Analysis of STAT1 Activation by Six FGFR3 Mutants Associated with Skeletal Dysplasia Undermines Dominant Role of STAT1 in FGFR3 Signaling in Cartilage

@article{Krejc2008AnalysisOS,
  title={Analysis of STAT1 Activation by Six FGFR3 Mutants Associated with Skeletal Dysplasia Undermines Dominant Role of STAT1 in FGFR3 Signaling in Cartilage},
  author={Pavel Krejc{\'i} and Lisa Fonseca Salazar and Tamara A. Kashiwada and Katarina Chlebova and Alena Sala{\vs}ov{\'a} and Leslie M. Thompson and V{\'i}tězslav Bryja and Alois Kozub{\'i}k and William R Wilcox},
  journal={PLoS ONE},
  year={2008},
  volume={3},
  pages={115 - 125}
}
Activating mutations in FGFR3 tyrosine kinase cause several forms of human skeletal dysplasia. Although the mechanisms of FGFR3 action in cartilage are not completely understood, it is believed that the STAT1 transcription factor plays a central role in pathogenic FGFR3 signaling. Here, we analyzed STAT1 activation by the N540K, G380R, R248C, Y373C, K650M and K650E-FGFR3 mutants associated with skeletal dysplasias. In a cell-free kinase assay, only K650M and K650E-FGFR3 caused activatory STAT1… CONTINUE READING

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