KREJČÍ, Pavel, Lisa SALAZAR, Tamara A. KASHIWADA, Katarína CHLEBOVÁ, Alena SALAŠOVÁ, Leslie Michels THOMPSON, Vítězslav BRYJA, Alois KOZUBÍK and William R. WILCOX. Analysis of STAT1 activation by six FGFR3 mutants associated with skeletal dysplasia undermines dominant role of STAT1 in FGFR3 signaling in cartilage. PLoS ONE. 2008, vol. 3, No 12, p. 72-81, 8 pp. ISSN 1932-6203.
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Basic information
Original name Analysis of STAT1 activation by six FGFR3 mutants associated with skeletal dysplasia undermines dominant role of STAT1 in FGFR3 signaling in cartilage
Name in Czech Analýza aktivace STAT1 pomocí 6ti FGFR3 mutantu asociovaných se skeletální dysplasii podkopává roli STAT1 jako hlavního mediátora patologického FGFR3 signalingu v chrupavce.
Authors KREJČÍ, Pavel (203 Czech Republic, guarantor, belonging to the institution), Lisa SALAZAR (840 United States of America), Tamara A. KASHIWADA (840 United States of America), Katarína CHLEBOVÁ (703 Slovakia), Alena SALAŠOVÁ (203 Czech Republic, belonging to the institution), Leslie Michels THOMPSON (840 United States of America), Vítězslav BRYJA (203 Czech Republic, belonging to the institution), Alois KOZUBÍK (203 Czech Republic, belonging to the institution) and William R. WILCOX (840 United States of America).
Edition PLoS ONE. 2008, 1932-6203.
Other information
Original language English
Type of outcome Article in a journal
Field of Study Genetics and molecular biology
Country of publisher United States of America
Confidentiality degree is not subject to a state or trade secret
RIV identification code RIV/00216224:14310/08:00024443
Organization unit Faculty of Science
UT WoS 000265458500007
Keywords in English FGFR3; STAT1; activation; skeletal dysplasia
Tags activation, FGFR3, skeletal dysplasia, STAT1
Changed by Changed by: Mgr. Jiřina Medalová, Ph.D., učo 176525. Changed: 20/3/2012 12:43.
Abstract
Article analyses activation of STAT1 by the six different FGFR3 mutants associated with skeletal dysplasia. We report that only the K650E and K650M mutants activate STAT1. As these mutants represent only a mionority of patients suffering from FGFR3-related skeletal dysplasia, it appears that STAT1 might not be the major intermediate of FGFR3 signaling in cartilage.
Abstract (in Czech)
Článek analyzuje aktivaci STAT1 pomocí 6ti FGFR3 mutantu asociovaných se skeletální dysplasií. Dle našich dat pouze K650E a K650M mutanti aktivují STAT1. Jelikož K650E a K650M mutace se vyskytují pouze u malé části pacientů se skeletální dysplasií, je nepravděpodobné, že STAT1 představuje hlavní mediátor patologického FGFR3 signalingu v chrupavce.
Links
MSM0021622415, plan (intention)Name: Molekulární podstata buněčných a tkáňových regulací
Investor: Ministry of Education, Youth and Sports of the CR, Molecular basis of cell and tissue regulations
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