Sixteen years and counting: the current understanding of fibroblast growth factorreceptor 3 (FGFR3) signaling in skeletal dysplasias.
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14310%2F12%3A00057264" target="_blank" >RIV/00216224:14310/12:00057264 - isvavai.cz</a>
Alternative codes found
RIV/68081707:_____/12:00375985 RIV/60077344:_____/12:00375985
Result on the web
<a href="http://dx.doi.org/10.1002/humu.21636" target="_blank" >http://dx.doi.org/10.1002/humu.21636</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1002/humu.21636" target="_blank" >10.1002/humu.21636</a>
Alternative languages
Result language
angličtina
Original language name
Sixteen years and counting: the current understanding of fibroblast growth factorreceptor 3 (FGFR3) signaling in skeletal dysplasias.
Original language description
In 1994, the field of bone biology was significantly advanced by the discovery that activating mutations in the fibroblast growth factor receptor 3 (FGFR3) receptor tyrosine kinase (TK) account for the common genetic form of dwarfism in humans, achondroplasia (ACH). Other conditions soon followed, with the list of human disorders caused by FGFR3 mutations now reaching at least 10. An array of vastly different diagnoses is caused by similar mutations in FGFR3, including syndromes affecting skeletal development (hypochondroplasia [HCH], ACH, thanatophoric dysplasia [TD]), skin (epidermal nevi, seborrhaeic keratosis, acanthosis nigricans), and cancer (multiple myeloma [MM], prostate and bladder carcinoma, seminoma). Despite many years of research, severalaspects of FGFR3 function in disease remain obscure or controversial. As FGFR3-related skeletal dysplasias are caused by growth attenuation of the cartilage, chondrocytes appear to be unique in their response to FGFR3 activation.
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
ED - Physiology
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)<br>Z - Vyzkumny zamer (s odkazem do CEZ)<br>S - Specificky vyzkum na vysokych skolach
Others
Publication year
2012
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Human Mutation
ISSN
1059-7794
e-ISSN
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Volume of the periodical
33
Issue of the periodical within the volume
1
Country of publishing house
US - UNITED STATES
Number of pages
13
Pages from-to
29-41
UT code for WoS article
000300705300005
EID of the result in the Scopus database
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