Bimodal antagonism of PKA signalling by ARHGAP36

Protein kinase A (PKA) is a key mediator of cyclic AMP signalling. Here, Eccles et al. show that ARHGAP36 antagonizes PKA by acting as a kinase inhibitor and targeting the catalytic subunit for endolysosomal degradation, thus reducing sensitivity of cells to cAMP and promoting Hedgehog signalling.

Bibliographic Details
Main Authors: Rebecca L. Eccles, Maciej T. Czajkowski, Carolin Barth, Paul Markus Müller, Erik McShane, Stephan Grunwald, Patrick Beaudette, Nora Mecklenburg, Rudolf Volkmer, Kerstin Zühlke, Gunnar Dittmar, Matthias Selbach, Annette Hammes, Oliver Daumke, Enno Klussmann, Sylvie Urbé, Oliver Rocks
Format: Article
Language:English
Published: Nature Publishing Group 2016-10-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/ncomms12963
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spelling doaj-4b603724ee39452aa970f9812ba070502021-05-11T11:00:47ZengNature Publishing GroupNature Communications2041-17232016-10-017111610.1038/ncomms12963Bimodal antagonism of PKA signalling by ARHGAP36Rebecca L. Eccles0Maciej T. Czajkowski1Carolin Barth2Paul Markus Müller3Erik McShane4Stephan Grunwald5Patrick Beaudette6Nora Mecklenburg7Rudolf Volkmer8Kerstin Zühlke9Gunnar Dittmar10Matthias Selbach11Annette Hammes12Oliver Daumke13Enno Klussmann14Sylvie Urbé15Oliver Rocks16Max-Delbrück-Center for Molecular MedicineMax-Delbrück-Center for Molecular MedicineMax-Delbrück-Center for Molecular MedicineMax-Delbrück-Center for Molecular MedicineMax-Delbrück-Center for Molecular MedicineMax-Delbrück-Center for Molecular MedicineMax-Delbrück-Center for Molecular MedicineMax-Delbrück-Center for Molecular MedicineLeibniz-Institut für Molekulare PharmakologieMax-Delbrück-Center for Molecular MedicineMax-Delbrück-Center for Molecular MedicineMax-Delbrück-Center for Molecular MedicineMax-Delbrück-Center for Molecular MedicineMax-Delbrück-Center for Molecular MedicineMax-Delbrück-Center for Molecular MedicineCellular and Molecular Physiology, Institute of Translational Medicine, University of LiverpoolMax-Delbrück-Center for Molecular MedicineProtein kinase A (PKA) is a key mediator of cyclic AMP signalling. Here, Eccles et al. show that ARHGAP36 antagonizes PKA by acting as a kinase inhibitor and targeting the catalytic subunit for endolysosomal degradation, thus reducing sensitivity of cells to cAMP and promoting Hedgehog signalling.https://doi.org/10.1038/ncomms12963
collection DOAJ
language English
format Article
sources DOAJ
author Rebecca L. Eccles
Maciej T. Czajkowski
Carolin Barth
Paul Markus Müller
Erik McShane
Stephan Grunwald
Patrick Beaudette
Nora Mecklenburg
Rudolf Volkmer
Kerstin Zühlke
Gunnar Dittmar
Matthias Selbach
Annette Hammes
Oliver Daumke
Enno Klussmann
Sylvie Urbé
Oliver Rocks
spellingShingle Rebecca L. Eccles
Maciej T. Czajkowski
Carolin Barth
Paul Markus Müller
Erik McShane
Stephan Grunwald
Patrick Beaudette
Nora Mecklenburg
Rudolf Volkmer
Kerstin Zühlke
Gunnar Dittmar
Matthias Selbach
Annette Hammes
Oliver Daumke
Enno Klussmann
Sylvie Urbé
Oliver Rocks
Bimodal antagonism of PKA signalling by ARHGAP36
Nature Communications
author_facet Rebecca L. Eccles
Maciej T. Czajkowski
Carolin Barth
Paul Markus Müller
Erik McShane
Stephan Grunwald
Patrick Beaudette
Nora Mecklenburg
Rudolf Volkmer
Kerstin Zühlke
Gunnar Dittmar
Matthias Selbach
Annette Hammes
Oliver Daumke
Enno Klussmann
Sylvie Urbé
Oliver Rocks
author_sort Rebecca L. Eccles
title Bimodal antagonism of PKA signalling by ARHGAP36
title_short Bimodal antagonism of PKA signalling by ARHGAP36
title_full Bimodal antagonism of PKA signalling by ARHGAP36
title_fullStr Bimodal antagonism of PKA signalling by ARHGAP36
title_full_unstemmed Bimodal antagonism of PKA signalling by ARHGAP36
title_sort bimodal antagonism of pka signalling by arhgap36
publisher Nature Publishing Group
series Nature Communications
issn 2041-1723
publishDate 2016-10-01
description Protein kinase A (PKA) is a key mediator of cyclic AMP signalling. Here, Eccles et al. show that ARHGAP36 antagonizes PKA by acting as a kinase inhibitor and targeting the catalytic subunit for endolysosomal degradation, thus reducing sensitivity of cells to cAMP and promoting Hedgehog signalling.
url https://doi.org/10.1038/ncomms12963
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