期刊
MOLECULAR AND CELLULAR ENDOCRINOLOGY
卷 449, 期 C, 页码 28-41出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2017.01.052
关键词
GPCR; beta-arrestins; Signalling bias; Hormones
资金
- ARTE2 from Region Centre
- MODUPHAC from Region Centre
- ARD Biomedicament from Region Centre
- LE STUDIUM(R) Loire Valley Institute for Advanced Studies and AgreenSkills Plus
- AgreenSkills
- Region Centre
- INRA
- LabEx MabImprove
G protein-coupled receptors (GPCRs) play crucial roles in the ability of target organs to respond to hormonal cues. GPCRs' activation mechanisms have long been considered as a two-state process connecting the agonist-bound receptor to heterotrimeric G proteins. This view is now challenged as mounting evidence point to GPCRs being connected to large arrays of transduction mechanisms involving heterotrimeric G proteins as well as other players. Amongst the G protein-independent transduction mechanisms, those elicited by beta-arrestins upon their recruitment to the active receptors are by far the best characterized and apply to most GPCRs. These concepts, in conjunction with remarkable advances made in the field of GPCR structural biology and biophysics, have supported the notion of ligand-selective signalling also known as pharmacological bias. Interestingly, recent reports have opened intriguing prospects to the way beta-arrestins control GPCR-mediated signalling in space and time within the cells. In the present paper, we review the existing evidence linking endocrine-related GPCRs to beta-arrestin recruitement, signalling, pathophysiological implications and selective activation by biased ligands and/or receptor modifications. Emerging concepts surrounding beta-arrestin-mediated transduction are discussed in the light of the peculiarities of endocrine systems. (C) 2017 Elsevier B.V. All rights reserved.
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