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The paradox of FGFR3 signaling in skeletal dysplasia: Why chondrocytes growth arrest while other cells over proliferate

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14110%2F14%3A00073450" target="_blank" >RIV/00216224:14110/14:00073450 - isvavai.cz</a>

  • Alternative codes found

    RIV/68081707:_____/14:00440129

  • Result on the web

    <a href="http://dx.doi.org/10.1016/j.mrrev.2013.11.001" target="_blank" >http://dx.doi.org/10.1016/j.mrrev.2013.11.001</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1016/j.mrrev.2013.11.001" target="_blank" >10.1016/j.mrrev.2013.11.001</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    The paradox of FGFR3 signaling in skeletal dysplasia: Why chondrocytes growth arrest while other cells over proliferate

  • Original language description

    Somatic mutations in receptor tyrosine kinase FGFR3 cause excessive cell proliferation, leading to cancer or skin overgrowth. Remarkably, the same mutations inhibit chondrocyte proliferation and differentiation in developing bones, resulting in skeletaldysplasias, such as hypochondroplasia, achondroplasia, SADDAN and thanatophoric dysplasia. A similar phenotype is observed in Noonan syndrome, Leopard syndrome, hereditary gingival fibromatosis, neurofibromatosis type 1, Costello syndrome, Legius syndrome and cardiofaciocutaneous syndrome. Collectively termed RASopathies, the latter syndromes are caused by germline mutations in components of the RAS/ERK MAP kinase signaling pathway. This article considers the evidence suggesting that FGFR3 activation inchondrocytes mimics the activation of major oncogenes signaling via the ERK pathway.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>x</sub> - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)

  • CEP classification

    CE - Biochemistry

  • OECD FORD branch

Result continuities

  • Project

    Result was created during the realization of more than one project. More information in the Projects tab.

  • Continuities

    P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Others

  • Publication year

    2014

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Mutation Research - Reviews in Mutation Research

  • ISSN

    1383-5742

  • e-ISSN

  • Volume of the periodical

    759

  • Issue of the periodical within the volume

    January?March

  • Country of publishing house

    NL - THE KINGDOM OF THE NETHERLANDS

  • Number of pages

    9

  • Pages from-to

    40-48

  • UT code for WoS article

    000333857600004

  • EID of the result in the Scopus database