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β-arrestin1 and 2 exhibit distinct phosphorylation-dependent conformations when coupling to the same GPCR in living cells

Nature communications, 2022-09, Vol.13 (1), p.5638-5638, Article 5638

2022

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Conformational flexibility of β‐arrestins – How these scaffolding proteins guide and transform the functionality of GPCRs

BioEssays, 2023-08, Vol.45 (8), p.e2300053-n/a

2023

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S1PR3 agonism and S1P lyase inhibition rescue mice in the severe state of experimental sepsis

Biomedicine & pharmacotherapy, 2024-05, Vol.174, p.116575-116575, Article 116575

2024

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Differential Regulation of GPCRs-Are GRK Expression Levels the Key?

Frontiers in cell and developmental biology, 2021-05, Vol.9, p.687489-687489

2021

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Circulating Bile Acids in Liver Failure Activate TGR5 and Induce Monocyte Dysfunction

Cellular and molecular gastroenterology and hepatology, 2021-01, Vol.12 (1), p.25-40

2021

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G Protein-Coupled Receptor Kinase 2 Selectively Enhances β-Arrestin Recruitment to the D2 Dopamine Receptor through Mechanisms That Are Independent of Receptor Phosphorylation

Biomolecules (Basel, Switzerland), 2023-10, Vol.13 (10), p.1552

2023

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Arrestin-1 engineering facilitates complex stabilization with native rhodopsin

Scientific reports, 2019-01, Vol.9 (1), p.439-439, Article 439

2019

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Microbially conjugated bile salts found in human bile activate the bile salt receptors TGR5 and FXR

Hepatology communications, 2024-04, Vol.8 (4)

2024

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To sense or not to sense—new insights from GPCR-based and arrestin-based biosensors

Current opinion in cell biology, 2019-04, Vol.57, p.16-24

2019

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Arrestin-centred interactions at the membrane and their conformational determinants

British journal of pharmacology, 2024-03

2024

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Rauchfreie Psychiatrie: Eine Bestandsaufnahme

Fortschritte der Neurologie, Psychiatrie, 2018-04, Vol.86 (4), p.213-218

2018

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The novel class of microbially conjugated bile salts activate the main host bile salt receptors FXR and TGR5

Journal of hepatology, 2023-06, Vol.78, p.S350-S351

2023

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THU-236 - The novel class of microbially conjugated bile salts activate the main host bile salt receptors FXR and TGR5

Journal of hepatology, 2023-06, Vol.78, p.S350-S351

2023

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Phosphorylation of the D1 Dopamine Receptor by G Protein‐Coupled Receptor Kinases: phosphorylation site identification and linkage to functional effects

The FASEB journal, 2021-05, Vol.35, p.n/a

2021

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Phosphorylation of the D 1 Dopamine Receptor by G Protein‐Coupled Receptor Kinases: phosphorylation site identification and linkage to functional effects

The FASEB journal, 2021-05, Vol.35 (S1), Article fasebj.2021.35.S1.02732

2021

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G protein‐coupled receptor kinase 2 can enhance β‐arrestin recruitment to the D 2 dopamine receptor in the absence of receptor phosphorylation

The FASEB journal, 2021-05, Vol.35 (S1), Article fasebj.2021.35.S1.02799

2021

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G protein‐coupled receptor kinase 2 can enhance β‐arrestin recruitment to the D2 dopamine receptor in the absence of receptor phosphorylation

The FASEB journal, 2021-05, Vol.35, p.n/a

2021

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G protein‐coupled receptor kinases regulate &[beta]‐arrestin interactions with the D2 dopamine receptor in an isoform‐specific manner and in the absence of direct receptor phosphorylation

The FASEB journal, 2022-05, Vol.36 (S1), p.n/a

2022

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β-arrestin–based biosensors: Tools to explore structural determinants of metabolic functions?

Current opinion in endocrine and metabolic research, 2021-02, Vol.16, p.66-74

2021

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G Protein-Coupled Receptor Kinase 2 Selectively Enhances beta-Arrestin Recruitment to the D[sub.2] Dopamine Receptor through Mechanisms That Are Independent of Receptor Phosphorylation

Biomolecules (Basel, Switzerland), 2023-10, Vol.13 (10)

2023

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G Protein-Coupled Receptor Kinase 2 Selectively Enhances β-Arrestin Recruitment to the D 2 Dopamine Receptor through Mechanisms That Are Independent of Receptor Phosphorylation

Biomolecules (Basel, Switzerland), 2023-10, Vol.13 (10)

2023

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Smoke-free psychiatry in Germany: A closer look

Fortschritte der Neurologie-Psychiatrie, 2018-04, Vol.86 (4), p.213

2018

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Circulating Bile Acids in Liver Failure Activate TGR5 and Induce Monocyte DysfunctionSummary

Cellular and molecular gastroenterology and hepatology, 2021-01, Vol.12 (1), p.25-40

2021

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Comprehensive Analysis of the Role of Arrestin Residues in Receptor Binding

The Structural Basis of Arrestin Functions, 2017, p.83-102

2017

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Pathway and network analysis of cancer genomes

Nature methods, 2015-07, Vol.12 (7), p.615-621

2015

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β-arrestin1 and 2 exhibit distinct phosphorylation-dependent conformations when coupling to the same GPCR in living cells

Conformational flexibility of β‐arrestins – How these scaffolding proteins guide and transform the functionality of GPCRs

S1PR3 agonism and S1P lyase inhibition rescue mice in the severe state of experimental sepsis

Differential Regulation of GPCRs-Are GRK Expression Levels the Key?

Circulating Bile Acids in Liver Failure Activate TGR5 and Induce Monocyte Dysfunction

G Protein-Coupled Receptor Kinase 2 Selectively Enhances β-Arrestin Recruitment to the D2 Dopamine Receptor through Mechanisms That Are Independent of Receptor Phosphorylation

Arrestin-1 engineering facilitates complex stabilization with native rhodopsin

Microbially conjugated bile salts found in human bile activate the bile salt receptors TGR5 and FXR

To sense or not to sense—new insights from GPCR-based and arrestin-based biosensors

Arrestin-centred interactions at the membrane and their conformational determinants

Rauchfreie Psychiatrie: Eine Bestandsaufnahme

The novel class of microbially conjugated bile salts activate the main host bile salt receptors FXR and TGR5

THU-236 - The novel class of microbially conjugated bile salts activate the main host bile salt receptors FXR and TGR5

Phosphorylation of the D1 Dopamine Receptor by G Protein‐Coupled Receptor Kinases: phosphorylation site identification and linkage to functional effects

Phosphorylation of the D 1 Dopamine Receptor by G Protein‐Coupled Receptor Kinases: phosphorylation site identification and linkage to functional effects

G protein‐coupled receptor kinase 2 can enhance β‐arrestin recruitment to the D 2 dopamine receptor in the absence of receptor phosphorylation

G protein‐coupled receptor kinase 2 can enhance β‐arrestin recruitment to the D2 dopamine receptor in the absence of receptor phosphorylation

G protein‐coupled receptor kinases regulate &[beta]‐arrestin interactions with the D2 dopamine receptor in an isoform‐specific manner and in the absence of direct receptor phosphorylation

β-arrestin–based biosensors: Tools to explore structural determinants of metabolic functions?

G Protein-Coupled Receptor Kinase 2 Selectively Enhances beta-Arrestin Recruitment to the D[sub.2] Dopamine Receptor through Mechanisms That Are Independent of Receptor Phosphorylation

G Protein-Coupled Receptor Kinase 2 Selectively Enhances β-Arrestin Recruitment to the D 2 Dopamine Receptor through Mechanisms That Are Independent of Receptor Phosphorylation

Smoke-free psychiatry in Germany: A closer look

Circulating Bile Acids in Liver Failure Activate TGR5 and Induce Monocyte DysfunctionSummary

Comprehensive Analysis of the Role of Arrestin Residues in Receptor Binding

Pathway and network analysis of cancer genomes

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