Journal
CELLULAR AND MOLECULAR LIFE SCIENCES
Volume 66, Issue 21, Pages 3487-3503Publisher
SPRINGER BASEL AG
DOI: 10.1007/s00018-009-0134-z
Keywords
p70S6K; G protein-coupled receptor; Dynamic model; Differentiation
Categories
Funding
- Region Centre
- Institut National de la Recherche Agronomique (INRA)
- Ministere de la Recherche et de la Technologie
- Fondation pour le Recherche Medicale
- INRA AgroBI AIP
- Centre National de la Recherche Scientifique
- Universite de Tours
- AE INRIA/INRA REGATE
Ask authors/readers for more resources
The mechanisms whereby G protein-coupled receptors (GPCR) activate signalling pathways involved in mRNA translation are ill-defined, in contrast to tyrosine kinase receptors (TKR). We compared a GPCR and a TKR, both endogenously expressed, for their ability to mediate phosphorylation of 70-kDa ribosomal S6 kinase p70S6K in primary rat Sertoli cells at two developmental stages. In proliferating cells stimulated with follicle-stimulating hormone (FSH), active p70S6K was phosphorylated on T389 and T421/S424, through cAMP-dependent kinase (PKA) and phosphatidyl-inositide-3 kinase (PI3K) antagonizing actions. In FSH-stimulated differentiating cells, active p70S6K was phosphorylated solely on T389, PKA and PI3K independently enhancing its activity. At both developmental stages, insulin-induced p70S6K regulation was consistent with reported data. Therefore, TKR and GPCR trigger distinct p70S6K active conformations. p70S6K developmental regulation was formalized in a dynamic mathematical model fitting the data, which led to experimentally inaccessible predictions on p70S6K phosphorylation rate.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available