,et al. [The genetic aspects of Williams-Beuren syndrome and the isolated form of the supravalvular aortic stenosis. Investigation of 128 families (author's transl)]. , 1980, Zeitschrift fur Kardiologie.