Lack of beta-arrestin signaling in the absence of active G proteins

Arrestins terminate signaling from GPCRs, but several lines of evidence suggest that they are also able to transduce signals independently of G proteins. Here, the authors systematically ablate G proteins in cell lines, and show that arrestins are unable to act as genuine signal initiators.

Bibliographic Details
Main Authors:	Manuel Grundmann, Nicole Merten, Davide Malfacini, Asuka Inoue, Philip Preis, Katharina Simon, Nelly Rüttiger, Nicole Ziegler, Tobias Benkel, Nina Katharina Schmitt, Satoru Ishida, Ines Müller, Raphael Reher, Kouki Kawakami, Ayumi Inoue, Ulrike Rick, Toni Kühl, Diana Imhof, Junken Aoki, Gabriele M. König, Carsten Hoffmann, Jesus Gomeza, Jürgen Wess, Evi Kostenis
Format:	Article
Language:	English
Published:	Nature Publishing Group 2018-01-01
Series:	Nature Communications
Online Access:	https://doi.org/10.1038/s41467-017-02661-3

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spelling	doaj-e038d4ec42a84fe0b5f232ccf68a180d2021-05-11T09:35:48ZengNature Publishing GroupNature Communications2041-17232018-01-019111610.1038/s41467-017-02661-3Lack of beta-arrestin signaling in the absence of active G proteinsManuel Grundmann0Nicole Merten1Davide Malfacini2Asuka Inoue3Philip Preis4Katharina Simon5Nelly Rüttiger6Nicole Ziegler7Tobias Benkel8Nina Katharina Schmitt9Satoru Ishida10Ines Müller11Raphael Reher12Kouki Kawakami13Ayumi Inoue14Ulrike Rick15Toni Kühl16Diana Imhof17Junken Aoki18Gabriele M. König19Carsten Hoffmann20Jesus Gomeza21Jürgen Wess22Evi Kostenis23Molecular, Cellular and Pharmacobiology Section, Institute for Pharmaceutical Biology, University of BonnMolecular, Cellular and Pharmacobiology Section, Institute for Pharmaceutical Biology, University of BonnMolecular, Cellular and Pharmacobiology Section, Institute for Pharmaceutical Biology, University of BonnGraduate School of Pharmaceutical Science, Tohoku UniversityMolecular, Cellular and Pharmacobiology Section, Institute for Pharmaceutical Biology, University of BonnMolecular, Cellular and Pharmacobiology Section, Institute for Pharmaceutical Biology, University of BonnInstitute for Molecular Cell Biology, CMB-Center for Molecular Biomedicine, University Hospital JenaBio-Imaging-Center/Rudolf-Virchow-Center, Institute of Pharmacology, University of WuerzburgMolecular, Cellular and Pharmacobiology Section, Institute for Pharmaceutical Biology, University of BonnMolecular, Cellular and Pharmacobiology Section, Institute for Pharmaceutical Biology, University of BonnGraduate School of Pharmaceutical Science, Tohoku UniversityMolecular, Cellular and Pharmacobiology Section, Institute for Pharmaceutical Biology, University of BonnInstitute for Pharmaceutical Biology, University of BonnGraduate School of Pharmaceutical Science, Tohoku UniversityGraduate School of Pharmaceutical Science, Tohoku UniversityMolecular, Cellular and Pharmacobiology Section, Institute for Pharmaceutical Biology, University of BonnPharmaceutical Biochemistry and Bioanalytics, Institute of Pharmacy, University of BonnPharmaceutical Biochemistry and Bioanalytics, Institute of Pharmacy, University of BonnGraduate School of Pharmaceutical Science, Tohoku UniversityInstitute for Pharmaceutical Biology, University of BonnInstitute for Molecular Cell Biology, CMB-Center for Molecular Biomedicine, University Hospital JenaMolecular, Cellular and Pharmacobiology Section, Institute for Pharmaceutical Biology, University of BonnMolecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)Molecular, Cellular and Pharmacobiology Section, Institute for Pharmaceutical Biology, University of BonnArrestins terminate signaling from GPCRs, but several lines of evidence suggest that they are also able to transduce signals independently of G proteins. Here, the authors systematically ablate G proteins in cell lines, and show that arrestins are unable to act as genuine signal initiators.https://doi.org/10.1038/s41467-017-02661-3
collection	DOAJ
language	English
format	Article
sources	DOAJ
author	Manuel Grundmann Nicole Merten Davide Malfacini Asuka Inoue Philip Preis Katharina Simon Nelly Rüttiger Nicole Ziegler Tobias Benkel Nina Katharina Schmitt Satoru Ishida Ines Müller Raphael Reher Kouki Kawakami Ayumi Inoue Ulrike Rick Toni Kühl Diana Imhof Junken Aoki Gabriele M. König Carsten Hoffmann Jesus Gomeza Jürgen Wess Evi Kostenis
spellingShingle	Manuel Grundmann Nicole Merten Davide Malfacini Asuka Inoue Philip Preis Katharina Simon Nelly Rüttiger Nicole Ziegler Tobias Benkel Nina Katharina Schmitt Satoru Ishida Ines Müller Raphael Reher Kouki Kawakami Ayumi Inoue Ulrike Rick Toni Kühl Diana Imhof Junken Aoki Gabriele M. König Carsten Hoffmann Jesus Gomeza Jürgen Wess Evi Kostenis Lack of beta-arrestin signaling in the absence of active G proteins Nature Communications
author_facet	Manuel Grundmann Nicole Merten Davide Malfacini Asuka Inoue Philip Preis Katharina Simon Nelly Rüttiger Nicole Ziegler Tobias Benkel Nina Katharina Schmitt Satoru Ishida Ines Müller Raphael Reher Kouki Kawakami Ayumi Inoue Ulrike Rick Toni Kühl Diana Imhof Junken Aoki Gabriele M. König Carsten Hoffmann Jesus Gomeza Jürgen Wess Evi Kostenis
author_sort	Manuel Grundmann
title	Lack of beta-arrestin signaling in the absence of active G proteins
title_short	Lack of beta-arrestin signaling in the absence of active G proteins
title_full	Lack of beta-arrestin signaling in the absence of active G proteins
title_fullStr	Lack of beta-arrestin signaling in the absence of active G proteins
title_full_unstemmed	Lack of beta-arrestin signaling in the absence of active G proteins
title_sort	lack of beta-arrestin signaling in the absence of active g proteins
publisher	Nature Publishing Group
series	Nature Communications
issn	2041-1723
publishDate	2018-01-01
description	Arrestins terminate signaling from GPCRs, but several lines of evidence suggest that they are also able to transduce signals independently of G proteins. Here, the authors systematically ablate G proteins in cell lines, and show that arrestins are unable to act as genuine signal initiators.
url	https://doi.org/10.1038/s41467-017-02661-3
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Lack of beta-arrestin signaling in the absence of active G proteins

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