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
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Czech description
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Classification
Type
J<sub>x</sub> - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)
CEP classification
CE - Biochemistry
OECD FORD branch
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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
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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
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