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• W2012102413 abstract "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." @default.
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• W2012102413 date "2007-03-01" @default.
• W2012102413 modified "2023-10-16" @default.
• W2012102413 title "Parallel inactivation of Y2 receptor and G-proteins in CHO cells by pertussis toxin" @default.
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• W2012102413 doi "https://doi.org/10.1016/j.regpep.2006.10.014" @default.
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