Literature DB >> 8742128

Mutations of the fibroblast growth factor receptor-3 gene in achondroplasia.

F Rousseau1, J Bonaventure, L Legeai-Mallet, A Pelet, J M Rozet, P Maroteaux, M Le Merrer, A Munnich.   

Abstract

Achondroplasia (ACH), the most common cause of chondrodysplasia in man (1 in 15,000 live births), is an autosomal dominant condition of unknown origin characterized by short-limbed dwarfism and macrocephaly. Recently, a gene for ACH has been mapped to chromosome 4p16.3. The genetic interval encompassing the disease gene contains a member of the fibroblast growth factor receptor (FGFR) family which is expressed in articular chondrocytes (FGFR3). We report here recurrent missense mutations, in a CpG doublet of the transmembrane domain of the FGFR3 protein (G380R) in 17 sporadic cases and 6 unrelated familial forms of ACH and show that the mutant genotype segregates with the disease in these families. Thus, it appears that recurrent mutations of a single amino acid in the transmembrane domain of the FGFR3 protein account for all cases (23/23) of achondroplasia in our series.

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Year:  1996        PMID: 8742128     DOI: 10.1159/000184768

Source DB:  PubMed          Journal:  Horm Res        ISSN: 0301-0163


  13 in total

Review 1.  FGFR3-related dwarfism and cell signaling.

Authors:  Daisuke Harada; Yoshitaka Yamanaka; Koso Ueda; Hiroyuki Tanaka; Yoshiki Seino
Journal:  J Bone Miner Metab       Date:  2008-12-09       Impact factor: 2.626

2.  Non-invasive prenatal detection of achondroplasia using circulating fetal DNA in maternal plasma.

Authors:  Ji Hyae Lim; Mee Jin Kim; Shin Young Kim; Hye Ok Kim; Mee Jin Song; Min Hyoung Kim; So Yeon Park; Jae Hyug Yang; Hyun Mee Ryu
Journal:  J Assist Reprod Genet       Date:  2010-10-21       Impact factor: 3.412

3.  Improvement of the sagittal alignment of the spine in patients with achondroplasia after subtrochanteric femoral lengthening.

Authors:  Rosa M Egea-Gámez; María Galán-Olleros; Javier Alonso-Hernández; Carlos Miranda-Gorozarri; Ignacio Martínez-Caballero; Ángel Palazón-Quevedo; Rafael González-Díaz
Journal:  Spine Deform       Date:  2022-06-02

4.  The ups and downs of mutation frequencies during aging can account for the Apert syndrome paternal age effect.

Authors:  Song-Ro Yoon; Jian Qin; Rivka L Glaser; Ethylin Wang Jabs; Nancy S Wexler; Rebecca Sokol; Norman Arnheim; Peter Calabrese
Journal:  PLoS Genet       Date:  2009-07-10       Impact factor: 5.917

Review 5.  Of hedgehogs and hereditary bone tumors: re-examination of the pathogenesis of osteochondromas.

Authors:  Kevin B Jones; Jose A Morcuende
Journal:  Iowa Orthop J       Date:  2003

Review 6.  Neurological Manifestations of Achondroplasia.

Authors:  John B Bodensteiner
Journal:  Curr Neurol Neurosci Rep       Date:  2019-11-28       Impact factor: 5.081

7.  The observed human sperm mutation frequency cannot explain the achondroplasia paternal age effect.

Authors:  Irene Tiemann-Boege; William Navidi; Raji Grewal; Dan Cohn; Brenda Eskenazi; Andrew J Wyrobek; Norman Arnheim
Journal:  Proc Natl Acad Sci U S A       Date:  2002-10-23       Impact factor: 11.205

Review 8.  Prion-like properties of disease-relevant proteins in amyotrophic lateral sclerosis.

Authors:  S Bräuer; V Zimyanin; A Hermann
Journal:  J Neural Transm (Vienna)       Date:  2018-02-08       Impact factor: 3.575

9.  Ligand activation leads to regulated intramembrane proteolysis of fibroblast growth factor receptor 3.

Authors:  Catherine R Degnin; Melanie B Laederich; William A Horton
Journal:  Mol Biol Cell       Date:  2011-08-24       Impact factor: 4.138

10.  Inducible dimerization of FGFR1: development of a mouse model to analyze progressive transformation of the mammary gland.

Authors:  Bryan E Welm; Kevin W Freeman; Mercy Chen; Alejandro Contreras; David M Spencer; Jeffrey M Rosen
Journal:  J Cell Biol       Date:  2002-05-13       Impact factor: 10.539

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