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Biol Reprod ; 66(1): 70-6, 2002 Jan.
Article in English | MEDLINE | ID: mdl-11751266

ABSTRACT

The FSH receptor (FSH-R) is a member of the rhodopsin-like subfamily of G protein-coupled receptors that undergoes homologous desensitization upon agonist stimulation. In immortalized cell lines overexpressing the FSH-R, G protein-coupled receptor kinases (GRKs) and beta-arrestins are involved in the phosphorylation, uncoupling, and internalization of this receptor. In an effort to appreciate the physiological relevance of GRK/beta-arrestin actions in natural FSH-R-bearing cells, we used primary rat Sertoli cells as a model. GRK2, -3, -5, -6a, and -6b and beta-arrestins 1 and 2 were expressed in primary rat Sertoli cells. Overexpression of these different GRKs and beta-arrestins in primary rat Sertoli cells significantly attenuated the FSH-induced cAMP response, and FSH rapidly triggered a relocalization of endogenously expressed GRK2, -3, -5, and -6 and beta-arrestins 1 and 2 from the cytosol to the membranes. These results highlight the relationship existing between the GRK/beta-arrestin regulatory system and the FSH-R signaling machinery in a physiological model.


Subject(s)
Arrestins/metabolism , Cyclic AMP/metabolism , Follicle Stimulating Hormone/pharmacology , Protein Serine-Threonine Kinases/metabolism , Sertoli Cells/metabolism , Animals , Cell Separation , Cells, Cultured , Cytosol/metabolism , G-Protein-Coupled Receptor Kinases , Immunoblotting , Male , Rats , Rats, Wistar , Receptors, FSH/metabolism , Reverse Transcriptase Polymerase Chain Reaction , Sertoli Cells/drug effects , Transfection , beta-Arrestins
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