Parallel inactivation of Y2 receptor and G-proteins in CHO cells by pertussis toxin.
Regul Pept
; 139(1-3): 128-35, 2007 Mar 01.
Article
en En
| MEDLINE
| ID: mdl-17175038
The Y(2) receptor for neuropeptide Y (NPY) interacts with pertussis toxin (PTX)-sensitive G-proteins, but little is known about interdependence of their levels and functions. We found that PTX reduces Y(2) receptors expressed in CHO cells in parallel to inactivation of Gi G-proteins, to loss of inhibition by Y(2) agonists of forskolin-stimulated adenylyl cyclase, and to decrease in the binding of GTP-gamma-S. These losses were attenuated by the endosome alkalinizer ammonium chloride. Affinity of the Y(2) receptor was not changed by PTX treatment. Prolonged treatment induced a large decrease of Y(2) receptor immunoreactivity (more than 70% in 48 h). The Gi(3) alpha-subunit immunoreactivity decreased slowly (about 46% in 48 h). There was a significant increase in Gq alpha immunoreactivity and in fraction of Y(2) binding sensitive to a Gq-selective antagonist. Possibly linked to that, the surface Y(2) sites and the internalization of the Y(2) receptor were less than 40% reduced. However, the abundant masked Y(2) sites were eliminated by the toxin, and could be mainly coupled to PTX-sensitive G-proteins.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Receptores de Neuropéptido Y
/
Proteínas de Unión al GTP
/
Toxina del Pertussis
Límite:
Animals
/
Humans
Idioma:
En
Revista:
Regul Pept
Año:
2007
Tipo del documento:
Article
Pais de publicación:
Países Bajos