Noncanonical interactions of G proteins and β-arrestins: from competitors to companions.
| Autor: | Smith JS; Department of Dermatology, Massachusetts General Hospital, Boston, MA, USA.; Department of Dermatology, Brigham and Women's Hospital, Boston, MA, USA.; Department of Dermatology, Beth Israel Deaconess Medical Center, Boston, MA, USA.; Dermatology Program, Boston Children's Hospital, Boston, MA, USA.; Harvard Medical School, Boston, MA, USA., Pack TF; Sio Gene Therapies, Durham, NC, USA. |
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| Jazyk: | angličtina |
| Zdroj: | The FEBS journal [FEBS J] 2021 Apr; Vol. 288 (8), pp. 2550-2561. Date of Electronic Publication: 2021 Feb 22. |
| DOI: | 10.1111/febs.15749 |
| Abstrakt: | G protein-coupled receptors (GPCRs) canonically couple to specific Gα protein subtypes and β-arrestin adaptor proteins to initiate cellular signaling events. G protein-mediated signaling and β-arrestin-mediated signaling have broadly been considered separable. However, noncanonical interactions between G proteins and GPCRs are now appreciated that do not result in nucleotide exchange and classical G protein signaling. New findings also demonstrate direct interactions between G proteins and β-arrestins that are required for certain signaling and physiological events. Further adding to the intrigue of these newly appreciated G protein:β-arrestin complexes, only the Gαi subtype family members, and not Gαs, Gαq/11, or Gα12/13 subtypes, appear to form direct interactions with β-arrestin. Here, we review the recent discovery and initial characterization of G protein:β-arrestin complexes and describe how these complexes provide mechanistic insight into seemingly disparate observations. G protein:β-arrestin complexes build upon other observations of noncanonical G protein and β-arrestin signaling events to add an additional dimension to our understanding of GPCR signaling. (© 2021 Federation of European Biochemical Societies.) |
| Databáze: | MEDLINE |
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