Arrestins

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  Subject Areas on Research

  • A beta-arrestin 2 signaling complex mediates lithium action on behavior. 
  • A beta-arrestin binding determinant common to the second intracellular loops of rhodopsin family G protein-coupled receptors. 
  • A beta-arrestin-biased agonist of the parathyroid hormone receptor (PTH1R) promotes bone formation independent of G protein activation. 
  • A beta-arrestin/green fluorescent protein biosensor for detecting G protein-coupled receptor activation. 
  • A central role for beta-arrestins and clathrin-coated vesicle-mediated endocytosis in beta2-adrenergic receptor resensitization. Differential regulation of receptor resensitization in two distinct cell types. 
  • A dopamine D1 receptor-dependent β-arrestin signaling complex potentially regulates morphine-induced psychomotor activation but not reward in mice. 
  • A stress response pathway regulates DNA damage through β2-adrenoreceptors and β-arrestin-1. 
  • A unique mechanism of beta-blocker action: carvedilol stimulates beta-arrestin signaling. 
  • Activation and targeting of extracellular signal-regulated kinases by beta-arrestin scaffolds. 
  • Activation-dependent conformational changes in {beta}-arrestin 2. 
  • Activity-dependent internalization of smoothened mediated by beta-arrestin 2 and GRK2. 
  • Agonist-specific regulation of delta-opioid receptor trafficking by G protein-coupled receptor kinase and beta-arrestin. 
  • Allosteric modulation of β-arrestin-biased angiotensin II type 1 receptor signaling by membrane stretch. 
  • An Akt/beta-arrestin 2/PP2A signaling complex mediates dopaminergic neurotransmission and behavior. 
  • Angiotensin II-stimulated signaling through G proteins and beta-arrestin. 
  • Antagonism of dopamine D2 receptor/beta-arrestin 2 interaction is a common property of clinically effective antipsychotics. 
  • Arrestin development: emerging roles for beta-arrestins in developmental signaling pathways. 
  • Arrestin interaction with E3 ubiquitin ligases and deubiquitinases: functional and therapeutic implications. 
  • Arresting a transient receptor potential (TRP) channel: beta-arrestin 1 mediates ubiquitination and functional down-regulation of TRPV4. 
  • Arresting developments in heptahelical receptor signaling and regulation. 
  • Arrestins as signaling molecules involved in apoptotic pathways: a real eye opener. 
  • Arrestins come of age: a personal historical perspective. 
  • Association of beta-arrestin with G protein-coupled receptors during clathrin-mediated endocytosis dictates the profile of receptor resensitization. 
  • Atypical responsiveness of the orphan receptor GPR55 to cannabinoid ligands. 
  • BRET biosensors to study GPCR biology, pharmacology, and signal transduction. 
  • Beta-Arrestins: new roles in regulating heptahelical receptors' functions. 
  • Beta-Arrestins: new roles in regulating heptahelical receptors' functions. 
  • Beta-arrestin 2 mediates endocytosis of type III TGF-beta receptor and down-regulation of its signaling. 
  • Beta-arrestin 2 regulates zebrafish development through the hedgehog signaling pathway. 
  • Beta-arrestin 2-dependent angiotensin II type 1A receptor-mediated pathway of chemotaxis. 
  • Beta-arrestin 2: a receptor-regulated MAPK scaffold for the activation of JNK3. 
  • Beta-arrestin and Mdm2 mediate IGF-1 receptor-stimulated ERK activation and cell cycle progression. 
  • Beta-arrestin goes nuclear. 
  • Beta-arrestin scaffolding of phosphatidylinositol 4-phosphate 5-kinase Ialpha promotes agonist-stimulated sequestration of the beta2-adrenergic receptor. 
  • Beta-arrestin- and G protein receptor kinase-mediated calcium-sensing receptor desensitization. 
  • Beta-arrestin- but not G protein-mediated signaling by the "decoy" receptor CXCR7. 
  • Beta-arrestin-2 regulates the development of allergic asthma. 
  • Beta-arrestin-biased ligands at seven-transmembrane receptors. 
  • Beta-arrestin-dependent formation of beta2 adrenergic receptor-Src protein kinase complexes. 
  • Beta-arrestin-dependent signaling and trafficking of 7-transmembrane receptors is reciprocally regulated by the deubiquitinase USP33 and the E3 ligase Mdm2. 
  • Beta-arrestin-mediated beta1-adrenergic receptor transactivation of the EGFR confers cardioprotection. 
  • Beta-arrestin-mediated localization of smoothened to the primary cilium. 
  • Beta-arrestin-mediated signaling in the heart. 
  • Beta-arrestin-mediated signaling regulates protein synthesis. 
  • Beta-arrestin1 mediates insulin-like growth factor 1 (IGF-1) activation of phosphatidylinositol 3-kinase (PI3K) and anti-apoptosis. 
  • Beta-arrestin2, a novel member of the arrestin/beta-arrestin gene family. 
  • Beta-arrestin2-mediated inotropic effects of the angiotensin II type 1A receptor in isolated cardiac myocytes. 
  • Beta-arrestins and cell signaling. 
  • Beta-arrestins regulate atherosclerosis and neointimal hyperplasia by controlling smooth muscle cell proliferation and migration. 
  • Beta-arrestins specifically constrain beta2-adrenergic receptor signaling and function in airway smooth muscle. 
  • Beta-arrestins: multifunctional cellular mediators. 
  • Beta-blockers alprenolol and carvedilol stimulate beta-arrestin-mediated EGFR transactivation. 
  • BiPS, a photocleavable, isotopically coded, fluorescent cross-linker for structural proteomics. 
  • Biased agonism as a mechanism for differential signaling by chemokine receptors. 
  • Both hematopoietic-derived and non-hematopoietic-derived {beta}-arrestin-2 regulates murine allergic airway disease. 
  • Cellular trafficking of G protein-coupled receptor/beta-arrestin endocytic complexes. 
  • Chronic loss of noradrenergic tone produces β-arrestin2-mediated cocaine hypersensitivity and alters cellular D2 responses in the nucleus accumbens. 
  • Circulating Exosomes Induced by Cardiac Pressure Overload Contain Functional Angiotensin II Type 1 Receptors. 
  • Classical and new roles of beta-arrestins in the regulation of G-protein-coupled receptors. 
  • Clathrin-mediated endocytosis of the beta-adrenergic receptor is regulated by phosphorylation/dephosphorylation of beta-arrestin1. 
  • Comparative studies of molecular mechanisms of dopamine D2 and D3 receptors for the activation of extracellular signal-regulated kinase. 
  • Competing G protein-coupled receptor kinases balance G protein and β-arrestin signaling. 
  • Constitutive arrestin-mediated desensitization of a human vasopressin receptor mutant associated with nephrogenic diabetes insipidus. 
  • Constitutive protease-activated receptor-2-mediated migration of MDA MB-231 breast cancer cells requires both beta-arrestin-1 and -2. 
  • Constitutively active alpha-1b adrenergic receptor mutants display different phosphorylation and internalization features. 
  • Defective lymphocyte chemotaxis in beta-arrestin2- and GRK6-deficient mice. 
  • Deletion of GSK3β in D2R-expressing neurons reveals distinct roles for β-arrestin signaling in antipsychotic and lithium action. 
  • Desensitization of G protein-coupled receptors and neuronal functions. 
  • Desensitization, internalization, and signaling functions of beta-arrestins demonstrated by RNA interference. 
  • Design, synthesis, and analysis of antagonists of GPR55: Piperidine-substituted 1,3,4-oxadiazol-2-ones. 
  • Deubiquitinases and their emerging roles in β-arrestin-mediated signaling. 
  • Diesel exhaust particles activate the matrix-metalloproteinase-1 gene in human bronchial epithelia in a beta-arrestin-dependent manner via activation of RAS. 
  • Different G protein-coupled receptor kinases govern G protein and beta-arrestin-mediated signaling of V2 vasopressin receptor. 
  • Differential affinities of visual arrestin, beta arrestin1, and beta arrestin2 for G protein-coupled receptors delineate two major classes of receptors. 
  • Differential kinetic and spatial patterns of beta-arrestin and G protein-mediated ERK activation by the angiotensin II receptor. 
  • Differential mechanisms of morphine antinociceptive tolerance revealed in (beta)arrestin-2 knock-out mice. 
  • Differential regulation of the dopamine D2 and D3 receptors by G protein-coupled receptor kinases and beta-arrestins. 
  • Direct binding of activated c-Src to the beta 3-adrenergic receptor is required for MAP kinase activation. 
  • Discovery of novel FFA4 (GPR120) receptor agonists with β-arrestin2-biased characteristics. 
  • Discovery of β-arrestin-biased dopamine D2 ligands for probing signal transduction pathways essential for antipsychotic efficacy. 
  • Dishevelled 2 recruits beta-arrestin 2 to mediate Wnt5A-stimulated endocytosis of Frizzled 4. 
  • Distinct beta-arrestin- and G protein-dependent pathways for parathyroid hormone receptor-stimulated ERK1/2 activation. 
  • Distinct conformational changes in beta-arrestin report biased agonism at seven-transmembrane receptors. 
  • Distinct phosphorylation sites on the β(2)-adrenergic receptor establish a barcode that encodes differential functions of β-arrestin. 
  • Distinct roles for β-arrestin2 and arrestin-domain-containing proteins in β2 adrenergic receptor trafficking. 
  • Dynamin and beta-arrestin reveal distinct mechanisms for G protein-coupled receptor internalization. 
  • Effects of β-Arrestin-Biased Dopamine D2 Receptor Ligands on Schizophrenia-Like Behavior in Hypoglutamatergic Mice. 
  • Elucidation of G-protein and β-arrestin functional selectivity at the dopamine D2 receptor. 
  • Emerging paradigms of β-arrestin-dependent seven transmembrane receptor signaling. 
  • Endocytosis of G protein-coupled receptors: roles of G protein-coupled receptor kinases and beta-arrestin proteins. 
  • Enhanced morphine analgesia in mice lacking beta-arrestin 2. 
  • Enhanced rewarding properties of morphine, but not cocaine, in beta(arrestin)-2 knock-out mice. 
  • Essential role for G protein-coupled receptor endocytosis in the activation of mitogen-activated protein kinase. 
  • Expanding roles for beta-arrestins as scaffolds and adapters in GPCR signaling and trafficking. 
  • Feedback regulation of beta-arrestin1 function by extracellular signal-regulated kinases. 
  • Functional antagonism of different G protein-coupled receptor kinases for beta-arrestin-mediated angiotensin II receptor signaling. 
  • Functional selectivity in adrenergic and angiotensin signaling systems. 
  • Functional specialization of beta-arrestin interactions revealed by proteomic analysis. 
  • G protein-coupled receptor adaptation mechanisms. 
  • G protein-coupled receptor desensitization as a measure of signaling: modeling of arrestin recruitment to activated CCK-B receptors. 
  • G protein-coupled receptor kinase 5 regulates beta 1-adrenergic receptor association with PSD-95. 
  • G protein-coupled receptor kinase and beta-arrestin-mediated desensitization of the angiotensin II type 1A receptor elucidated by diacylglycerol dynamics. 
  • G protein-coupled receptor kinase function is essential for chemosensation in C. elegans. 
  • G protein-coupled receptor kinase regulates dopamine D3 receptor signaling by modulating the stability of a receptor-filamin-beta-arrestin complex. A case of autoreceptor regulation. 
  • G protein-coupled receptor kinase/beta-arrestin systems and drugs of abuse: psychostimulant and opiate studies in knockout mice. 
  • G protein-coupled receptors. III. New roles for receptor kinases and beta-arrestins in receptor signaling and desensitization. 
  • G-protein-coupled receptor (GPCR) kinase phosphorylation and beta-arrestin recruitment regulate the constitutive signaling activity of the human cytomegalovirus US28 GPCR. 
  • G-protein-coupled receptor kinase specificity for beta-arrestin recruitment to the beta2-adrenergic receptor revealed by fluorescence resonance energy transfer. 
  • G-protein-coupled receptor kinases and arrestins: regulators of G-protein-coupled receptor sequestration. 
  • GPCRs and arrestins in airways: implications for asthma. 
  • GRKs and beta-arrestins: roles in receptor silencing, trafficking and signaling. 
  • Genetic Deletion of β-Arrestin-2 and the Mitigation of Established Airway Hyperresponsiveness in a Murine Asthma Model. 
  • Genetic mapping of the beta-arrestin 1 and 2 genes on mouse chromosomes 7 and 11 respectively. 
  • Global phosphorylation analysis of beta-arrestin-mediated signaling downstream of a seven transmembrane receptor (7TMR). 
  • Heptahelical terpsichory. Who calls the tune? 
  • Human substance P receptor lacking the C-terminal domain remains competent to desensitize and internalize. 
  • Identification of Drosophila neuropeptide receptors by G protein-coupled receptors-beta-arrestin2 interactions. 
  • Identification of NSF as a beta-arrestin1-binding protein. Implications for beta2-adrenergic receptor regulation. 
  • Identification of a motif in the carboxyl terminus of beta -arrestin2 responsible for activation of JNK3. 
  • Identification of select glucocorticoids as Smoothened agonists: potential utility for regenerative medicine. 
  • Independent beta-arrestin 2 and G protein-mediated pathways for angiotensin II activation of extracellular signal-regulated kinases 1 and 2. 
  • Independent beta-arrestin2 and Gq/protein kinase Czeta pathways for ERK stimulated by angiotensin type 1A receptors in vascular smooth muscle cells converge on transactivation of the epidermal growth factor receptor. 
  • Lgr4 and Lgr5 drive the formation of long actin-rich cytoneme-like membrane protrusions. 
  • Modeling of bias for the analysis of receptor signaling in biochemical systems. 
  • Molecular determinants underlying the formation of stable intracellular G protein-coupled receptor-beta-arrestin complexes after receptor endocytosis*. 
  • Molecular mechanism of desensitization of the chemokine receptor CCR-5: receptor signaling and internalization are dissociable from its role as an HIV-1 co-receptor. 
  • Molecular mechanism of β-arrestin-biased agonism at seven-transmembrane receptors. 
  • Molecular mechanisms of G protein-coupled receptor desensitization and resensitization. 
  • Morphine side effects in beta-arrestin 2 knockout mice. 
  • Mu-opioid receptor desensitization by beta-arrestin-2 determines morphine tolerance but not dependence. 
  • Multifaceted roles of beta-arrestins in the regulation of seven-membrane-spanning receptor trafficking and signalling. 
  • Muscarinic acetylcholine receptor M3 modulates odorant receptor activity via inhibition of β-arrestin-2 recruitment. 
  • Myosin III illuminates the mechanism of arrestin translocation. 
  • N-formyl peptide receptors internalize but do not recycle in the absence of arrestins. 
  • N-terminal tyrosine modulation of the endocytic adaptor function of the beta-arrestins. 
  • Nedd4 mediates agonist-dependent ubiquitination, lysosomal targeting, and degradation of the beta2-adrenergic receptor. 
  • New roles for beta-arrestins in cell signaling: not just for seven-transmembrane receptors. 
  • Novel roles for β-arrestins in the regulation of pharmacological sequestration to predict agonist-induced desensitization of dopamine D3 receptors. 
  • Odorant receptors and desensitization proteins colocalize in mammalian sperm. 
  • Opposite function of dopamine D1 and N-methyl-D-aspartate receptors in striatal cannabinoid-mediated signaling. 
  • Overexpression of beta-arrestin and beta-adrenergic receptor kinase augment desensitization of beta 2-adrenergic receptors. 
  • Pharmacological blockade of a β(2)AR-β-arrestin-1 signaling cascade prevents the accumulation of DNA damage in a behavioral stress model. 
  • Phenotypic regulation of the sphingosine 1-phosphate receptor miles apart by G protein-coupled receptor kinase 2. 
  • Phosphoinositide 3-kinase regulates beta2-adrenergic receptor endocytosis by AP-2 recruitment to the receptor/beta-arrestin complex. 
  • Phosphorylation and desensitization of the human beta 1-adrenergic receptor. Involvement of G protein-coupled receptor kinases and cAMP-dependent protein kinase. 
  • Phosphorylation of beta-arrestin2 regulates its function in internalization of beta(2)-adrenergic receptors. 
  • Physiologic and cardiac roles of beta-arrestins. 
  • Properties of secretin receptor internalization differ from those of the beta(2)-adrenergic receptor. 
  • Protein kinase activity of phosphoinositide 3-kinase regulates beta-adrenergic receptor endocytosis. 
  • Quantification of beta adrenergic receptor subtypes in beta-arrestin knockout mouse airways. 
  • RNA editing induces variation in desensitization and trafficking of 5-hydroxytryptamine 2c receptor isoforms. 
  • Real-time visualization of the cellular redistribution of G protein-coupled receptor kinase 2 and beta-arrestin 2 during homologous desensitization of the substance P receptor. 
  • Receptor regulation: beta-arrestin moves up a notch. 
  • Receptor, Ligand and Transducer Contributions to Dopamine D2 Receptor Functional Selectivity. 
  • 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. 
  • Receptor-specific ubiquitination of beta-arrestin directs assembly and targeting of seven-transmembrane receptor signalosomes. 
  • Reciprocal regulation of angiotensin receptor-activated extracellular signal-regulated kinases by beta-arrestins 1 and 2. 
  • Regulated expression of G protein-coupled receptor kinases (GRK's) and beta-arrestins in osteoblasts. 
  • Regulation of G protein-coupled receptor kinases and arrestins during receptor desensitization. 
  • Regulation of G protein-coupled receptor signaling by scaffold proteins. 
  • Regulation of V2 vasopressin receptor degradation by agonist-promoted ubiquitination. 
  • Regulation of arrestin-3 phosphorylation by casein kinase II. 
  • Regulation of beta-adrenergic receptor signaling by S-nitrosylation of G-protein-coupled receptor kinase 2. 
  • Regulation of epidermal growth factor receptor internalization by G protein-coupled receptors. 
  • Regulation of receptor fate by ubiquitination of activated beta 2-adrenergic receptor and beta-arrestin. 
  • Regulation of tyrosine kinase cascades by G-protein-coupled receptors. 
  • Relative opioid efficacy is determined by the complements of the G protein-coupled receptor desensitization machinery. 
  • Resonating to the music of ubiquitination. 
  • Role for β-arrestin in mediating paradoxical β2AR and PAR2 signaling in asthma. 
  • Role of beta-adrenergic receptor signaling and desensitization in heart failure: new concepts and prospects for treatment. 
  • Role of beta-arrestin in mediating agonist-promoted G protein-coupled receptor internalization. 
  • Role of beta-arrestins in the intracellular trafficking of G-protein-coupled receptors. 
  • Role of the cytoplasmic tails of CXCR1 and CXCR2 in mediating leukocyte migration, activation, and regulation. 
  • Role of the sphingosine-1-phosphate receptor EDG-1 in PDGF-induced cell motility. 
  • S-nitrosylation of beta-arrestin regulates beta-adrenergic receptor trafficking. 
  • Selective engagement of G protein coupled receptor kinases (GRKs) encodes distinct functions of biased ligands. 
  • Seven transmembrane receptors: something old, something new. 
  • Seven-transmembrane receptor signaling through beta-arrestin. 
  • Signaling, desensitization, and trafficking of G protein-coupled receptors revealed by green fluorescent protein conjugates. 
  • Smoothened signal transduction is promoted by G protein-coupled receptor kinase 2. 
  • Specificity of arrestin subtypes in regulating airway smooth muscle G protein-coupled receptor signaling and function. 
  • Spinophilin blocks arrestin actions in vitro and in vivo at G protein-coupled receptors. 
  • Stable interaction between beta-arrestin 2 and angiotensin type 1A receptor is required for beta-arrestin 2-mediated activation of extracellular signal-regulated kinases 1 and 2. 
  • Structure of active β-arrestin-1 bound to a G-protein-coupled receptor phosphopeptide. 
  • Structure-functional selectivity relationship studies of β-arrestin-biased dopamine D₂ receptor agonists. 
  • Synergistic regulation of beta2-adrenergic receptor sequestration: intracellular complement of beta-adrenergic receptor kinase and beta-arrestin determine kinetics of internalization. 
  • Targeted disruption of β-arrestin 2-mediated signaling pathways by aptamer chimeras leads to inhibition of leukemic cell growth. 
  • Targeting of cyclic AMP degradation to beta 2-adrenergic receptors by beta-arrestins. 
  • Targeting of diacylglycerol degradation to M1 muscarinic receptors by beta-arrestins. 
  • Targeting of the orphan receptor GPR35 by pamoic acid: a potent activator of extracellular signal-regulated kinase and β-arrestin2 with antinociceptive activity. 
  • Targeting β-arrestin2 in the treatment of L-DOPA-induced dyskinesia in Parkinson's disease. 
  • Teaching old receptors new tricks: biasing seven-transmembrane receptors. 
  • The Akt-GSK-3 signaling cascade in the actions of dopamine. 
  • The active conformation of beta-arrestin1: direct evidence for the phosphate sensor in the N-domain and conformational differences in the active states of beta-arrestins1 and -2. 
  • The adaptor protein beta-arrestin2 enhances endocytosis of the low density lipoprotein receptor. 
  • The beta2-adrenergic receptor/betaarrestin complex recruits the clathrin adaptor AP-2 during endocytosis. 
  • The deubiquitinases USP33 and USP20 coordinate beta2 adrenergic receptor recycling and resensitization. 
  • The interaction of beta-arrestin with the AP-2 adaptor is required for the clustering of beta 2-adrenergic receptor into clathrin-coated pits. 
  • The interaction of endoglin with beta-arrestin2 regulates transforming growth factor-beta-mediated ERK activation and migration in endothelial cells. 
  • The role of arrestins in development. 
  • The role of beta-arrestins in the termination and transduction of G-protein-coupled receptor signals. 
  • The role of beta-arrestins in the termination and transduction of G-protein-coupled receptor signals. 
  • The role of the prostaglandin EP4 receptor in the regulation of human outflow facility. 
  • The role of β-arrestin2-dependent signaling in thoracic aortic aneurysm formation in a murine model of Marfan syndrome. 
  • The stability of the G protein-coupled receptor-beta-arrestin interaction determines the mechanism and functional consequence of ERK activation. 
  • The stem cell-expressed receptor Lgr5 possesses canonical and functionally active molecular determinants critical to β-arrestin-2 recruitment. 
  • The superfamily of heptahelical receptors. 
  • The sustainability of interactions between the orexin-1 receptor and beta-arrestin-2 is defined by a single C-terminal cluster of hydroxy amino acids and modulates the kinetics of ERK MAPK regulation. 
  • The transforming growth factor-beta type III receptor mediates distinct subcellular trafficking and downstream signaling of activin-like kinase (ALK)3 and ALK6 receptors. 
  • The type III TGF-beta receptor regulates epithelial and cancer cell migration through beta-arrestin2-mediated activation of Cdc42. 
  • The type III TGFbeta receptor regulates directional migration: new tricks for an old dog. 
  • The type III transforming growth factor-beta receptor negatively regulates nuclear factor kappa B signaling through its interaction with beta-arrestin2. 
  • Therapeutic potential of β-arrestin- and G protein-biased agonists. 
  • Trafficking patterns of beta-arrestin and G protein-coupled receptors determined by the kinetics of beta-arrestin deubiquitination. 
  • Transduction of receptor signals by beta-arrestins. 
  • Triphenylmethane dye activation of beta-arrestin. 
  • Troglitazone stimulates beta-arrestin-dependent cardiomyocyte contractility via the angiotensin II type 1A receptor. 
  • TβRIII/β-arrestin2 regulates integrin α5β1 trafficking, function, and localization in epithelial cells. 
  • Ubiquitin-specific Protease 20 Regulates the Reciprocal Functions of β-Arrestin2 in Toll-like Receptor 4-promoted Nuclear Factor κB (NFκB) Activation. 
  • Ubiquitination of beta-arrestin links seven-transmembrane receptor endocytosis and ERK activation. 
  • Vasoactive intestinal polypeptide type-1 receptor regulation. Desensitization, phosphorylation, and sequestration. 
  • Visualization of arrestin recruitment by a G-protein-coupled receptor. 
  • beta -Arrestin-mediated recruitment of the Src family kinase Yes mediates endothelin-1-stimulated glucose transport. 
  • beta -Arrestins regulate protease-activated receptor-1 desensitization but not internalization or Down-regulation. 
  • beta-Arrestin 1 and 2 differentially regulate heptahelical receptor signaling and trafficking. 
  • beta-Arrestin 1 and Galphaq/11 coordinately activate RhoA and stress fiber formation following receptor stimulation. 
  • beta-Arrestin 2 expression determines the transcriptional response to lysophosphatidic acid stimulation in murine embryo fibroblasts. 
  • beta-Arrestin inhibits NF-kappaB activity by means of its interaction with the NF-kappaB inhibitor IkappaBalpha. 
  • beta-Arrestin mediates beta1-adrenergic receptor-epidermal growth factor receptor interaction and downstream signaling. 
  • beta-Arrestin scaffolding of the ERK cascade enhances cytosolic ERK activity but inhibits ERK-mediated transcription following angiotensin AT1a receptor stimulation. 
  • beta-Arrestin-biased agonism of the angiotensin receptor induced by mechanical stress. 
  • beta-Arrestin-dependent activation of Ca(2+)/calmodulin kinase II after beta(1)-adrenergic receptor stimulation. 
  • beta-Arrestin-dependent constitutive internalization of the human chemokine decoy receptor D6. 
  • beta-Arrestin-mediated ADP-ribosylation factor 6 activation and beta 2-adrenergic receptor endocytosis. 
  • beta-Arrestin-mediated PDE4 cAMP phosphodiesterase recruitment regulates beta-adrenoceptor switching from Gs to Gi. 
  • beta-Arrestin/AP-2 interaction in G protein-coupled receptor internalization: identification of a beta-arrestin binging site in beta 2-adaptin. 
  • beta-Arrestin1 mediates nicotinic acid-induced flushing, but not its antilipolytic effect, in mice. 
  • beta-Arrestin1 modulates lymphoid enhancer factor transcriptional activity through interaction with phosphorylated dishevelled proteins. 
  • beta-arrestin-1 competitively inhibits insulin-induced ubiquitination and degradation of insulin receptor substrate 1. 
  • beta-arrestin-biased agonism at the beta2-adrenergic receptor. 
  • beta-arrestin-dependent, G protein-independent ERK1/2 activation by the beta2 adrenergic receptor. 
  • beta-arrestin1 interacts with the catalytic domain of the tyrosine kinase c-SRC. Role of beta-arrestin1-dependent targeting of c-SRC in receptor endocytosis. 
  • beta-arrestin1 interacts with the catalytic domain of the tyrosine kinase c-SRC. Role of beta-arrestin1-dependent targeting of c-SRC in receptor endocytosis. 
  • beta-arrestins regulate mitogenic signaling and clathrin-mediated endocytosis of the insulin-like growth factor I receptor. 
  • beta-arrestins regulate mitogenic signaling and clathrin-mediated endocytosis of the insulin-like growth factor I receptor. 
  • beta-arrestins: traffic cops of cell signaling. 
  • {beta}-Arrestin is crucial for ubiquitination and down-regulation of the insulin-like growth factor-1 receptor by acting as adaptor for the MDM2 E3 ligase. 
  • {beta}-Arrestin-2 Mediates Anti-apoptotic Signaling through Regulation of BAD Phosphorylation. 
  • Β-arrestin: a signaling molecule and potential therapeutic target for heart failure. 
  • β-Arrestin and dishevelled coordinate biased signaling. 
  • β-Arrestin mediates oxytocin receptor signaling, which regulates uterine contractility and cellular migration. 
  • β-Arrestin-2 desensitizes the transient receptor potential vanilloid 1 (TRPV1) channel. 
  • β-Arrestin-2 mediates the proinflammatory effects of proteinase-activated receptor-2 in the airway. 
  • β-Arrestin-biased AT1R stimulation promotes cell survival during acute cardiac injury. 
  • β-Arrestin-mediated receptor trafficking and signal transduction. 
  • β-Arrestin2 mediates the initiation and progression of myeloid leukemia. 
  • β-arrestin deficiency protects against pulmonary fibrosis in mice and prevents fibroblast invasion of extracellular matrix. 
  • β-arrestin-biased signaling by the β-adrenergic receptors. 
  • β-arrestin1-biased β1-adrenergic receptor signaling regulates microRNA processing. 
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  Keywords of People

  • Oas, Terrence Gilbert, Professor of Biochemistry, Duke Cancer Institute