Opioid-induced adenylyl cyclase supersensitization in human embryonic kidney 293 cells requires pertussis toxin-sensitive G proteins other than Gi1 and Gi3
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Acknowledgements
This work was supported in part by the Hong Kong Jockey Club and the Research Grants Council of Hong Kong (HKUST 567/95M and HKUST 6096/98M).
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Gα<inf>i/o</inf>-coupled receptor-mediated sensitization of adenylyl cyclase: 40 years later
2015, European Journal of PharmacologyCitation Excerpt :Pretreatment with pertussis toxin leads to ADP-ribosylation of Gαi/o subunits, ultimately preventing their activation by receptors. Because pertussis toxin inhibits all isoforms of Gαi (i.e. Gαi1, Gαi2, Gαi3), and Gαo (Gαoa and Gαob), pertussis toxin insensitive (PTXi) isoforms of inhibitory Gα have been employed to determine the isoforms involved in heterologous sensitization for a number of receptors (Clark et al., 2004; Taussig et al., 1992; Tso and Wong, 2000, 2001; Watts et al., 1998; Zhang et al., 2006). Despite receptor dependency, PTXi-Gαo robustly rescued sensitization through the dopamine D2 receptor and μ-opioid receptor (Clark et al., 2004; Watts et al., 1998).
Role of receptor internalization in opioid tolerance and dependence
2008, Pharmacology and TherapeuticsSensitization of adenylate cyclase by Gα<inf>i/o</inf>-coupled receptors
2005, Pharmacology and TherapeuticsSensitization of adenylate cyclase by short-term activation of 5-HT1A receptors
2003, Cellular Signalling