GRK specificity and Gβγ dependency determines the potential of a GPCR for arrestin-biased agonism
- Location
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Deutsche Nationalbibliothek Frankfurt am Main
- Extent
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1 Online-Ressource.
- Language
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Englisch
- Bibliographic citation
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GRK specificity and Gβγ dependency determines the potential of a GPCR for arrestin-biased agonism ; volume:7 ; number:1 ; day:3 ; month:7 ; year:2024 ; pages:1-12 ; date:12.2024
Communications biology ; 7, Heft 1 (3.7.2024), 1-12, 12.2024
- Creator
-
Matthees, Edda
Filor, Jenny
Jaiswal, Natasha
Reichel, Mona
Youssef, Noureldine
D’Uonnolo, Giulia
Szpakowska, Martyna
Drube, Julia
König, Gabriele M.
Kostenis, Eva
Chevigné, Andy
Godbole, Amod
Hoffmann, Carsten
- Contributor
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SpringerLink (Online service)
- DOI
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10.1038/s42003-024-06490-1
- URN
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urn:nbn:de:101:1-2409202125299.253564101266
- Rights
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Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Last update
-
15.08.2025, 7:32 AM CEST
Data provider
This object is provided by:
Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Associated
- Matthees, Edda
- Filor, Jenny
- Jaiswal, Natasha
- Reichel, Mona
- Youssef, Noureldine
- D’Uonnolo, Giulia
- Szpakowska, Martyna
- Drube, Julia
- König, Gabriele M.
- Kostenis, Eva
- Chevigné, Andy
- Godbole, Amod
- Hoffmann, Carsten
- SpringerLink (Online service)
Other Objects (12)
Dynamic mechanism of GPCR-mediated β-arrestin: a potential therapeutic agent discovery of biased drug
Exploring GPCR‐arrestin interfaces with genetically encoded crosslinkers
Characterization of GPCR-arrestin interfaces via genetically incorporated crosslinkers
GPCR kinase knockout cells reveal the impact of individual GRKs on arrestin binding and GPCR regulation
CXCR7: a β-arrestin-biased receptor that potentiates cell migration and recruits β-arrestin2 exclusively through Gβγ subunits and GRK2
Unique Roles of β-Arrestin in GPCR Trafficking Revealed by Photoinducible Dimerizers
β-Arrestin-independent endosomal cAMP signaling by a polypeptide hormone GPCR
Highly biased agonism for GPCR ligands via nanobody tethering
Allosteric modulation of GPCR-induced β-arrestin trafficking and signaling by a synthetic intrabody
A bead-based GPCR phosphorylation immunoassay for high-throughput ligand profiling and GRK inhibitor screening
Gαi is required for carvedilol-induced β1 adrenergic receptor β-arrestin biased signaling
Revisionsberichte GRK
Dynamic mechanism of GPCR-mediated β-arrestin: a potential therapeutic agent discovery of biased drug
Exploring GPCR‐arrestin interfaces with genetically encoded crosslinkers
Characterization of GPCR-arrestin interfaces via genetically incorporated crosslinkers
GPCR kinase knockout cells reveal the impact of individual GRKs on arrestin binding and GPCR regulation
CXCR7: a β-arrestin-biased receptor that potentiates cell migration and recruits β-arrestin2 exclusively through Gβγ subunits and GRK2
Unique Roles of β-Arrestin in GPCR Trafficking Revealed by Photoinducible Dimerizers
β-Arrestin-independent endosomal cAMP signaling by a polypeptide hormone GPCR
Highly biased agonism for GPCR ligands via nanobody tethering
Allosteric modulation of GPCR-induced β-arrestin trafficking and signaling by a synthetic intrabody
A bead-based GPCR phosphorylation immunoassay for high-throughput ligand profiling and GRK inhibitor screening
Gαi is required for carvedilol-induced β1 adrenergic receptor β-arrestin biased signaling
Revisionsberichte GRK
Dynamic mechanism of GPCR-mediated β-arrestin: a potential therapeutic agent discovery of biased drug
Exploring GPCR‐arrestin interfaces with genetically encoded crosslinkers
Characterization of GPCR-arrestin interfaces via genetically incorporated crosslinkers
GPCR kinase knockout cells reveal the impact of individual GRKs on arrestin binding and GPCR regulation
CXCR7: a β-arrestin-biased receptor that potentiates cell migration and recruits β-arrestin2 exclusively through Gβγ subunits and GRK2
Unique Roles of β-Arrestin in GPCR Trafficking Revealed by Photoinducible Dimerizers
β-Arrestin-independent endosomal cAMP signaling by a polypeptide hormone GPCR
Highly biased agonism for GPCR ligands via nanobody tethering
Allosteric modulation of GPCR-induced β-arrestin trafficking and signaling by a synthetic intrabody
A bead-based GPCR phosphorylation immunoassay for high-throughput ligand profiling and GRK inhibitor screening
Gαi is required for carvedilol-induced β1 adrenergic receptor β-arrestin biased signaling