Attributes | Values |
---|
rdf:type
| |
Description
| - 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.
- 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. (en)
|
Title
| - STAT1 and STAT3 do not participate in FGF-mediated growth arrest in chondrocytes
- STAT1 and STAT3 do not participate in FGF-mediated growth arrest in chondrocytes (en)
|
skos:prefLabel
| - STAT1 and STAT3 do not participate in FGF-mediated growth arrest in chondrocytes
- STAT1 and STAT3 do not participate in FGF-mediated growth arrest in chondrocytes (en)
|
skos:notation
| - RIV/00216224:14310/08:00067178!RIV14-MSM-14310___
|
http://linked.open...avai/riv/aktivita
| |
http://linked.open...avai/riv/aktivity
| - S, Z(AV0Z50040507), Z(AV0Z50040702), Z(MSM0021622430)
|
http://linked.open...iv/cisloPeriodika
| |
http://linked.open...vai/riv/dodaniDat
| |
http://linked.open...aciTvurceVysledku
| |
http://linked.open.../riv/druhVysledku
| |
http://linked.open...iv/duvernostUdaju
| |
http://linked.open...titaPredkladatele
| |
http://linked.open...dnocenehoVysledku
| |
http://linked.open...ai/riv/idVysledku
| - RIV/00216224:14310/08:00067178
|
http://linked.open...riv/jazykVysledku
| |
http://linked.open.../riv/klicovaSlova
| - FACTOR RECEPTOR-3 FGFR3; THANATOPHORIC DYSPLASIA; SERINE PHOSPHORYLATION; INHIBITS PROLIFERATION; INTERFERON-GAMMA; PC12 CELLS; ACTIVATION; INDUCTION; KINASE; APOPTOSIS (en)
|
http://linked.open.../riv/klicoveSlovo
| |
http://linked.open...odStatuVydavatele
| - US - Spojené státy americké
|
http://linked.open...ontrolniKodProRIV
| |
http://linked.open...i/riv/nazevZdroje
| |
http://linked.open...in/vavai/riv/obor
| |
http://linked.open...ichTvurcuVysledku
| |
http://linked.open...cetTvurcuVysledku
| |
http://linked.open...UplatneniVysledku
| |
http://linked.open...v/svazekPeriodika
| |
http://linked.open...iv/tvurceVysledku
| - Krejčí, Pavel
- Jelínková, Petra
- Salazar, Lisa
- Wilcox, William
- Kashiwada, Tamara
- Goodridge, Helen
- Schibler, Matthew
- Thompson,, Leslie Michels
|
http://linked.open...ain/vavai/riv/wos
| |
http://linked.open...n/vavai/riv/zamer
| |
issn
| |
number of pages
| |
http://localhost/t...ganizacniJednotka
| |