. "2014-07-01+02:00"^^ . "Hlavn\u00ED p\u0159\u00EDnos projektu spo\u010D\u00EDval v odhalen\u00ED a popisu n\u011Bkolika nov\u00FDch proces\u016F patologick\u00E9 funkce FGFR. Konkr\u00E9tn\u011B \u0161lo o charakterizaci molekul\u00E1rn\u00EDho mechanizmu interakce FGFR3 s kanonickou WNT/beta-kateninovou dr\u00E1hou a roli t\u00E9to interakce v regulaci bun\u011B\u010Dn\u00E9 differenciace. Projekt podpo\u0159il publikaci 7 p\u016Fvodn\u00EDch v\u011Bdeck\u00FDch \u010Dl\u00E1nk\u016F a 2 review. P\u011Bt student\u016F se z\u00FA\u010Dastnilo \u0159e\u0161en\u00ED projektu."@cs . . . . . "GAP305/11/0752" . "2011-01-01+01:00"^^ . "0"^^ . . . . . "1"^^ . "The main objective of the proposal was to (A) discover novel intermediates of pathological FGFR3 signaling and to (B) characterize their role in cellular phenotypes regulated by FGFR3. The grant supported publication of 7 original research articles and 2 critical reviews. Project also enabled scientific training of 5 students,"@en . "Activating mutations in the FGFR3 tyrosine kinase account for several forms of human dwarfism, including achondroplasia and a thanatophoric dysplasia. Although achondroplasia is considered potentially treatable condition, there is no cure available at present. This is mostly due to our poor understanding of the mechanism of FGFR3 action in cartilage. Among the least characterized areas of FGFR3 signaling lies the nature of protein complexes participating in transduction of the FGFR3 signal into the nucleus. This proposal aims on characterization of novel proteins integral to the FGFR3 signaling and determination of their role in known cellular phenotypes of pathological FGFR3 signaling in cartilage such as growth inhibition, degradation of the extracellular matrix, changes in cellular shape and induction of premature cellular senescence."@en . "2013-06-07+02:00"^^ . . . "Molecular basis of FGFR3 signal transduction in skeletal dysplasia"@en . "0"^^ . . . "2013-12-31+01:00"^^ . "Molekul\u00E1rn\u00ED z\u00E1klady FGFR3 signalingu v kostn\u00ED dyspl\u00E1zii" . "9"^^ . "9"^^ . "http://www.isvav.cz/projectDetail.do?rowId=GAP305/11/0752"^^ . . . "Aktivuj\u00EDc\u00ED mutace v FGFR3 receptorov\u00E9 tyrozinov\u00E9 kin\u00E1ze jsou p\u0159\u00ED\u010Dinou vzniku n\u011Bkolika z\u00E1va\u017En\u00FDch poruch r\u016Fstu kosti jako je achondropl\u00E1zie a thanatoforick\u00E1 dyspl\u00E1zie. P\u0159esto\u017Ee je achondropl\u00E1zie v\u0161eobecn\u011B pova\u017Eov\u00E1na za l\u00E9\u010Diteln\u00E9 onemocn\u011Bn\u00ED, v sou\u010Dastnosti \u017E\u00E1dn\u00E1 \u00FA\u010Dinn\u00E1 l\u00E9\u010Dba neexistuje. To je d\u00E1no p\u0159edev\u0161\u00EDm na\u0161imi omezen\u00FDmi znalostmi molekul\u00E1rn\u00EDch mechanizm\u016F signalingu FGFR3 v chrupavce. Mezi nejm\u00E9n\u011B charakterizovan\u00E9 oblasti FGFR3 signalingu pat\u0159\u00ED zejm\u00E9na proteinov\u00E9 komplexy, kter\u00E9 se \u00FA\u010Dastn\u00ED p\u0159enosu sign\u00E1lu do j\u00E1dra. C\u00EDlem navrhovan\u00E9ho projektu je charakterizovat nov\u00E9 proteiny, kter\u00E9\u00A0jsou sou\u010D\u00E1st\u00ED mechanizmu\u00A0sign\u00E1lov\u00E1n\u00ED FGFR3\u00A0kin\u00E1zy a definovat jejich funk\u010Dn\u00ED v\u00FDznam pro bun\u011B\u010Dn\u00E9 fenotypy (inhibice r\u016Fstu, degradace vn\u011Bbun\u011B\u010Dn\u00E9 hmoty, zm\u011Bny bun\u011B\u010Dn\u00E9ho tvaru, indukce p\u0159ed\u010Dasn\u00E9ho bun\u011B\u010Dn\u00E9ho st\u00E1rnut\u00ED) regulovan\u00E9 patologick\u00FDm FGFR3 signalingem v chrupavce." . . "FGFR3 kinase cartilage achondroplasia signal transduction."@en . . .