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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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