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Differential β-Arrestin–Dependent Conformational Signaling and Cellular Responses Revealed by Angiotensin Analogs

https://doi.org/10.1126/scisignal.2002522

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What this work says

Outgoing claims: the papers this work cites, builds on, or argues with.

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Identification of amino acid residues of rat angiotensin II receptor for ligand binding by site directed mutagenesis

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Regulation of cell proliferation and growth by angiotensin II

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Multiplexing of Multicolor Bioluminescence Resonance Energy Transfer

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c-Src-mediated phosphorylation of AP-2 reveals a general mechanism for receptors internalizing through the clathrin pathway

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Receptor-specific desensitization with purified proteins. Kinase dependence and receptor specificity of beta-arrestin and arrestin in the beta 2-adrenergic receptor and rhodopsin systems.

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Side-Chain Substitutions within Angiotensin II Reveal Different Requirements for Signaling, Internalization, and Phosphorylation of Type 1A Angiotensin Receptors

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The tyrosine within the NPXnY motif of the human angiotensin II type 1 receptor is involved in mediating signal transduction but is not essential for internalization.

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International Union of Pharmacology. XXIII. The Angiotensin II Receptors

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Monitoring agonist‐promoted conformational changes of β‐arrestin in living cells by intramolecular BRET

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Effects of an Angiotensin-Converting–Enzyme Inhibitor, Ramipril, on Cardiovascular Events in High-Risk Patients

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Functional antagonism of different G protein-coupled receptor kinases for β-arrestin-mediated angiotensin II receptor signaling

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β-Arrestin2-mediated inotropic effects of the angiotensin II type 1A receptor in isolated cardiac myocytes

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β-Arrestin-mediated activation of MAPK by inverse agonists reveals distinct active conformations for G protein-coupled receptors

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Studies on angiotensin II and analogs: impact of substitution in position 8 on conformation and activity.

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Interaction of Phe8 of Angiotensin II with Lys199 and His256 of AT1 Receptor in Agonist Activation

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A Novel Biased Allosteric Compound Inhibitor of Parturition Selectively Impedes the Prostaglandin F2α-mediated Rho/ROCK Signaling Pathway

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Differential Kinetic and Spatial Patterns of β-Arrestin and G Protein-mediated ERK Activation by the Angiotensin II Receptor

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Distinct β-Arrestin- and G Protein-dependent Pathways for Parathyroid Hormone Receptor-stimulated ERK1/2 Activation

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β-Arrestin-biased Agonism at the β2-Adrenergic Receptor

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Independent β-Arrestin2 and Gq/Protein Kinase Cζ Pathways for ERK Stimulated by Angiotensin Type 1A Receptors in Vascular Smooth Muscle Cells Converge on Transactivation of the Epidermal Growth Factor Receptor

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Endogenous ARF6 Interacts with Rac1 upon Angiotensin II Stimulation to Regulate Membrane Ruffling and Cell Migration

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Operational models of pharmacological agonism

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Functional Selectivity of Natural and Synthetic Prostaglandin EP4 Receptor Ligands

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Selectively Engaging β-Arrestins at the Angiotensin II Type 1 Receptor Reduces Blood Pressure and Increases Cardiac Performance

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Distinct Signaling Profiles of β1 and β2 Adrenergic Receptor Ligands toward Adenylyl Cyclase and Mitogen-Activated Protein Kinase Reveals the Pluridimensionality of Efficacy

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The Angiotensin II Type 1 Receptor Induces Membrane Blebbing by Coupling to Rho A, Rho Kinase, and Myosin Light Chain Kinase

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Allosteric Ligands of the Glucagon-Like Peptide 1 Receptor (GLP-1R) Differentially Modulate Endogenous and Exogenous Peptide Responses in a Pathway-Selective Manner: Implications for Drug Screening

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β-Arrestin–Biased Agonism of the Angiotensin Receptor Induced by Mechanical Stress

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Distinct Phosphorylation Sites on the β 2 -Adrenergic Receptor Establish a Barcode That Encodes Differential Functions of β-Arrestin

inferredcites →https://doi.org/10.1146/annurev.physiol.69.022405.154749openalex-snapshot

β-Arrestins and Cell Signaling

inferredcites →https://doi.org/10.1152/ajpcell.00287.2006openalex-snapshot

Angiotensin II cell signaling: physiological and pathological effects in the cardiovascular system

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Protective effect of long-term angiotensin II inhibition

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Angiotensin II Type 1 Receptor–Induced Extracellular Signal–Regulated Protein Kinase Activation Is Mediated by Ca 2+ /Calmodulin-Dependent Transactivation of Epidermal Growth Factor Receptor

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Cardiorenal Actions of TRV120027, a Novel ß-Arrestin–Biased Ligand at the Angiotensin II Type I Receptor, in Healthy and Heart Failure Canines

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Angiotensin II-mediated hypertension in the rat increases vascular superoxide production via membrane NADH/NADPH oxidase activation. Contribution to alterations of vasomotor tone.

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c-Src Regulates Clathrin Adapter Protein 2 Interaction with β-Arrestin and the Angiotensin II Type 1 Receptor during Clathrin- Mediated Internalization

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Biased Signaling of the Angiotensin II Type 1 Receptor Can Be Mediated through Distinct Mechanisms

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What points at this work

Incoming claims: where this work appears in other papers’ reference lists and arguments.

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Signaling Pathways

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Conclusion

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Signaling Lipids

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Mitogen-Activated Protein Kinase Module

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Prostaglandin F2α and angiotensin II type 1 receptors exhibit differential cognate G protein coupling regulation

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G protein–coupled receptor kinase phosphorylation of distal C-tail sites specifies βarrestin1-mediated signaling by chemokine receptor CXCR4

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Angiotensin receptor conformations stabilized by biased ligands differentially modulate β-arrestin interactions

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Biased Agonist TRV027 Determinants in AT1R by Molecular Dynamics Simulations

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Size-Reduced Macrocyclic Analogues of [Pyr1]-apelin-13 Showing Negative Gα12 Bias Still Produce Prolonged Cardiac Effects

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Molecular Biology Techniques Applied to GPCR Allosteric and Biased Ligands

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Structure–activity relationship of novel macrocyclic biased apelin receptor agonists

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Ligand bias at the μ-opioid receptor

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Receptor sequestration in response to β-arrestin-2 phosphorylation by ERK1/2 governs steady-state levels of GPCR cell-surface expression

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Functional New World monkey oxytocin forms elicit an altered signaling profile and promotes parental care in rats

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Biased Signaling Favoring Gi over β-Arrestin Promoted by an Apelin Fragment Lacking the C-terminal Phenylalanine

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Differential Regulation of Endosomal GPCR/β-Arrestin Complexes and Trafficking by MAPK

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Allosteric Modulation of β-Arrestin-biased Angiotensin II Type 1 Receptor Signaling by Membrane Stretch

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Arrestin-dependent Angiotensin AT1 Receptor Signaling Regulates Akt and mTor-mediated Protein Synthesis

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Angiotensin II Type I and Prostaglandin F2α Receptors Cooperatively Modulate Signaling in Vascular Smooth Muscle Cells

inferred← citeshttps://doi.org/10.1074/jbc.m115.684357openalex-snapshot

β-Arrestin-mediated Angiotensin II Signaling Controls the Activation of ARF6 Protein and Endocytosis in Migration of Vascular Smooth Muscle Cells

inferred← citeshttps://doi.org/10.1074/jbc.m116.763854openalex-snapshot

Conformational Profiling of the AT1 Angiotensin II Receptor Reflects Biased Agonism, G Protein Coupling, and Cellular Context

inferred← citeshttps://doi.org/10.1074/jbc.m117.793877openalex-snapshot

Conformational biosensors reveal allosteric interactions between heterodimeric AT1 angiotensin and prostaglandin F2α receptors

inferred← citeshttps://doi.org/10.1074/jbc.ra119.010324openalex-snapshot

Genetic code expansion and photocross-linking identify different β-arrestin binding modes to the angiotensin II type 1 receptor

inferred← citeshttps://doi.org/10.1074/jbc.ra120.014330openalex-snapshot

Angiotensin II type 1 receptor variants alter endosomal receptor–β-arrestin complex stability and MAPK activation

inferred← citeshttps://doi.org/10.1096/fj.14-249771openalex-snapshot

Biased signaling regulates the pleiotropic effects of the urotensin II receptor to modulate its cellular behaviors

inferred← citeshttps://doi.org/10.1101/2020.06.11.146605openalex-snapshot

Biased agonists of the chemokine receptor CXCR3 differentially drive formation of G αi :β-arrestin complexes

inferred← citeshttps://doi.org/10.1101/2020.11.09.375162openalex-snapshot

Diverse chemotypes drive biased signaling by cannabinoid receptors

inferred← citeshttps://doi.org/10.1101/2021.01.28.427950openalex-snapshot

Vasopressin V2 is a promiscuous G protein-coupled receptor that is biased by its peptide ligands

inferred← citeshttps://doi.org/10.1101/2021.05.17.444454openalex-snapshot

Decoding Angiotensin II Type 1 Receptor Allosteric Communication to Gq and β-arrestin

inferred← citeshttps://doi.org/10.1101/2023.04.01.535208openalex-snapshot

β-arrestin-dependent and -independent endosomal G protein activation by the vasopressin type 2 receptor

inferred← citeshttps://doi.org/10.1111/bph.13072openalex-snapshot

GPCR ‐mediated EGF receptor transactivation regulates TRPV 4 action in the vasculature

inferred← citeshttps://doi.org/10.1111/febs.15826openalex-snapshot

Allosteric communication regulates ligand‐specific GPCR activity

inferred← citeshttps://doi.org/10.1113/jphysiol.2014.279109openalex-snapshot

Photoreleasable ligands to study intracrine angiotensin II signalling

inferred← citeshttps://doi.org/10.1124/mol.113.088880openalex-snapshot

Quantification of Ligand Bias for Clinically Relevant β2-Adrenergic Receptor Ligands: Implications for Drug Taxonomy

inferred← citeshttps://doi.org/10.1124/mol.114.097337openalex-snapshot

Characterization of Angiotensin II Molecular Determinants Involved in AT1 Receptor Functional Selectivity

inferred← citeshttps://doi.org/10.1124/mol.115.098087openalex-snapshot

Cyclic Adenosine 3′,5′-Monophosphate Elevation and Biological Signaling through a Secretin Family Gs-Coupled G Protein–Coupled Receptor Are Restricted to a Single Adenylate Cyclase Isoform

inferred← citeshttps://doi.org/10.1124/mol.115.099630openalex-snapshot

Fulfilling the Promise of "Biased" G Protein–Coupled Receptor Agonism

inferred← citeshttps://doi.org/10.1124/mol.116.105940openalex-snapshot

A Pluridimensional View of Biased Agonism

inferred← citeshttps://doi.org/10.1124/molpharm.120.000192openalex-snapshot

Arrestin-Dependent and -Independent Internalization of G Protein–Coupled Receptors: Methods, Mechanisms, and Implications on Cell Signaling

inferred← citeshttps://doi.org/10.1124/molpharm.122.000497openalex-snapshot

Michaelis-Menten Quantification of Ligand Signaling Bias Applied to the Promiscuous Vasopressin V2 Receptor

inferred← citeshttps://doi.org/10.1124/pr.114.010454openalex-snapshot

International Union of Basic and Clinical Pharmacology. XCIX. Angiotensin Receptors: Interpreters of Pathophysiological Angiotensinergic Stimuli

inferred← citeshttps://doi.org/10.1124/pr.116.013367openalex-snapshot

The Diverse Roles of Arrestin Scaffolds in G Protein–Coupled Receptor Signaling

inferred← citeshttps://doi.org/10.1124/pr.118.016790openalex-snapshot

Biased Receptor Signaling in Drug Discovery

inferred← citeshttps://doi.org/10.1126/science.aay9813openalex-snapshot

Angiotensin and biased analogs induce structurally distinct active conformations within a GPCR

inferred← citeshttps://doi.org/10.1126/scisignal.aat1631openalex-snapshot

Functional selectivity profiling of the angiotensin II type 1 receptor using pathway-wide BRET signaling sensors

inferred← citeshttps://doi.org/10.1126/scisignal.abg5203openalex-snapshot

Biased agonists of the chemokine receptor CXCR3 differentially signal through Gα i :β-arrestin complexes

inferred← citeshttps://doi.org/10.1126/scisignal.adf2173openalex-snapshot

Unraveling allostery within the angiotensin II type 1 receptor for Gα q and β-arrestin coupling

inferred← citeshttps://doi.org/10.1126/scisignal.adf6206openalex-snapshot

Sustained Gα s signaling mediated by vasopressin type 2 receptors is ligand dependent but endocytosis and β-arrestin independent

inferred← citeshttps://doi.org/10.1126/scisignal.adi0934openalex-snapshot

G protein–coupled receptor endocytosis generates spatiotemporal bias in β-arrestin signaling

inferred← citeshttps://doi.org/10.1126/scisignal.adk5736openalex-snapshot

Phosphorylation patterns in the AT1R C-terminal tail specify distinct downstream signaling pathways

inferred← citeshttps://doi.org/10.1146/annurev-pharmtox-052120-091058openalex-snapshot

Biased Agonism: Lessons from Studies of Opioid Receptor Agonists

inferred← citeshttps://doi.org/10.11606/t.42.2014.tde-19112014-112006openalex-snapshot

Efeito da variação do conteúdo de K+ na dieta sobre a expressão renal de AT1R, ATRAP e WNKs.

inferred← citeshttps://doi.org/10.1161/circheartfailure.112.969220openalex-snapshot

TRV120027, a Novel β-Arrestin Biased Ligand at the Angiotensin II Type I Receptor, Unloads the Heart and Maintains Renal Function When Added to Furosemide in Experimental Heart Failure

inferred← citeshttps://doi.org/10.1161/hypertensionaha.116.08118openalex-snapshot

Cardioprotective Angiotensin-(1–7) Peptide Acts as a Natural-Biased Ligand at the Angiotensin II Type 1 Receptor

inferred← citeshttps://doi.org/10.1161/hypertensionaha.121.17977openalex-snapshot

Angiotensin II Type 1 Receptor Tachyphylaxis Is Defined by Agonist Residence Time

inferred← citeshttps://doi.org/10.1161/hypertensionaha.123.19419openalex-snapshot

Insights Into the Role of Angiotensin-II AT 1 Receptor-Dependent β-Arrestin Signaling in Cardiovascular Disease

inferred← citeshttps://doi.org/10.1165/rcmb.2024-0111ocopenalex-snapshot

Enhanced Gαq Signaling in TSC2 -Deficient Cells Is Required for Their Neoplastic Behavior

inferred← citeshttps://doi.org/10.1172/jci71951openalex-snapshot

CXCL11-dependent induction of FOXP3-negative regulatory T cells suppresses autoimmune encephalomyelitis

inferred← citeshttps://doi.org/10.1189/jlb.2mr0915-441ropenalex-snapshot

Biased signaling pathways via CXCR3 control the development and function of CD4+ T cell subsets

inferred← citeshttps://doi.org/10.1210/en.2013-1286openalex-snapshot

β-Arrestin 2 Is a Mediator of GnRH-(1–5) Signaling in Immortalized GnRH Neurons

inferred← citeshttps://doi.org/10.1210/me.2013-1314openalex-snapshot

Minireview: More Than Just a Hammer: Ligand “Bias” and Pharmaceutical Discovery

inferred← citeshttps://doi.org/10.15252/embr.201949886openalex-snapshot

Key phosphorylation sites in GPCRs orchestrate the contribution of β‐Arrestin 1 in ERK1/2 activation

inferred← citeshttps://doi.org/10.1530/jme-14-0125openalex-snapshot

Structural determinants for binding, activation, and functional selectivity of the angiotensin AT1 receptor

inferred← citeshttps://doi.org/10.3389/fendo.2017.00032openalex-snapshot

A Comprehensive View of the β-Arrestinome

inferred← citeshttps://doi.org/10.3389/fendo.2019.00162openalex-snapshot

Asymmetric Recruitment of β-Arrestin1/2 by the Angiotensin II Type I and Prostaglandin F2α Receptor Dimer

inferred← citeshttps://doi.org/10.3389/fimmu.2015.00609openalex-snapshot

The Role of Chemokines in Shaping the Balance Between CD4+ T Cell Subsets and Its Therapeutic Implications in Autoimmune and Cancer Diseases

inferred← citeshttps://doi.org/10.3389/fphar.2015.00131openalex-snapshot

Comparative analyses of downstream signal transduction targets modulated after activation of the AT1 receptor by two β-arrestin-biased agonists

inferred← citeshttps://doi.org/10.3390/biom11020218openalex-snapshot

Receptor-Arrestin Interactions: The GPCR Perspective

inferred← citeshttps://doi.org/10.3390/cells14161284openalex-snapshot

Decoding ADGRE5: How Proteolytic Cleavage and Mechanical Forces Unleash Cellular Signals

inferred← citeshttps://doi.org/10.3390/ijms23021000openalex-snapshot

Scaffolding of Mitogen-Activated Protein Kinase Signaling by β-Arrestins

inferred← citeshttps://doi.org/10.3410/f.735441026.793559485openalex-snapshot

Faculty Opinions recommendation of Asymmetric Recruitment of β-Arrestin1/2 by the Angiotensin II Type I and Prostaglandin F2α Receptor Dimer.

inferred← citeshttps://doi.org/10.64898/2026.05.11.724365openalex-snapshot

GRK-dependent ACKR3 endocytosis and chemokine scavenging is independent of receptor phosphorylation and β-arrestin

inferred← citeshttps://doi.org/10.70675/3d2ffd20z5280z48adzbfe2z0d17920a5eeaopenalex-snapshot

Voies de signalisation activées lors de la stimulation du récepteur de l'apéline, responsables de l'effet hypotenseur de l'apéline

inferred← citeshttps://doi.org/10.70675/44901d9bz7728z47efz816dze698ae966bbdopenalex-snapshot

Régulation des tyrosine kinases FAK et Pyk2 par les ß-arrestines

inferred← citeshttps://doi.org/10.7554/elife.74101openalex-snapshot

Effector membrane translocation biosensors reveal G protein and βarrestin coupling profiles of 100 therapeutically relevant GPCRs

inferred← citeshttps://doi.org/10.7554/elife.87754openalex-snapshot

β-Arrestin-dependent and -independent endosomal G protein activation by the vasopressin type 2 receptor

inferred← citeshttps://doi.org/10.7554/elife.87754.2openalex-snapshot

β-arrestin-dependent and -independent endosomal G protein activation by the vasopressin type 2 receptor

inferred← citeshttps://doi.org/10.7554/elife.87754.3openalex-snapshot

β-Arrestin-dependent and -independent endosomal G protein activation by the vasopressin type 2 receptor

inferred← citeshttps://doi.org/10.7554/elife.99373openalex-snapshot

Endosomal chemokine receptor signalosomes regulate central mechanisms underlying cell migration

inferred← citeshttps://doi.org/10.7554/elife.99373.1openalex-snapshot

Endosomal Chemokine Receptor Signalosomes Regulate Central Mechanisms Underlying Cell Migration

inferred← citeshttps://doi.org/10.7554/elife.99373.1.sa0openalex-snapshot

Reviewer #2 (Public Review): Endosomal Chemokine Receptor Signalosomes Regulate Central Mechanisms Underlying Cell Migration

inferred← citeshttps://doi.org/10.7554/elife.99373.1.sa1openalex-snapshot

Reviewer #1 (Public Review): Endosomal Chemokine Receptor Signalosomes Regulate Central Mechanisms Underlying Cell Migration

inferred← citeshttps://doi.org/10.7554/elife.99373.1.sa2openalex-snapshot

eLife Assessment: Endosomal Chemokine Receptor Signalosomes Regulate Central Mechanisms Underlying Cell Migration

inferred← citeshttps://doi.org/10.7554/elife.99373.2openalex-snapshot

Endosomal Chemokine Receptor Signalosomes Regulate Central Mechanisms Underlying Cell Migration

inferred← citeshttps://doi.org/10.7554/elife.99373.3openalex-snapshot

Endosomal chemokine receptor signalosomes regulate central mechanisms underlying cell migration

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