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@article{879430, author = {Krejčí, Pavel and Salazar, Lisa and Goodridge, Helen and Kashiwada, Tamara and Schibler, Matthew and Jelínková, Petra and Thompson,, Leslie Michels and Wilcox, William}, article_number = {3}, keywords = {FACTOR RECEPTOR-3 FGFR3; THANATOPHORIC DYSPLASIA; SERINE PHOSPHORYLATION; INHIBITS PROLIFERATION; INTERFERON-GAMMA; PC12 CELLS; ACTIVATION; INDUCTION; KINASE; APOPTOSIS}, language = {eng}, issn = {0021-9533}, journal = {JOURNAL OF CELL SCIENCE}, title = {STAT1 and STAT3 do not participate in FGF-mediated growth arrest in chondrocytes}, volume = {121}, year = {2008} }
TY - JOUR ID - 879430 AU - Krejčí, Pavel - Salazar, Lisa - Goodridge, Helen - Kashiwada, Tamara - Schibler, Matthew - Jelínková, Petra - Thompson,, Leslie Michels - Wilcox, William PY - 2008 TI - STAT1 and STAT3 do not participate in FGF-mediated growth arrest in chondrocytes JF - JOURNAL OF CELL SCIENCE VL - 121 IS - 3 SP - 272-81 EP - 272-81 SN - 00219533 KW - FACTOR RECEPTOR-3 FGFR3 KW - THANATOPHORIC DYSPLASIA KW - SERINE PHOSPHORYLATION KW - INHIBITS PROLIFERATION KW - INTERFERON-GAMMA KW - PC12 CELLS KW - ACTIVATION KW - INDUCTION KW - KINASE KW - APOPTOSIS N2 - Activating mutations in fibroblast growth factor receptor 3 (FGFR3) cause several human skeletal dysplasias as a result of attenuation of cartilage growth. It is believed that FGFR3 inhibits chondrocyte proliferation via activation of signal transducers and activators of transcription ( STAT) proteins, although the exact mechanism of both STAT activation and STAT-mediated inhibition of chondrocyte growth is unclear. We show that FGFR3 interacts with STAT1 in cells and is capable of activating phosphorylation of STAT1 in a kinase assay, thus potentially serving as a STAT1 kinase in chondrocytes. However, as demonstrated by western blotting with phosphorylation-specific antibodies, imaging of STAT nuclear translocation, STAT transcription factor assays and STAT luciferase reporter assays, FGF does not activate STAT1 or STAT3 in RCS chondrocytes, which nevertheless respond to a FGF stimulus with potent growth arrest. Moreover, addition of active STAT1 and STAT3 to the FGF signal, by means of cytokine treatment, SRC-mediated STAT activation or expression of constitutively active STAT mutants does not sensitize RCS chondrocytes to FGF-mediated growth arrest. Since FGF-mediated growth arrest is rescued by siRNA-mediated downregulation of the MAP kinase ERK1/2 but not STAT1 or STAT3, our data support a model whereby the ERK arm but not STAT arm of FGF signaling in chondrocytes accounts for the growth arrest phenotype. ER -
KREJČÍ, Pavel, Lisa SALAZAR, Helen GOODRIDGE, Tamara KASHIWADA, Matthew SCHIBLER, Petra JELÍNKOVÁ, Leslie Michels THOMPSON, and William WILCOX. STAT1 and STAT3 do not participate in FGF-mediated growth arrest in chondrocytes. \textit{JOURNAL OF CELL SCIENCE}. 2008, vol.~121, No~3, p.~272-81, 11 pp. ISSN~0021-9533.
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