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GPR158/179 regulate G protein signaling by controlling localization and activity of the RGS7 complexes

Academic Article
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Overview

authors

  • Orlandi, C.
  • Posokhova, E.
  • Masuho, I.
  • Ray, T. A.
  • Hasan, N.
  • Gregg, R. G.
  • Martemyanov, Kirill

publication date

  • June 2012

journal

  • Journal of Cell Biology  Journal

abstract

  • The extent and temporal characteristics of G protein-coupled receptor (GPCR) signaling are shaped by the regulator of G protein signaling (RGS) proteins, which promote G protein deactivation. With hundreds of GPCRs and dozens of RGS proteins, compartmentalization plays a key role in establishing signaling specificity. However, the molecular details and mechanisms of this process are poorly understood. In this paper, we report that the R7 group of RGS regulators is controlled by interaction with two previously uncharacterized orphan GPCRs: GPR158 and GPR179. We show that GPR158/179 recruited RGS complexes to the plasma membrane and augmented their ability to regulate GPCR signaling. The loss of GPR179 in a mouse model of night blindness prevented targeting of RGS to the postsynaptic compartment of bipolar neurons in the retina, illuminating the role of GPR179 in night vision. We propose that the interaction of RGS proteins with orphan GPCRs promotes signaling selectivity in G protein pathways.

subject areas

  • Animals
  • Cell Communication
  • Cell Membrane
  • Disease Models, Animal
  • GTP-Binding Proteins
  • HEK293 Cells
  • Humans
  • Immunoprecipitation
  • Mass Spectrometry
  • Mice
  • Microscopy, Confocal
  • Neurons
  • RGS Proteins
  • Receptors, G-Protein-Coupled
  • Signal Transduction
  • Transfection
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Identity

PubMed Central ID

  • PMC3373406

International Standard Serial Number (ISSN)

  • 0021-9525

Digital Object Identifier (DOI)

  • 10.1083/jcb.201202123

PubMed ID

  • 22689652
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Additional Document Info

start page

  • 711

end page

  • 719

volume

  • 197

issue

  • 6

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