{"volume":5,"_id":"3150","doi":"10.1038/ncb941","title":"Spontaneous receptor-independent heterotrimeric G-protein signalling in an RGS mutant","date_updated":"2021-01-12T07:41:24Z","month":"03","author":[{"first_name":"Daria E","full_name":"Daria Siekhaus","last_name":"Siekhaus","id":"3D224B9E-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-8323-8353"},{"full_name":"Drubin, David G","last_name":"Drubin","first_name":"David"}],"type":"journal_article","citation":{"ieee":"D. E. Siekhaus and D. Drubin, “Spontaneous receptor-independent heterotrimeric G-protein signalling in an RGS mutant,” <i>Nature Cell Biology</i>, vol. 5, no. 3. Nature Publishing Group, pp. 231–235, 2003.","ama":"Siekhaus DE, Drubin D. Spontaneous receptor-independent heterotrimeric G-protein signalling in an RGS mutant. <i>Nature Cell Biology</i>. 2003;5(3):231-235. doi:<a href=\"https://doi.org/10.1038/ncb941\">10.1038/ncb941</a>","short":"D.E. Siekhaus, D. Drubin, Nature Cell Biology 5 (2003) 231–235.","ista":"Siekhaus DE, Drubin D. 2003. Spontaneous receptor-independent heterotrimeric G-protein signalling in an RGS mutant. Nature Cell Biology. 5(3), 231–235.","mla":"Siekhaus, Daria E., and David Drubin. “Spontaneous Receptor-Independent Heterotrimeric G-Protein Signalling in an RGS Mutant.” <i>Nature Cell Biology</i>, vol. 5, no. 3, Nature Publishing Group, 2003, pp. 231–35, doi:<a href=\"https://doi.org/10.1038/ncb941\">10.1038/ncb941</a>.","chicago":"Siekhaus, Daria E, and David Drubin. “Spontaneous Receptor-Independent Heterotrimeric G-Protein Signalling in an RGS Mutant.” <i>Nature Cell Biology</i>. Nature Publishing Group, 2003. <a href=\"https://doi.org/10.1038/ncb941\">https://doi.org/10.1038/ncb941</a>.","apa":"Siekhaus, D. E., &#38; Drubin, D. (2003). Spontaneous receptor-independent heterotrimeric G-protein signalling in an RGS mutant. <i>Nature Cell Biology</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/ncb941\">https://doi.org/10.1038/ncb941</a>"},"publication":"Nature Cell Biology","publication_status":"published","date_created":"2018-12-11T12:01:41Z","day":"01","date_published":"2003-03-01T00:00:00Z","status":"public","extern":1,"page":"231 - 235","year":"2003","abstract":[{"text":"Tripartite G-protein-coupled receptors (GPCRs) represent one of the largest groups of signal transducers, transmitting signals from hormones, neuropeptides, odorants, food and light. Ligand-bound receptors catalyse GDP/GTP exchange on the G-protein α-subunit (Gα), leading to α-GTP separation from the βγ subunits and pathway activation. Activating mutations in the receptors or G proteins underlie many human diseases, including some cancers, dwarfism and premature puberty. Regulators of G-protein signalling (RGS proteins) are known to modulate the level and duration of ligand-induced signalling by accelerating the intrinsic GTPase activity of the Gα subunit, and thus reformation of the inactive GDP-bound Gα. Here we find that even in the absence of receptor, mutation of the RGS family member Sst2 (refs 6-9) permits spontaneous activation of the G-protein-coupled mating pathway in Saccharomyces cerevisiae at levels normally seen only in the presence of ligand. Our work demonstrates the occurence of spontaneous tripartite G-protein signalling in vivo and identifies a requirement for RGS proteins in preventing such receptor-independent activation.","lang":"eng"}],"publisher":"Nature Publishing Group","quality_controlled":0,"issue":"3","publist_id":"3544","intvolume":"         5"}