Transforming growth factor-beta1 induces junB mRNA accumulation, G1-phase arrest, and pRb dephosphorylation in human leukemia HL-60 cells
Jazyk angličtina Země Česko Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
11232867
Knihovny.cz E-zdroje
- MeSH
- fosforylace MeSH
- G1 fáze * MeSH
- HL-60 buňky MeSH
- lidé MeSH
- messenger RNA genetika metabolismus MeSH
- protoonkogenní proteiny c-jun genetika MeSH
- retinoblastomový protein metabolismus MeSH
- transformující růstový faktor beta farmakologie MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- messenger RNA MeSH
- protoonkogenní proteiny c-jun MeSH
- retinoblastomový protein MeSH
- transformující růstový faktor beta MeSH
Although TGF-beta1 unambiguously functions as a regulator of hematopoietic differentiation, its significance for the development of myeloid lineage is still questionable. In this study three components of early response to TGF-beta1 treatment were investigated in human promyelocytic leukemia HL-60 cells. Changes in junB mRNA accumulation and pRb dephosphorylation were accompained by accumulation of cells in G1 phase of the cell cycle. Time dependence of these changes may implicate mutual cooperation of the pRb and junB in the cell cycle control. It can be concluded that, although myeloid HL-60 cells are known to require rather complex cytokine stimulation to fully differentiate, they clearly possess the ability to respond to TGF-beta1.
