Skip Nav Destination
Close Modal
Update search
Filter
- Title
- Author
- Author Affiliations
- Full Text
- Abstract
- Keyword
- DOI
- ISSN
- EISSN
- Issue
- Volume
- References
Filter
- Title
- Author
- Author Affiliations
- Full Text
- Abstract
- Keyword
- DOI
- ISSN
- EISSN
- Issue
- Volume
- References
Filter
- Title
- Author
- Author Affiliations
- Full Text
- Abstract
- Keyword
- DOI
- ISSN
- EISSN
- Issue
- Volume
- References
Filter
- Title
- Author
- Author Affiliations
- Full Text
- Abstract
- Keyword
- DOI
- ISSN
- EISSN
- Issue
- Volume
- References
Filter
- Title
- Author
- Author Affiliations
- Full Text
- Abstract
- Keyword
- DOI
- ISSN
- EISSN
- Issue
- Volume
- References
Filter
- Title
- Author
- Author Affiliations
- Full Text
- Abstract
- Keyword
- DOI
- ISSN
- EISSN
- Issue
- Volume
- References
NARROW
Format
Article Type
Date
Availability
1-1 of 1
Paul J. DAVIS
Close
Follow your search
Access your saved searches in your account
Would you like to receive an alert when new items match your search?
Sort by
Articles
Journal:
Biochemical Journal
Biochem J (1999) 338 (2): 427–432.
Published: 22 February 1999
Abstract
We have examined the effects of l -thyroxine (T 4 ) on the activation of signal transducer and activator of transcription 3 (STAT3) and on the STAT3-dependent induction of c-Fos expression by epidermal growth factor (EGF). T 4 , at a physiological concentration of 100 nM, caused tyrosine phosphorylation and nuclear translocation (i.e. activation) of STAT3 in HeLa cells in as little as 10–20 min. Activation by T 4 of STAT3 was maximal at 30 min (15±4-fold enhancement; mean±S.E.M.) in 18 experiments. This effect was reproduced by T 4 –agarose (100 nM) and blocked by CGP 41251, genistein, PD 98059 and geldanamycin, inhibitors of protein kinase C (PKC), protein tyrosine kinase (PTK), mitogen-activated protein kinase (MAPK) kinase and Raf-1 respectively. Tyrosine-phosphorylated MAPK also appeared in nuclear fractions within 10 min of treatment with T 4 . In the nuclear fraction of T 4 -treated cells, MAPK immunoprecipitate also contained STAT3. The actions of T 4 were similar in HeLa and CV-1 cells, which lack thyroid hormone receptor (TR), and in TR-replete skin fibroblasts (BG-9). T 4 also potentiated the EGF-induced nuclear translocation of activated STAT1α and STAT3 and enhanced the EGF-stimulated expression of c-Fos. Hormone potentiation of EGF-induced signal transduction and c-Fos expression was inhibited by CGP 41251, geldanamycin and PD 98059. Therefore the non-genomically induced activation by T 4 of STAT3, and the potentiation of EGF by T 4 , require activities of PKC, PTK and an intact MAPK pathway.