AnatomyOrganismsChemicals and DrugsPsychiatry and PsychologyPhenomena and ProcessesHumanities
ArrestinG-Protein-Coupled Receptor Kinase 1Eye ProteinsTransducinRod Cell Outer SegmentAntigensLightVision, OcularCattlePhotoreceptor Cells, InvertebrateRetinal Rod Photoreceptor CellsG-Protein-Coupled Receptor Kinase 3Dark AdaptationPhosphorylationProtein BindingOpsinsMitogen-Activated Protein Kinase 10Receptors, Adrenergic, beta-2Ocular Physiological ProcessesRetinal Cone Photoreceptor CellsPectenMyosin Type IIIProtein TransportRod OpsinsHistory
Arrestin
A 48-Kd protein of the outer segment of the retinal rods and a component of the phototransduction cascade. Arrestin quenches G-protein activation by binding to phosphorylated photolyzed rhodopsin. Arrestin causes experimental autoimmune uveitis when injected into laboratory animals.
G-Protein-Coupled Receptor Kinase 1
A PROTEIN-SERINE-THREONINE KINASE that is found in PHOTORECEPTOR CELLS. It mediates light-dependent PHOSPHORYLATION of RHODOPSIN and plays an important role in PHOTOTRANSDUCTION.
Eye Proteins
Transducin
A heterotrimeric GTP-binding protein that mediates the light activation signal from photolyzed rhodopsin to cyclic GMP phosphodiesterase and is pivotal in the visual excitation process. Activation of rhodopsin on the outer membrane of rod and cone cells causes GTP to bind to transducin followed by dissociation of the alpha subunit-GTP complex from the beta/gamma subunits of transducin. The alpha subunit-GTP complex activates the cyclic GMP phosphodiesterase which catalyzes the hydrolysis of cyclic GMP to 5'-GMP. This leads to closure of the sodium and calcium channels and therefore hyperpolarization of the rod cells. EC 3.6.1.-.
Rod Cell Outer Segment
The portion of a retinal rod cell situated between the ROD INNER SEGMENT and the RETINAL PIGMENT EPITHELIUM. It contains a stack of photosensitive disk membranes laden with RHODOPSIN.
Antigens
Substances that are recognized by the immune system and induce an immune reaction.
Light
That portion of the electromagnetic spectrum in the visible, ultraviolet, and infrared range.
Vision, Ocular
The process in which light signals are transformed by the PHOTORECEPTOR CELLS into electrical signals which can then be transmitted to the brain.
Cattle
Domesticated bovine animals of the genus Bos, usually kept on a farm or ranch and used for the production of meat or dairy products or for heavy labor.
Photoreceptor Cells, Invertebrate
Specialized cells in the invertebrates that detect and transduce light. They are predominantly rhabdomeric with an array of photosensitive microvilli. Illumination depolarizes invertebrate photoreceptors by stimulating Na+ influx across the plasma membrane.
Retinal Rod Photoreceptor Cells
Photosensitive afferent neurons located in the peripheral retina, with their density increases radially away from the FOVEA CENTRALIS. Being much more sensitive to light than the RETINAL CONE CELLS, the rod cells are responsible for twilight vision (at scotopic intensities) as well as peripheral vision, but provide no color discrimination.
G-Protein-Coupled Receptor Kinase 3
A ubiquitously expressed G-protein-coupled receptor kinase subtype that has specificity for the agonist-occupied form of BETA-ADRENERGIC RECEPTORS and a variety of other G-PROTEIN-COUPLED RECEPTORS. Although it is highly homologous to G-PROTEIN-COUPLED RECEPTOR KINASE 2, it is not considered to play an essential role in regulating myocardial contractile response.
Dark Adaptation
Adjustment of the eyes under conditions of low light. The sensitivity of the eye to light is increased during dark adaptation.
Phosphorylation
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
Protein Binding
The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.
Opsins
Photosensitive proteins in the membranes of PHOTORECEPTOR CELLS such as the rods and the cones. Opsins have varied light absorption properties and are members of the G-PROTEIN-COUPLED RECEPTORS family. Their ligands are VITAMIN A-based chromophores.
Mitogen-Activated Protein Kinase 10
A c-jun amino-terminal kinase that is found predominantly within NEURONS of the BRAIN, suggesting a role in stress-induced neuronal APOPTOSIS. Several isoforms of the protein with molecular sizes of 47 kDa and 52 kDa exist due to multiple ALTERNATIVE SPLICING.
Receptors, Adrenergic, beta-2
A subclass of beta-adrenergic receptors (RECEPTORS, ADRENERGIC, BETA). The adrenergic beta-2 receptors are more sensitive to EPINEPHRINE than to NOREPINEPHRINE and have a high affinity for the agonist TERBUTALINE. They are widespread, with clinically important roles in SKELETAL MUSCLE; LIVER; and vascular, bronchial, gastrointestinal, and genitourinary SMOOTH MUSCLE.
Ocular Physiological Processes
Biological action and events that support the functions of the EYE and VISION, OCULAR.
Retinal Cone Photoreceptor Cells
Photosensitive afferent neurons located primarily within the FOVEA CENTRALIS of the MACULA LUTEA. There are three major types of cone cells (red, blue, and green) whose photopigments have different spectral sensitivity curves. Retinal cone cells operate in daylight vision (at photopic intensities) providing color recognition and central visual acuity.
Pecten
A genus of scallops in the family PECTINIDAE, class BIVALVIA. The shell is usually radially ribbed.
Myosin Type III
A subclass of myosins originally found in the photoreceptor of DROSOPHILA. The heavy chains can occur as two alternatively spliced isoforms of 132 and 174 KDa. The amino terminal of myosin type III is highly unusual in that it contains a protein kinase domain which may be an important component of the visual process.
Protein Transport
The process of moving proteins from one cellular compartment (including extracellular) to another by various sorting and transport mechanisms such as gated transport, protein translocation, and vesicular transport.
Rod Opsins
Photosensitive proteins expressed in the ROD PHOTORECEPTOR CELLS. They are the protein components of rod photoreceptor pigments such as RHODOPSIN.
History

How does arrestin respond to the phosphorylated state of rhodopsin? (1/474)

Visual arrestin quenches light-induced signaling by binding to light-activated, phosphorylated rhodopsin (P-Rh*). Here we present structure-function data, which in conjunction with the refined crystal structure of arrestin (Hirsch, J. A., Schubert, C., Gurevich, V. V., and Sigler, P. B. (1999) Cell, in press), support a model for the conversion of a basal or "inactive" conformation of free arrestin to one that can bind to and inhibit the light activated receptor. The trigger for this transition is an interaction of the phosphorylated COOH-terminal segment of the receptor with arrestin that disrupts intramolecular interactions, including a hydrogen-bonded network of buried, charged side chains, referred to as the "polar core." This disruption permits structural adjustments that allow arrestin to bind to the receptor. Our mutational survey identifies residues in arrestin (Arg175, Asp30, Asp296, Asp303, Arg382), which when altered bypass the need for the interaction with the receptor's phosphopeptide, enabling arrestin to bind to activated, nonphosphorylated rhodopsin (Rh*). These mutational changes disrupt interactions and substructures which the crystallographic model and previous biochemical studies have shown are responsible for maintaining the inactive state. The molecular basis for these disruptions was confirmed by successfully introducing structure-based second site substitutions that restored the critical interactions. The nearly absolute conservation of the mutagenically sensitive residues throughout the arrestin family suggests that this mechanism is likely to be applicable to arrestin-mediated desensitization of most G-protein-coupled receptors.  (+info)

The 2.8 A crystal structure of visual arrestin: a model for arrestin's regulation. (2/474)

G protein-coupled signaling is utilized by a wide variety of eukaryotes for communicating information from the extracellular environment. Signal termination is achieved by the action of the arrestins, which bind to activated, phosphorylated G protein-coupled receptors. We describe here crystallographic studies of visual arrestin in its basal conformation. The salient features of the structure are a bipartite molecule with an unusual polar core. This core is stabilized in part by an extended carboxy-terminal tail that locks the molecule into an inactive state. In addition, arrestin is found to be a dimer of two asymmetric molecules, suggesting an intrinsic conformational plasticity. In conjunction with biochemical and mutagenesis data, we propose a molecular mechanism by which arrestin is activated for receptor binding.  (+info)

G-protein coupled receptor kinases as modulators of G-protein signalling. (3/474)

G-protein coupled receptors (GPCRs) comprise one of the largest classes of signalling molecules. A wide diversity of activating ligands induce the active conformation of GPCRs and lead to signalling via heterotrimeric G-proteins and downstream effectors. In addition, a complex series of reactions participate in the 'turn-off' of GPCRs in both physiological and pharmacological settings. Some key players in the inactivation or 'desensitization' of GPCRs have been identified, whereas others remain the target of ongoing studies. G-protein coupled receptor kinases (GRKs) specifically phosphorylate activated GPCRs and initiate homologous desensitization. Uncoupling proteins, such as members of the arrestin family, bind to the phosphorylated and activated GPCRs and cause desensitization by precluding further interactions of the GPCRs and G-proteins. Adaptor proteins, including arrestins, and endocytic machinery participate in the internalization of GPCRs away from their normal signalling milieu. In this review we discuss the roles of these regulatory molecules as modulators of GPCR signalling.  (+info)

Immediate upstream sequence of arrestin directs rod-specific expression in Xenopus. (4/474)

Arrestins are a family of proteins that modulate G protein-coupled receptor responses with distinct arrestin genes expressed in rods and cones. To understand the regulatory mechanisms controlling rod-specific expression, the abundant Xenopus rod arrestin cDNA and a partial genomic clone, containing the immediate upstream region and amino terminus of the polypeptide, have been characterized. The deduced polypeptide has approximately 69% identity to other vertebrate rod arrestins. Southern blot analysis and polymerase chain reaction of intronic sequences demonstrated multiple alleles for rod arrestin. DNase I footprinting with retinal proteins revealed four major DNA binding sites in the proximal promoter, coinciding with consensus sequences reported in mammalian promoters. Purified bovine Crx homeodomain and mouse Nrl proteins protected a number of these sites. A dual approach of transient embryo transfections and transgenesis was used to locate transcriptional control sequences essential for rod-specific expression in Xenopus. Constructs containing -1287/+113 of 5' upstream sequence with or without intron 1 directed high level expression, specifically in rods. A construct containing only -287/+113 directed expression of green fluorescent protein solely in rod cells. These results suggest that the Crx and Nrl binding sites in the proximal promoter are the primary cis-acting sequences regulating arrestin gene expression in rods.  (+info)

Successful cotransplantation of intact sheets of fetal retina with retinal pigment epithelium. (5/474)

PURPOSE: Many retinal diseases, such as macular degeneration, affect both retinal pigment epithelium (RPE) and photoreceptors. Therefore, retinal repair may require transplantation of both tissues together as a cograft. METHODS: As recipients of retina-RPE cografts, 7- to 10-week-old albino Royal College of Surgeons rats that lose their photoreceptors because of a pigment epithelium defect were used. Freshly harvested intact sheets of RPE with neural retina from pigmented normal rat fetuses were gel embedded for protection and transplanted into the subretinal space. RESULTS: After 6 to 7 weeks, with the support of the cografted RPE sheet, transplanted photoreceptors developed fully in organized parallel layers in the subretinal space. Immunohistochemistry for rhodopsin, rod alpha-transducin, and S-antigen and peanut agglutinin labeling for cone interphotoreceptor matrix domains suggested that the photoreceptors in the graft were capable of normal function. CONCLUSIONS: Freshly harvested intact sheets of fetal RPE and retina, transplanted together into the subretinal space, can develop a normal morphology. Such transplants have the potential to benefit retinal diseases with dysfunctional RPE and photoreceptors.  (+info)

Photoreceptor function of retinal transplants implicated by light-dark shift of S-antigen and rod transducin. (6/474)

The aim was to demonstrate functional properties of transplanted histologically normal photoreceptors. Subretinal intact-sheet transplants of fetal E17-E20 rat retinas to light-damaged albino rat eyes were fixed in light or dark, 2 to 42 weeks after transplantation, and stained immunohistochemically for certain phototransduction proteins. In light adapted transplants, transducin was predominantly found in inner segments of parallel-organized photoreceptors. Transducin shifted to the outer segments with dark-adaptation. S-antigen distribution was opposite to transducin. Rhodopsin distribution did not change. The shift of signal transduction proteins correlated to the light conditions indicates that normal phototransduction processes were established in photoreceptors of transplanted retinal sheets.  (+info)

Visual arrestin activity may be regulated by self-association. (7/474)

Visual arrestin is the protein responsible for rapid quenching of G-protein-coupled receptor signaling. Arrestin exists as a latent inhibitor which must be 'activated' upon contact with a phosphorylated receptor. X-ray crystal structures of visual arrestin exhibit a tetrameric arrangement wherein an asymmetric dimer with an extensive interface between conformationally different subunits is related to a second asymmetric dimer by a local two-fold rotation axis. To test the biological relevance of this molecular organization in solution, we carried out a sedimentation equilibrium analysis of arrestin at both crystallographic and physiological protein concentrations. While the tetrameric form can exist at the high concentrations used in crystallography experiments, we find that arrestin participates in a monomer/dimer equilibrium at concentrations more likely to be physiologically relevant. Solution interaction analysis of a proteolytically modified, constitutively active form of arrestin shows diminished dimerization. We propose that self-association of arrestin may provide a mechanism for regulation of arrestin activity by (i) ensuring an adequate supply for rapid quenching of the visual signal and (ii) limiting the availability of active monomeric species, thereby preventing inappropriate signal termination.  (+info)

Differential expression of nitric oxide synthase in experimental uveoretinitis. (8/474)

PURPOSE: To investigate the site and the cellular source of inducible nitric oxide synthase (iNOS) expression in human S-antigen peptide-induced experimental autoimmune uveoretinitis (EAU). METHODS: Twenty-one Lewis rats were sensitized with human S-antigen peptides. Three rats were killed each consecutive day from day 6 through day 12 after sensitization. Frozen sections of the enucleated eyes were analyzed for iNOS by the dual immunohistochemical method. Primary antibodies included rabbit anti-mouse iNOS combined with anti-human endothelium NOS, anti-rat lysosomal protein (ED1), or anti-rat major histocompatibility complex class II molecule (OX6) monoclonal antibodies. Secondary antibodies were fluorescein-conjugated anti-mouse IgG and streptavidin rhodamine-labeled anti-rabbit IgG. The adjacent sections were separately stained with ED1, iNOS, and glial fibrillary acidic protein (GFAP). The mouse macrophage cell line RAW 264.7 was exposed to either interferon (IFN)gamma/lipopolysaccharide (LPS) or S-antigen and to interphotoreceptor retinoid-binding protein (IRBP), myelin basic protein, and bovine serum albumin for 12 hours. Cells were harvested for detection of iNOS expression by northern blot analysis hybridization and detection of protein by immunohistochemistry. RESULTS: In the retina of eyes with EAU, ED1+/iNOS+ and OX6+/iNOS+ cells were first detected on day 9 after sensitization. These iNOS+ cells increased in number on subsequent days in parallel with the increasing severity of retinal damage. Most of the cells localized around the outer retina. In contrast, a large number of ED1+ and OX6+ cells that were localized in the uvea and conjunctiva were negative for iNOS. Retinal pigment epithelial cells did not stain for iNOS. Macrophages exposed to IFNgamma/LPS, S-antigen, and IRBP showed expression of iNOS mRNA and the protein. CONCLUSIONS: Macrophages are an important source of NO production in eyes with EAU. These macrophages preferentially express iNOS in the retina. Such a differential expression of iNOS by the macrophages appears to be related to retinal soluble proteins.  (+info)

The Role Of Amphipathic Alpha-helix I in Arrestin Membrane Translocation | IOVS | ARVO JournalsThe Role Of Amphipathic Alpha-helix I in Arrestin Membrane Translocation | IOVS | ARVO Journals
Abstract: : Purpose: Arrestin rapidly binds both in vivo and in vitro to phosphorylated light-activated rhodopsin (P-Rh*), thereby quenching signaling in rods. However, in vivo arrestin apparently stays in the complex with P-Rh* for a long time, at least until P-Rh* decays into phospho-opsin. To identify the mechanism that slows down arrestin dissociation, we studied it in direct binding assay. Methods: Tritiated arrestin was pre-bound to P-Rh* for 5 min at 37oC, then diluted 50-fold and allowed to dissociate on ice. Aliquots were taken every 15 min. and bound arrestin was measured using gel-filtration-based assay. Results: The half-life of the complex was found to be 123 + 7 min, i.e., extremely long. Our recent mutagenesis data suggest that in the process of arrestin binding to P-Rh* the three-element interaction involving beta-strand I, alpha-helix one, and arrestin C-tail is disrupted. One of the released elements, alpha-helix I (residues 100-111), is a typical amphipathic helix closely ...
http://iovs.arvojournals.org/article.aspx?articleid=2418667
Two Elements In The Two Domains of The Arrestin Molecule Determine Its Receptor Specificity | IOVS | ARVO JournalsTwo Elements In The Two Domains of The Arrestin Molecule Determine Its Receptor Specificity | IOVS | ARVO Journals
Abstract: : Purpose: To elucidate the structural basis for arrestins receptor specificity. Four cloned arrestin proteins participate in homologous desensitization of hundreds of G protein-coupled receptors. Although the receptor specificity of the two non-visual arrestins is not known, the specificity of rod and cone arrestins for their respective pigments is inferred from their selective expression in these two types of photoreceptor cells. Recently we found that cone arrestin has a 50-fold lower affinity for phosphorylated light-activated rhodopsin (P-Rh*) than rod visual arrestin (VA). The difference in affinity of bovine and salamander VA for P-Rh* of the corresponding vs the other species is of similar magnitude. Methods: Experimentally the preference of VA for P-Rh* and that of beta-arrestin (BA) for agonist-activated phosphorylated m2 muscarinic cholinergic receptor (P-m2*) can be measured in the direct binding assay. Each arrestin demonstrates about 6-fold higher binding to the ...
http://iovs.arvojournals.org/article.aspx?articleid=2418666
A homozygous 1-base pair deletion in the arrestin gene is a frequent cause of Oguchi disease in Japanese | Hereditary Ocular...A homozygous 1-base pair deletion in the arrestin gene is a frequent cause of Oguchi disease in Japanese | Hereditary Ocular...
Fuchs S, Nakazawa M, Maw M, Tamai M, Oguchi Y, Gal A. A homozygous 1-base pair deletion in the arrestin gene is a frequent cause of Oguchi disease in Japanese. Nat Genet. 1995 Jul;10(3):360-2.. ...
https://disorders.eyes.arizona.edu/references/homozygous-1-base-pair-deletion-arrestin-gene-frequent-cause-oguchi-disease-japanese
Retinal S-antigen Antibody [PDS1] - ImmuQuest
Target AntigenRetinal S antigen Quantity50ulClonePDS1HostMouse ImmunogenPorcine retinal S-antigen (arrestin)Myeloma/fusion partnersBalb/c Ag 8.653 myeloma cellsSpecies ReactivityRat, Cow, Human, PigPurificationProtein GFormatPurified antibody (from supernatant) containing PBS 0.1% sodium azideApplicationsWB, IHC-Fr, IC
https://immuquest.com/products/retinal-s-antigen-antibody-pds1
Regulation of Epithelial Morphogenesis by β-Arrestin Kurtz by Katarzyna Maria PiotrowskaRegulation of Epithelial Morphogenesis by β-Arrestin Kurtz by Katarzyna Maria Piotrowska
Arrestins are ubiquitous adaptor proteins that are implicated in diverse signaling pathways. Arrestins are involved in the regulation of G-protein coupled receptors (GPCRs) via endocytosis and desensitization followed by degradation or recycling of the receptor. There are two β-arrestin homologs in mammals, which are largely redundant and therefore difficult to study. Drosophila has a single β-arrestin, Kurtz (Krz), and hence presents unique opportunities to study the functions of β-arrestin. krz maternal mutants have been shown to cause defects in the gastrulation of Drosophila embryos. These were attributed to effects of Krz on Toll signaling pathway. To investigate the origins of the defects, the early hours of embryo development needed to be examined. One of the main pathways activated during the first hours of gastrulation that enables epithelial remodeling and ventral furrow formation is Fog-Mist signaling. Mist is a GPCR that is activated by Fog, which triggers a cascade of downstream
https://scholarworks.umb.edu/masters_theses/330/
Plus itPlus it
CCR2 is a well studied chemokine receptor that meets considerable clinical interest. Yet, few studies have been investigating recruitment of β-arrestin to CCR2, with CCL2 as the sole analyzed CCR2 ligand (Aragay et al., 1998; García Lopez et al., 2009). Thus, we report the first study dedicated to the investigation of the effects of different CCR2 ligands on β-arrestin recruitment. We demonstrate that the effects of different CCR2 ligands on β-arrestin recruitment to the receptor are quantitatively and qualitatively distinct from one another. Differences were found in recruitment efficacy, identifying CCL7, CCL8, and CCL13 as partial agonists, with submaximal responses despite full receptor occupancy. Comparing β-arrestin 1 or 2, we found potential bias toward β-arrestin 2 of CCL13 and CCL8, overall weak β-arrestin recruiters. Experiments addressing the decline of the CCR2/β-arrestin interaction over time revealed striking differences between the ligands. Although CCL7-induced ...
http://molpharm.aspetjournals.org/content/79/3/488
SMART: Pfam domain Arrestin NSMART: Pfam domain Arrestin N
G protein-coupled receptors are a large family of signalling molecules that respond to a wide variety of extracellular stimuli. The receptors relay the information encoded by the ligand through the activation of heterotrimeric G proteins and intracellular effector molecules. To ensure the appropriate regulation of the signalling cascade, it is vital to properly inactivate the receptor. This inactivation is achieved, in part, by the binding of a soluble protein, arrestin, which uncouples the receptor from the downstream G protein after the receptors are phosphorylated by G protein-coupled receptor kinases. In addition to the inactivation of G protein-coupled receptors, arrestins have also been implicated in the endocytosis of receptors and cross talk with other signalling pathways. Arrestin (retinal S-antigen) is a major protein of the retinal rod outer segments. It interacts with photo-activated phosphorylated rhodopsin, inhibiting or arresting its ability to interact with transducin ...
http://smart.embl.de/smart/do_annotation.pl?DOMAIN=Pfam:Arrestin_N&START=7&END=139&E_VALUE=8.5e-19&TYPE=PFAM&BLAST=FEIRLSQGRVVYGPGEPLAGTVHLRLGAPLPFRAIRVTCMGSCGVSTKANDGAWVVEESYFNSSLSLADKGSLPAGEHNFPFQFLLPATAPTSFEGPFGKIVHQVRASIDTPRFSKDHKCSLVFYILSPLNLN
β-Arrestin Deficiency Protects Against Pulmonary Fibrosis in Mice and Prevents Fibroblast Invasion of Extracellular Matrix |...β-Arrestin Deficiency Protects Against Pulmonary Fibrosis in Mice and Prevents Fibroblast Invasion of Extracellular Matrix |...
Idiopathic pulmonary fibrosis is a progressive disease that causes unremitting extracellular matrix deposition with resulting distortion of pulmonary architecture and impaired gas exchange. β-Arrestins regulate G protein (heterotrimeric guanine nucleotide-binding protein)-coupled receptors through receptor desensitization while also acting as signaling scaffolds to facilitate numerous effector pathways. Here, we examine the role of β-arrestin1 and β-arrestin2 in the pathobiology of pulmonary fibrosis. In the bleomycin-induced mouse lung fibrosis model, loss of either β-arrestin1 or β-arrestin2 resulted in protection from mortality, inhibition of matrix deposition, and protected lung function. Fibrosis was prevented despite preserved recruitment of inflammatory cells and fibroblast chemotaxis. However, isolated lung fibroblasts from bleomycin-treated β-arrestin-null mice failed to invade extracellular matrix and displayed altered expression of genes involved in matrix production and ...
https://stm.sciencemag.org/content/3/74/74ra23
Novel function of β-arrestin2 in the nucleus of mature spermatozoa | Journal of Cell ScienceNovel function of β-arrestin2 in the nucleus of mature spermatozoa | Journal of Cell Science
β-arrestin2 is well known to function as a scaffold for some MAP kinase modules thereby contributing to the activation of mitogen-activated protein kinases by GPCRs. We investigated activation of MAPKs in spermatozoa upon bourgeonal treatment and found that activation of hOR17-4 leads to phosphorylation of ERK1/2 and p38 MAPK. Interestingly, activated ERK1/2 showed nuclear localization. MAPK activation by GPCR-bound arrestin is generally thought to target the MAPK to specific extranuclear locations (Luttrell, 2003; Lefkowitz and Shenoy, 2005). In spite of this, it was recently shown that β-arrestin2 promotes a subset of ERK1/2-mediated transcriptional responses to lysophosphatidic acid receptor activation (Gesty-Palmer et al., 2005) and β2-adrenergic receptor-mediated nuclear translocation of ERK (Kobayashi et al., 2005). Whether the observed nuclear translocation of β-arrestin2 upon hOR17-4 activation in spermatozoa causes the nuclear translocation of ERK1/2, as in the cases of activated ...
http://jcs.biologists.org/content/119/15/3047
Crystal structure of cone arrestin at 2.3A: evolution of receptor specificityCrystal structure of cone arrestin at 2.3A: evolution of receptor specificity
Arrestins play a fundamental role in the regulation and signal transduction of G protein-coupled receptors. Here we describe the crystal structure of cone arrestin at 2.3A resolution. The overall structure of cone visual arrestin is similar to the crystal structures of rod visual and the non-visual …
https://pubmed.ncbi.nlm.nih.gov/16289201/
MEK1 binds βarrestin1 directly, influencing both its phosphorylation by ERK and the timing of its isoprenaline-stimulated...MEK1 binds βarrestin1 directly, influencing both its phosphorylation by ERK and the timing of its isoprenaline-stimulated...
cAMP is a well studied second messenger that is ubiquitously expressed in mammals. It conducts its function by activating its downstream effectors: protein kinase A (PKA), exchange proteins regulated by cAMP (EPAC) and cyclic nucleotide gated ion-channels. The sole mechanism to inactivate cAMP is through degradation via cyclic-phosphodiesterases (PDEs). The PDEs, especially PDE4s, are involved in many diseases including asthma, chronic obstructive pulmonary disease (COPD) and depression. Therefore, PDEs have been a consistently popular research subject for decades and pharmaceutical companies have devoted considerable effort in developing PDE inhibitors. β-arrestin interacts with PDE4D5 and is a multifunctional protein that plays pivotal roles in signal transduction. It functions as an adaptor protein in the c-Raf/MEK/ERK cascade by interacting with c-Raf and ERK ...
http://theses.gla.ac.uk/1614/
C5AR1 CHO-K1 β-Arrestin GPCR Assay Kit Kit-1132 - Creative BioMart
Purified C5AR1 CHO-K1 β-Arrestin GPCR Assay Kit from Creative Biomart. C5AR1 CHO-K1 β-Arrestin GPCR Assay Kit can be used for research.
https://www.creativebiomart.net/c5ar1-cho-k1-beta-arrestin-gpcr-assay-kit-462420.htm
CCR4 CHO-K1 β-Arrestin GPCR Assay Kit Kit-1152 - Creative BioMart
Purified CCR4 CHO-K1 β-Arrestin GPCR Assay Kit from Creative Biomart. CCR4 CHO-K1 β-Arrestin GPCR Assay Kit can be used for research.
https://www.creativebiomart.net/ccr4-cho-k1-beta-arrestin-gpcr-assay-kit-462513.htm
Enhanced Morphine Analgesia in Mice Lacking β-Arrestin 2 | ScienceEnhanced Morphine Analgesia in Mice Lacking β-Arrestin 2 | Science
GPCRs have important roles in mediating fundamental physiological processes such as vision, olfaction, cardiovascular function, and pain perception. Cellular communication through GPCRs requires the coordination of processes governing receptor activation, desensitization, and resensitization. However, the relative contribution of desensitization mechanisms to the overall homeostatic process still remains largely unexplored in vivo. GPCR kinases (GRKs) act to phosphorylate activated receptors and promote their interaction with β-arrestins. This, in turn, prevents further coupling with G proteins and disrupts normal activation of the second messenger signaling cascade. By this mechanism, GRKs and β-arrestins can act to dampen GPCR signaling, thereby leading to desensitization of the receptor (1). At least six GRKs (GRK1 to GRK6) and four arrestins (visual and cone arrestin, β-arrestins 1 and 2) have been discovered; however, the functional importance of such redundancy is unclear. ...
https://science.sciencemag.org/content/286/5449/2495?ijkey=2e90334538824d6cd5a7d59ac157cec1e8f5606f&keytype2=tf_ipsecsha
Distinct phosphorylation sites in a prototypical GPCR differently orchestrate β-arrestin interaction, trafficking, and...Distinct phosphorylation sites in a prototypical GPCR differently orchestrate β-arrestin interaction, trafficking, and...
The Nature Index tracks the affiliations of high-quality scientific articles. Updated monthly, the Nature Index presents research outputs by institution and country. Use the Nature Index to interrogate publication patterns and to benchmark research performance.
https://www.natureindex.com/article/10.1126/sciadv.abb8368
Differential role of beta-arrestin ubiquitination in agonist-promoted down-regulation of M1 vs M2 muscarinic acetylcholine...Differential role of beta-arrestin ubiquitination in agonist-promoted down-regulation of M1 vs M2 muscarinic acetylcholine...
Our recent work established the essential role of β-arrestin in the internalization of the M2 mAChR [9]. The present study extends the observations of previous work and demonstrates that the agonist-promoted down-regulation of M1 and M2 mAChRs is β-arrestin dependent, and that the ubiquitination pattern of β-arrestin has a critical role in the differential down-regulation for M1 vs M2 mAChRs.. It has been previously established in a variety of cell lines that a prolonged activation of M1 or M2 mAChRs induces receptor down-regulation. In agreement with these findings, long-term stimulation of M1 or M2 mAChRs induced receptor down-regulation with the M1 mAChR showing significantly more down-regulation than M2 subtype. This observation suggests that the two subtypes are differentially regulated by endogenous β-arrestins. No down-regulation of either mAChR subtype occurred in the absence of β-arrestin and either β-arrestin subtype was able to rescue receptor down-regulation.. The observations ...
https://jmolecularsignaling.com/articles/10.1186/1750-2187-3-20/
β-Arrestin1-Biased β1-Adrenergic Receptor Signaling Regulates MicroRNA Processing | Circulation Researchβ-Arrestin1-Biased β1-Adrenergic Receptor Signaling Regulates MicroRNA Processing | Circulation Research
Rationale: MicroRNAs (miRs) are small, non-coding RNAs that function to post-transcriptionally regulate gene expression. First transcribed as long primary miR transcripts (pri-miRs), they are enzymatically processed in the nucleus by Drosha into hairpin intermediate miRs (pre-miRs) and further processed in the cytoplasm by Dicer into mature miRs where they regulate cellular processes following activation by a variety of signals such as those stimulated by β-adrenergic receptors (βARs). Initially discovered to desensitize βAR signaling, β-arrestins are now appreciated to transduce multiple effector pathways independent of G protein-mediated second messenger accumulation, a concept known as biased signaling. We previously showed that the β-arrestin-biased βAR agonist carvedilol activates cellular pathways in the heart. Objective: Here, we tested whether carvedilol could activate β-arrestin-mediated miR maturation, thereby providing a novel potential mechanism for its cardioprotective ...
http://circres.ahajournals.org/content/early/2013/12/13/CIRCRESAHA.114.302766
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The nuclear translocation of ERKs is normally regulated by the phosphorylation status of MEK1 (Whitmarsh and Davis, 1999). MEK1 binds to ERKs and prevents nuclear translocation of ERKs by its nucleus export signal. Phosphorylation of MEK1 leads to the activation of ERKs and the dissociation of MEK1-ERK complexes, which results in the subsequent nuclear translocation of activated ERKs. In several Gq-coupled GPCR systems, the G protein-dependent pathway activates ERKs through PKC, and the activated ERKs translocate into the nucleus, whereas the β-arrestin functions as a scaffold for both MEK1 and ERKs, thereby preventing the nuclear translocation of β-arrestin-activated ERKs (Tohgo et al., 2002; Shenoy and Lefkowitz, 2005). In addition, the prevention of the nuclear translocation of β-arrestin-activated ERKs is related to the interaction between receptor and β-arrestin. With the reduction in receptor-β-arrestin interaction allowing the recycling of the internalized receptor, a certain amount ...
http://molpharm.aspetjournals.org/content/73/1/178
Abstract 17572: Regulation of Myocardial Collagen Synthesis and Degradation by Beta-Arrestin 1/2 in Maladaptive Ventricular...Abstract 17572: Regulation of Myocardial Collagen Synthesis and Degradation by Beta-Arrestin 1/2 in Maladaptive Ventricular...
Cardiac fibroblasts (CF) produce and degrade extracellular matrix and are critical in regulating myocardial remodeling which can lead to heart failure. β-arrestins regulate G protein-coupled receptor (GPCR) function and also mediate GPCR-independent signaling. This study investigates the role of β-arrestin signaling in adult human CF isolated from normal and failing left ventricles. β-arrestin-1 expression is increased 1.5-fold in failing CF relative to normal controls. siRNA-mediated knockdown of β-arrestin 1 or 2 in failing CF decreased the expression of α-smooth muscle actin, suggesting that β-arrestins play an important role in the transformation of CF to activated myofibroblasts in the failing ventricle. This effect was more pronounced by decreasing β-arrestin 1 expression. Knockdown of β-arrestin 1 or 2 in failing CF led to increased β-agonist-stimulated cAMP production and restoration of β-agonist-mediated inhibition of collagen synthesis similar to normal CF. This effect was ...
http://circ.ahajournals.org/content/126/Suppl_21/A17572
Cutting Edge: Differential Regulation of Chemoattractant Receptor-Induced Degranulation and Chemokine Production by Receptor...Cutting Edge: Differential Regulation of Chemoattractant Receptor-Induced Degranulation and Chemokine Production by Receptor...
We have previously shown that fMLP, C3a, and C5a stimulated CCL2 production in a human mast cell line, HMC-1 (8). We suggested that chemoattractant receptor-induced ERK phosphorylation interacts synergistically with Ca2+/calcineurin-dependent activation of NFAT to induce chemokine gene expression (8). Receptor phosphorylation by GRK and subsequent β-arrestin-mediated internalization via clathrin-coated pits is an important mechanism for activation of ERK by a number of G protein-coupled receptors (27, 28). This raises the possibility that chemoattractant receptor-induced chemokine production could involve receptor phosphorylation and β-arrestin-dependent ERK activation. To test this possibility, transient transfectants were generated in RBL-2H3 cells coexpressing C3aR or ΔST-C3aR and βarr2-GFP conjugate. As shown in Fig. 4⇓A, C3a caused a rapid translocation of βarr2-GFP from the cytosol to the membrane in C3aR cells. In contrast, C3a did not induce this response in ΔST-C3aR cells. PTX, ...
http://www.jimmunol.org/content/167/7/3559
Cutting Edge: Differential Regulation of Chemoattractant Receptor-Induced Degranulation and Chemokine Production by Receptor...Cutting Edge: Differential Regulation of Chemoattractant Receptor-Induced Degranulation and Chemokine Production by Receptor...
We have previously shown that fMLP, C3a, and C5a stimulated CCL2 production in a human mast cell line, HMC-1 (8). We suggested that chemoattractant receptor-induced ERK phosphorylation interacts synergistically with Ca2+/calcineurin-dependent activation of NFAT to induce chemokine gene expression (8). Receptor phosphorylation by GRK and subsequent β-arrestin-mediated internalization via clathrin-coated pits is an important mechanism for activation of ERK by a number of G protein-coupled receptors (27, 28). This raises the possibility that chemoattractant receptor-induced chemokine production could involve receptor phosphorylation and β-arrestin-dependent ERK activation. To test this possibility, transient transfectants were generated in RBL-2H3 cells coexpressing C3aR or ΔST-C3aR and βarr2-GFP conjugate. As shown in Fig. 4⇓A, C3a caused a rapid translocation of βarr2-GFP from the cytosol to the membrane in C3aR cells. In contrast, C3a did not induce this response in ΔST-C3aR cells. PTX, ...
http://www.jimmunol.org/content/167/7/3559.full
GPCRs - B-arrestinGPCRs - B-arrestin
β-Arrestins are ubiquitously expressed and function in the activation of GPCRs, desensitization of most 7-transmembrane receptors, and regulation of other signaling molecules such as protein kinases. For GPCRs, ligand-induced β-arrestin recruitment activates signaling cascades independent of G-protein signaling to provide a non-amplified signal which is ideal for antagonist mode screening, studying ligand pharmacologies, and deorphanizing GPCRs. With decades of experience and hundreds of customer publications, DiscoverX provides a complete set of tools to analyze β-arrestin biology. The PathHunter β-arrestin assays and reagents offer a powerful and universal screening and profiling platform that can be used for virtually any Gi-, Gs-, or Gq-coupled receptor ...
https://discoverx.com/arrestin
Illuminating an Arrestin Pathway to Blindness | Science SignalingIlluminating an Arrestin Pathway to Blindness | Science Signaling
Using Drosophila as a model system, Lee and Montell uncovered a surprising divergence between the pathway leading to light-induced blindness and that underlying retinal degeneration. In many vertebrates, sustained exposure to even low-intensity light leads to blindness, which has long been attributed to the retinal degeneration that takes place under these conditions. Lee and Montell showed that Drosophila exposed to continuous light also displayed a progressive reduction in the visual response (measured with an electroretinogram), as well as retinal degeneration. The photoresponse was substantially reduced after 9 days of exposure to continuous light and drastically reduced--or abolished--after 17 days of exposure. Western analysis of head extracts indicated that the concentration of Rh1, the major rhodopsin, declined in parallel with attenuation of the photoresponse, whereas that of various other signaling proteins did not. Genetic analysis revealed that mutations in arrestin (which encodes a ...
https://stke.sciencemag.org/content/2004/264/tw456
β-Arrestin and Mdm2, Unsuspected Partners in Signaling from the Cell Surface | Science Signalingβ-Arrestin and Mdm2, Unsuspected Partners in Signaling from the Cell Surface | Science Signaling
Mdm2 is a ubiquitin-protein ligase known to ubiquitinate p53, promoting its degradation by the ubiquitin-proteasome system. Shenoy and co-workers showed that Mdm2 can act as a key factor in the sequestration of the cell surface β2-adrenergic receptor (β-AR) through interactions with β-arrestin. Strous and Schantl discuss how Mdm2 may be a switch connecting extracellular signals mediated through G protein-coupled receptors (GPCRs) to p53 and its functions in apoptosis and cell cycle progression.. ...
http://stke.sciencemag.org/content/2001/110/pe41
LinkLight™ U2-OS GPR101 / β-arrestin Cell Line | Bon Opus BiosciencesLinkLight™ U2-OS GPR101 / β-arrestin Cell Line | Bon Opus Biosciences
LinkLight™ U2-OS GPR101 / β-arrestin Cell Line is a stable monoclonal cell line in U2-OS cells, targeting Human GPR101 pathway via b-arrestin. The proprietary LinkLight™ technology uses a standard Luciferase Assay as the detection method. Bon Opus Cat. #BC050061
https://www.bonopusbio.com/product-page/linklight-u2-os-gpr101-%CE%B2-arrestin-cell-line
β-Arrestin 2: A receptor-regulated MAPK scaffold for the activation of JNK3 - Fingerprint - Albert Einstein College of...β-Arrestin 2: A receptor-regulated MAPK scaffold for the activation of JNK3 - Fingerprint - Albert Einstein College of...
Fingerprint Dive into the research topics of β-Arrestin 2: A receptor-regulated MAPK scaffold for the activation of JNK3. Together they form a unique fingerprint. ...
https://einstein.pure.elsevier.com/en/publications/%CE%B2-arrestin-2-a-receptor-regulated-mapk-scaffold-for-the-activatio-2/fingerprints/
Download A Pharmacology Primer. Techniques for More Effective and by Terry Kenakin PDF - khlinikthantkrrm Book ArchiveDownload A Pharmacology Primer. Techniques for More Effective and by Terry Kenakin PDF - khlinikthantkrrm Book Archive
Pleiotropic G-protein activation 2. Selective G-protein activation 3. Selective G-protein activation 4. Receptor dimerization 5. β-arrestin-Receptor interaction 9. 6. Receptor internalization 7. Receptor/Co-protein interaction 8. 8. β-arrestin-associated signaling 9. 24 Schematic showing some of the properties of seven transmembrane receptors. While many of these behaviors are interdependent upon each other, others are not, and receptors can be made to demonstrate partial panels of these behaviors selectively through binding of different ligands. In fact, new vantage points to view agonist activity can lead to reclassification of ligands. 23 shows a collection of β-blockers reclassified in terms of their activity on β-adrenoceptors as activators of Gproteins and ERK via β-arrestin binding [16,17]. This polyfunctional view of receptors extends beyond cellular signaling, as it is now known that modification of receptor behavior does not require activation of conventional signaling pathways. ...
http://sukhumvitskytraindental.com/pdf/a-pharmacology-primer-techniques-for-more-effective-and-strategic-drug
7:12 pm7:12 pm
Starting research in the Caron lab has been an exciting, yet terrifying experience. As the recipient of prestigious awards such as the Lieber Prize for Outstanding Achievement in Schizophrenia Research, Dr. Caron has set the standards high for his lab.. Upon first arriving, I was thrown in at the deep end and expectations were high. I witnessed many procedures and took notes as I watched, hoping that I would be able to replicate the techniques on my own when needed. Such is the case with transfecting and splitting cells, which is how I spent most of my time in lab this past week. While my mentor, Tom Pack, no longer has to overbook the hood for me (though he still does just in case), I find that I still have much to learn in the next 7 weeks.. As the summer progresses, I hope to not only increase my technical proficiency in lab, but also gain a greater understanding of GPCR signaling and the lab equipment that exists for studying it. While my current focus is on arrestin signaling following ...
https://sites.duke.edu/adhoc_org_trinity_hhr_fellows/?p=2251
Arrestin Orchestrates Crosstalk Between G Protein-Coupled Receptors to Modulate the Spatiotemporal Activation of ERK MAPK |...Arrestin Orchestrates Crosstalk Between G Protein-Coupled Receptors to Modulate the Spatiotemporal Activation of ERK MAPK |...
In cardiac fibroblasts and MEFs, our data indicate that the α1ARs make the primary contribution to ERK activation, supporting the dominant roles of these receptor subtypes in cardiac remodeling.34 Consistent with previous studies,35 stimulation of the α1ARs with Phe induces the classic Gq-dependent activation of PLC and PKC, leading to ERK activation through Raf-MEK1 kinase cascade. Under this signaling cascade, activated ERK translocates to the nucleus.35 Interestingly, this scenario is completely reshaped when β2ARs are coactivated with the α1AR on Epi stimulation. Coactivation of the α1 and β2ARs leads to sequestration of phospho-ERK within the cytosol. Under Epi stimulation, it was possible that two pools of ERK existed; a transient pool activated by the β2AR and a prolonged pool activated by the α1AR. The first pool becomes dominant simply because β2ARs are more prominent in cardiac tissues than α1ARs. This explanation is unlikely for several reasons. First, α1AR antagonist ...
http://circres.ahajournals.org/content/106/1/79
INT116674 - wiki-pain
By contrast, specific inhibition of endogenous GRK2 by dominant-negative mutants robustly inhibited OTR phosphorylation and internalization as well as arrestin/OTR interactions ...
http://gnteam.cs.manchester.ac.uk/demos/wiki-pain/vhosts/wikipaints/mediawiki-1.19.1/index.php/INT116674
Tekmira
Four HBV Product Candidates Advancing In Human Clinical Trials in 1H16 Three IND Filings in 2016 for Oral HBV Drug Candidates Targeting cccDNA, S-Antigen, and Core Protein New Business Unit Established to Maximize Value of Tekmiras Non-HBV Assets VANCOUVER, British … Continue reading →. ...
http://hepatitisb.hcvadvocate.org/category/tekmira/
Primary and secondary structure of bovine retinal S antigen (48-kDa protein) | PNASPrimary and secondary structure of bovine retinal S antigen (48-kDa protein) | PNAS
The complete amino acid sequence of bovine S antigen (48-kDa protein) has been determined by cDNA and partial amino acid sequencing. A 1623-base-pair (bp) cDNA contains an open reading frame coding for a protein of 404 amino acids (45,275 Da). Tryptic peptides and cyanogen bromide peptides of native bovine S antigen were purified and partially sequenced. All of these peptides were accounted for in the long open reading frame. Searching of the National Biomedical Research Foundation data bank revealed no extensive sequence homology between S antigen and other proteins. However, there are local regions of sequence similarity with alpha transducin, including the sites subject to ADP-ribosylation by Bordetella pertussis and cholera toxins and the phosphoryl binding-sites. Secondary structure prediction and circular dichroic spectroscopy show that S antigen is composed predominantly of beta-sheet conformation. Acid-catalyzed methanolysis suggests the presence of low levels of carbohydrate in the ...
https://www.pnas.org/content/84/20/6975?ijkey=70bf6d891513a262f906f10f1c663a9f6b6c6489&keytype2=tf_ipsecsha
Cellular Morphine Tolerance Produced by βArrestin-2-Dependent Impairment of μ-Opioid Receptor Resensitization | Journal of...Cellular Morphine Tolerance Produced by βArrestin-2-Dependent Impairment of μ-Opioid Receptor Resensitization | Journal of...
This study suggests that, unlike the mechanisms of β2 adrenoceptor regulation (Zhang et al., 1997b; Oakley et al., 1999; Gainetdinov et al., 2004), MOR resensitization in LC neurons does not require βarr-2-dependent mechanisms. When MOR endocytosis was presumably impaired by deletion of βarr-2, disruption of GRK2 function, or disruption of dynamin function, MOR resensitization was similarly accelerated rather than inhibited. Furthermore, intracellular application of a phosphatase inhibitor in the absence of βarrestin-dependent receptor trafficking (GRK2 inhibition in βarr-2 k.o.) prevented full recovery of MOR function, suggesting that MOR dephosphorylation is required for MOR resensitization and that this can occur independently of βarr-2-dependent MOR trafficking and endocytosis. The ability of MOR to dephosphorylate and resensitize rapidly when GRK2 and βarr-2 processes are disrupted is consistent with the observation that blocking endocytosis with concanavalin A in cultured LC neurons ...
https://www.jneurosci.org/content/31/19/7122?ijkey=92b16c7ebf5970487993bfcd58151fbde0e23fb9&keytype2=tf_ipsecsha
G Protein-Coupled Receptor Kinase 2, With β-Arrestin 2, Impairs Insulin-Induced Akt/Endothelial Nitric Oxide Synthase Signaling...G Protein-Coupled Receptor Kinase 2, With β-Arrestin 2, Impairs Insulin-Induced Akt/Endothelial Nitric Oxide Synthase Signaling...
In the current study, the most important question was whether GRK2 negatively controlled the insulin-induced Akt/eNOS pathway in aortas from diabetic mice with hyperinsulinemia. An important vascular action of insulin is its vasodilator effect, which is associated with increased NO production by endothelial cells (4,5,22,23). The results shown in the present Fig. 1A and B are consistent with our previous report (14). In that previous report, we discussed why GRK2 was increased in the diabetic aorta and how it affected the dysfunction of the endothelium-dependent relaxation to insulin that is mediated via the Akt pathway. We drew the conclusion that PKC activation mediated GRK2 overactivation and that the upregulation of GRK2 led to inhibition of the insulin-induced stimulation of the Akt/eNOS pathway (14). In the current study, we were interested in the pathway downstream of GRK2. From the results, we can propose that GRK2 acts by competing for β-arrestin 2 upon insulin-induced Akt/eNOS ...
http://diabetes.diabetesjournals.org/content/61/8/1978?with-ds=yes
S-Antigen: Adoptive Transfer of Experimental Autoimmune Uveitis Following Immunization With a Small Synthetic Peptide | JAMA...S-Antigen: Adoptive Transfer of Experimental Autoimmune Uveitis Following Immunization With a Small Synthetic Peptide | JAMA...
• Experimental autoimmune uveitis was observed following the adoptive transfer of T cell lymphocytes (T cells) from Lewis rats previously immunized with a small
https://jamanetwork.com/journals/jamaophthalmology/article-abstract/636738
Genetic Similarities to Humans - mollusks
Mollusks and human are different species, but because of convergent evolution that led them to have similar genetic expression. There have been studies that proved octopus eyes are similar to humans. In their study, they used a set of 1052 genes of the octopus eye and 13 303 genes of the human eye. For one of the research, they discovered that the protein in the eye were similar. When then compared the genes, they identified that a total of 729 genes were commonly expressed, a total of 69.3%. On other various tests,they found that six3, lhx2, retinal arrestin, retinal dehydrogenase, and human nuclear-transport receptor karyopherin were found to be expressed in the octopus eye ...
http://mollusk.weebly.com/genetic-similarities-to-humans.html
Molecular Regulation of Opioid Receptor SignalingMolecular Regulation of Opioid Receptor Signaling
The varied behavioral effects of kappa opioid receptors (KOR) are mediated through different signaling cascades. KOR activation of G protein-dependent signaling results in analgesia, whereas the dysphoric effects are mediated by a different pathway involving G protein-coupled receptor kinase (GRK) and arrestin. Therefore, a partial KOR agonist that does not efficiently activate arrestin-dependent signaling may produce analgesia without dysphoria. No selective KOR partial agonists are currently available, and preclinical assessment is complicated by sequence differences between rodent (r) and human (h) KOR. KOR antagonists are also of therapeutic interest for their potential anxiolytic and antidepressant effects, but many KOR antagonists have long durations of action resulting from selective activation of cJun kinase (JNK). In this thesis, I compared the signaling events initiated by agonist stimulation of hKOR and rKOR. Although a partial agonist at both hKOR and rKOR, pentazocine was more ...
https://digital.lib.washington.edu/researchworks/handle/1773/22023
Beltran, Mol Vis 2005; 11:232-244. Figure 1.Beltran, Mol Vis 2005; 11:232-244. Figure 1.
Figure 1. Immunolocalization of CNTFRα in the adult mouse retina. A: Negative control. B: Pattern of immunoenzymatic labeling with the anti-chick CNTFRα antibody. C: Pattern of immunoenzymatic labeling with the anti-rat CNTFRα antibody. D: Sequential section (to B) labeled with mouse cone arrestin antibody. E: Immunofluorescence labeling (overlaid images) with the anti-chick CNTFRα antibody (green), DAPI (blue), and peanut agglutinin (red). Intense labeling with the CNTFRα antibodies (B,E) was limited to ganglion cells, nerve fibers, and cells located predominantly at the vitreal and scleral borders of the inner nuclear layer (INL). Less intense labeling was also present at the inner plexiform layer (IPL) and outer plexiform layer (OPL). Nonspecific staining was observed at the photoreceptor layer (A-C) and was distinct from the specific cone inner segment labeling (arrows in D) obtained with the mouse cone arrestin antibody. Fluorescence immunocytochemistry confirmed the absence of ...
http://www.molvis.org/molvis/v11/a27/beltran-fig1.html
Modulation of methuselah expression targeted to Drosophila insulin-producing cells extends life and enhances oxidative stress...Modulation of methuselah expression targeted to Drosophila insulin-producing cells extends life and enhances oxidative stress...
Ubiquitously reduced signaling via Methuselah (MTH), a G-protein-coupled receptor (GPCR) required for neurosecretion, has previously been reported to extend life and enhance stress resistance in flies. Whether these effects are due to reduced MTH signalling in specific tissues remains unknown. We determined that reduced expression of mth targeted to the insulin-producing cells (IPCs) of the fly brain was sufficient to extend life and enhance oxidative stress resistance. Paradoxically, we discovered that overexpression of mth targeted to the same cells has similar phenotypic effects to reduced expression due to MTHs interaction with β-arrestin, which uncouples GPCRs from their G-proteins. We confirmed the functional relationship between MTH and β-arrestin by finding that IPC-targeted overexpression of β-arrestin alone mimics the longevity phenotype of reduced MTH signaling. As reduced MTH signaling also inhibits insulin secretion from the IPCs, the most parsimonious mechanistic explanation of ...
http://scholars.uab.edu/display/pub114065
Plus itPlus it
Heptahelical G protein-coupled receptors are the most diverse and therapeutically important family of receptors in the human genome. Ligand binding activates heterotrimeric G proteins that transmit intracellular signals by regulating effector enzymes or ion channels. G protein signaling is terminated, in large part, by arrestin binding, which uncouples the receptor and G protein and targets the receptor for internalization. It is clear, however, that heptahelical receptor signaling does not end with desensitization. Arrestins bind a host of catalytically active proteins and serve as ligand-regulated scaffolds that recruit protein and lipid kinase, phosphatase, phosphodiesterase, and ubiquitin ligase activity into the receptor-arrestin complex. Although many of these arrestin-bound effectors serve to modulate G protein signaling, degrading second messengers and regulating endocytosis and trafficking, other signals seem to extend beyond the receptor-arrestin complex to regulate such processes as ...
http://pharmrev.aspetjournals.org/content/early/2010/04/27/pr.109.002436
Biological membranes | Essays in BiochemistryBiological membranes | Essays in Biochemistry
Figure 12. GPCR and heterotrimeric G-protein signalling.. The ligand bound to the GPCR is shown in red. Binding allows the exchange of GDP for GTP by the associated G protein, and dissociation of the protein into Gα and Gβγ subunits. These then have downstream effects on a range of proteins, thereby propagating the signal from the bound ligand. Yellow arrows indicate either activation (up arrow) or inhibition (down arrow) of the targets. Regulators of G-protein signalling (RGS) proteins aid the GTPase activity of the G protein to turn off the signal. Arrestin can bind the receptor following GPCR phosphorylation by G-protein receptor kinase (GRK), desensitizing the receptor to further signalling. Reproduced from Berridge, M.J. (2012) Cell Signalling Biology; doi:10.1042/csb0001002, with permission. ...
http://essays.biochemistry.org/content/59/43.figures-only
kurtz, a Novel Nonvisual Arrestin, Is an Essential Neural Gene in Drosophila | Geneticskurtz, a Novel Nonvisual Arrestin, Is an Essential Neural Gene in Drosophila | Genetics
The Genetics Society of America (GSA), founded in 1931, is the professional membership organization for scientific researchers and educators in the field of genetics. Our members work to advance knowledge in the basic mechanisms of inheritance, from the molecular to the population level.. Online ISSN: 1943-2631. ...
https://www.genetics.org/content/155/3/1281.article-info
β‐arrestin‐1 mediates the TCR‐triggered re‐routing of distal receptors to the immunological synapse by a PKC‐mediated mechanism...β‐arrestin‐1 mediates the TCR‐triggered re‐routing of distal receptors to the immunological synapse by a PKC‐mediated mechanism...
In this study, we have adopted a proteomic approach to characterize new ligands of the TCR‐signaling ITAM motifs. In this way, we identified the GPCR‐interacting protein β‐Arr1 as a novel direct ligand of the TCR that is recruited to unphosphorylated ITAMs in a manner dependent on TCR triggering. While β‐Arr1 was previously described as a cytoplasmic effector of both GPCRs and RTKs (Hupfeld & Olefsky, 2007), this is the first demonstration of β‐Arr1 binding to the TCR, a multi‐subunit receptor without intrinsic enzymatic activity. We found that β‐Arr1 recruitment to the TCR was induced by TCR triggering. However, in contrast to the recruitment of other TCR signaling effectors, such as the tyrosine kinase ZAP‐70 or the adaptor protein Nck (Gil et al, 2002), that is mediated by changes in the TCR itself, recruitment of β‐Arr1 to the TCR was mediated by modifying β‐Arr1. The mechanism by which TCR triggering induces the recruitment of β‐Arr1 to non‐triggered TCRs ...
http://emboj.embopress.org/content/33/6/559
WikiGenes - ARR3 - arrestin 3, retinal (X-arrestin)WikiGenes - ARR3 - arrestin 3, retinal (X-arrestin)
The worlds first wiki where authorship really matters. Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts.
https://www.wikigenes.org/e/gene/e/407.html
Arrestin C-terminal-like domain (IPR011022) | InterPro | EMBL-EBIArrestin C-terminal-like domain (IPR011022) | InterPro | EMBL-EBI
InterPro provides functional analysis of proteins by classifying them into families and predicting domains and important sites. We combine protein signatures from a number of member databases into a single searchable resource, capitalising on their individual strengths to produce a powerful integrated database and diagnostic tool.
http://www.ebi.ac.uk/interpro/entry/IPR011022
Arrestin C domain-containing protein - Anopheles farautiArrestin C domain-containing protein - Anopheles farauti
p>The checksum is a form of redundancy check that is calculated from the sequence. It is useful for tracking sequence updates.,/p> ,p>It should be noted that while, in theory, two different sequences could have the same checksum value, the likelihood that this would happen is extremely low.,/p> ,p>However UniProtKB may contain entries with identical sequences in case of multiple genes (paralogs).,/p> ,p>The checksum is computed as the sequence 64-bit Cyclic Redundancy Check value (CRC64) using the generator polynomial: x,sup>64,/sup> + x,sup>4,/sup> + x,sup>3,/sup> + x + 1. The algorithm is described in the ISO 3309 standard. ,/p> ,p class=publication>Press W.H., Flannery B.P., Teukolsky S.A. and Vetterling W.T.,br /> ,strong>Cyclic redundancy and other checksums,/strong>,br /> ,a href=http://www.nrbook.com/b/bookcpdf.php>Numerical recipes in C 2nd ed., pp896-902, Cambridge University Press (1993),/a>),/p> Checksum:i ...
https://www.uniprot.org/uniprot/A0A182QD30
The TXNIP gene and its putative association with human ageingThe TXNIP gene and its putative association with human ageing
This gene encodes a thioredoxin-binding protein that is a member of the alpha arrestin protein family. Thioredoxin is a thiol-oxidoreductase that is a major regulator of cellular redox signaling which protects cells from oxidative stress. This protein inhibits the antioxidative function of thioredoxin resulting in the accumulation of reactive oxygen species and cellular stress. This protein also functions as a regulator of cellular metabolism and of endoplasmic reticulum (ER) stress. This protein may also function as a tumor suppressor. Alternate splicing results in multiple transcript variants. [provided by RefSeq, Sep 2015 ...
http://genomics.senescence.info/cells/gene.php?gene_name=TXNIP
RAX - Retinal homeobox protein Rx - Homo sapiens (Human) - RAX gene & proteinRAX - Retinal homeobox protein Rx - Homo sapiens (Human) - RAX gene & protein
Plays a critical role in eye formation by regulating the initial specification of retinal cells and/or their subsequent proliferation. Binds to the photoreceptor conserved element-I (PCE-1/Ret 1) in the photoreceptor cell-specific arrestin promoter.
https://www.uniprot.org/uniprot/Q9Y2V3
Differential expression of alternative splice variants of β-arrestin-1 and -2 in rat central nervous system and peripheral...Differential expression of alternative splice variants of β-arrestin-1 and -2 in rat central nervous system and peripheral...
TY - JOUR. T1 - Differential expression of alternative splice variants of β-arrestin-1 and -2 in rat central nervous system and peripheral tissues. AU - Komori, Naoka. AU - Cain, Sandra D.. AU - Roch, Jean Marc. AU - Miller, Kenneth E.. AU - Matsumoto, Hiroyuki. N1 - Copyright: Copyright 2007 Elsevier B.V., All rights reserved.. PY - 1998. Y1 - 1998. N2 - Members of arrestin/β-arrestin protein family are thought to participate in agonist-mediated desensitization of G-protein-coupled receptors, including rhodopsin and β2-adrenergic receptor. Unlike in human and cow, splice variants of this protein family in rat have not been studied extensively, and there has been no report on their existence at protein level. Hence, a previous report by others on the localization of both β-arrestin-1 and -2 in a wide range of innervated rat tissues could imply their broad receptor specificity. In this report we show the presence of two alternatively spliced forms of β-arrestin-1 in several rat tissues using ...
https://scholars.okstate.edu/en/publications/differential-expression-of-alternative-splice-variants-of-%CE%B2-arres
Thioredoxin-Interacting Protein Mediates Sustained VEGFR2 Signaling in Endothelial Cells Required for AngiogenesisSignificance ...Thioredoxin-Interacting Protein Mediates Sustained VEGFR2 Signaling in Endothelial Cells Required for AngiogenesisSignificance ...
TXNIP is a member of the α-arrestin family that functions as an intracellular scaffold, which participates in cellular signaling by formation of signaling complexes and localization of signaling components in the cell.11,12 VEGF-VEGFR2 signaling in EC seems to be dependent on TXNIP as shown in the present study. We showed previously that TXNIP was required for VEGFR2 activation and EC survival in response to low concentrations of H2O2 and tumor necrosis factor-α.15 These data support our concept that TXNIP plays a critical role in regulating VEGFR2 signaling and angiogenesis in EC.. A novel finding of the present study is that TXNIP seems to be required for the earliest stage of VEGFR2 internalization. Receptor tyrosine kinases are regulated by endocytosis through the internalization of plasma membrane receptors.25-27 For example, the internalization of epidermal growth factor receptor is mediated by clathrin-mediated endocytosis and is essential for sustained epidermal growth factor receptor ...
http://atvb.ahajournals.org/content/33/4/737
The formation of stable rhodopsin-arrestin complexes induces apoptosis and photoreceptor cell degenerationThe formation of stable rhodopsin-arrestin complexes induces apoptosis and photoreceptor cell degeneration
Although many different mutations in humans and Drosophila cause retinal degeneration, in most cases, a molecular mechanism for the degeneration has not been found. We now demonstrate the existence of stable, persistent complexes between rhodopsin and its regulatory protein arrestin in several diffe …
https://pubmed.ncbi.nlm.nih.gov/11086989/?dopt=Abstract
Distinct CCK-2 Receptor Conformations Associated with β-Arrestin-2 Recruitment or Phospholipase-C Activation Revealed by a...
TY - JOUR. T1 - Distinct CCK-2 Receptor Conformations Associated with β-Arrestin-2 Recruitment or Phospholipase-C Activation Revealed by a Biased Antagonist. AU - Magnan, Rémi. AU - Escrieut, Chantal. AU - Gigoux, Véronique. AU - De, Kavita. AU - Clerc, Pascal. AU - Niu, Fan. AU - Azema, Joelle. AU - Masri, Bernard. AU - Cordomi, Arnau. AU - Baltas, Michel. AU - Tikhonova, Irina G. AU - Fourmy, Daniel. PY - 2013/2/20. Y1 - 2013/2/20. N2 - Seven-transmembrane receptors (7TMRs), also termed G protein-coupled receptors (GPCRs), form the largest class of cell surface membrane receptors, involving several hundred members in the human genome. Near 30% of marketed pharmacological agents target 7TMRs. 7TMRs adopt multiple conformations upon agonist binding. Biased agonists, in contrast to non-biased agonists, are believed to stabilize conformations preferentially activating either G-protein- or ß-arrestin-dependent signalling pathways. However, proof that cognate conformations of receptors display ...
https://pure.qub.ac.uk/en/publications/distinct-cck-2-receptor-conformations-associated-with-%CE%B2-arrestin-
β-arrestin-biased agonism of β-adrenergic receptor regulates Dicer-mediated microRNA maturation to promote cardioprotective...
TY - JOUR. T1 - β-arrestin-biased agonism of β-adrenergic receptor regulates Dicer-mediated microRNA maturation to promote cardioprotective signaling. AU - Teoh, Jian Peng. AU - Bayoumi, Ahmed S.. AU - Aonuma, Tatsuya. AU - Xu, Yanyan. AU - Johnson, John A.. AU - Su, Huabo. AU - Weintraub, Neal L.. AU - Tang, Yaoliang. AU - Kim, Il Man. PY - 2018/5. Y1 - 2018/5. N2 - Rationale: MicroRNAs (miRs) are small, non-coding RNAs that function to post-transcriptionally regulate target genes. First transcribed as primary miR transcripts (pri-miRs), they are enzymatically processed by Drosha into premature miRs (pre-miRs) and further cleaved by Dicer into mature miRs. Initially discovered to desensitize β-adrenergic receptor (βAR) signaling, β-arrestins are now well-appreciated to modulate multiple pathways independent of G protein signaling, a concept known as biased signaling. Using the β-arrestin-biased βAR ligand carvedilol, we previously showed that β-arrestin1 (not β-arrestin2)-biased β1AR ...
https://indiana.pure.elsevier.com/en/publications/%CE%B2-arrestin-biased-agonism-of-%CE%B2-adrenergic-receptor-regulates-dice
Publications - Yamina.org
3. Berchiche Y.A., Gravel S., Pelletier M-E.,Ste-Onge G., Heveker N. Different effects of the different natural CCR2 ligands on β-arrestin recruitment, Gαi signalling and receptor internalization.(2011) Molecular Pharmacology 79(3):488-98. http://www.ncbi.nlm.nih.gov/pubmed/21088225. 4. Gravel S. Malouf C., Boulais P., Berchiche Y.A., Oishi S., Fujii N., Leduc R., Sinnett D., Heveker N. The Peptidomimetic CXCR4 antagonist TC14012 Recruits Beta-Arrestin to CXCR7-Roles of Receptor Domains.(2010) Journal of Biological Chemistry 285(49):37939-43. http://www.ncbi.nlm.nih.gov/pubmed/20956518. 5. Kalatskaya I*, Berchiche Y.A.*, Gravel S, Limberg B. J., Rosenbaum J.S, Heveker N. AMD3100 is a CXCR7 Ligand with Allosteric Agonist Properties. (2009) Molecular Pharmacology 75:1-8. * Contributed equally to this work. http://www.ncbi.nlm.nih.gov/pubmed/19255243. 6. Rafei M., Berchiche Y.A., Birman E., Boivin MN., Young Y.K., Wu J. H., Heveker N., Galipeau J. An Engineered GMCSF-CCL2 Fusokine is a Potent ...
http://yamina.org/publications/
How the protease thrombin talks to cells | PNASHow the protease thrombin talks to cells | PNAS
The mechanism of PAR1 activation is strikingly irreversible. Cleavage of PAR1 by thrombin is irrevocable, and the tethered ligand generated cannot diffuse away from the receptor. In the absence of the reversible ligation that characterizes most receptor systems, how is PAR1 shut off? The β2-adrenergic receptor has served as a prototype for dissecting the molecular events responsible for G protein-coupled receptor desensitization and resensitization (10-13). Upon activation, β2-adrenergic receptor is rapidly phosphorylated. It then binds arrestin, preventing further interaction with G proteins. Arrestin also mediates internalization of β2-adrenergic receptors via clathrin-coated pits (14, 15). Within an endosomal compartment, receptors dissociate from ligand, are dephosphorylated, and recycle back to the cell surface competent to signal again. Thus trafficking serves to remove activated β2-adrenergic receptors from the cell surface and to return the receptors to the surface in an off state, ...
https://www.pnas.org/content/96/20/11023?ijkey=d2fdf03db6f920ea4ced813ae3a3a8c257adf13d&keytype2=tf_ipsecsha
OPN1MW - WikipediaOPN1MW - Wikipedia
Zhu X, Brown B, Li A et al. (2003). GRK1-dependent phosphorylation of S and M opsins and their binding to cone arrestin during cone phototransduction in the mouse retina.. J. Neurosci. 23 (14): 6152-60. PMID 12853434. CS1 održavanje: Eksplicitna upotreba et al. (link) ...
https://sh.wikipedia.org/wiki/OPN1MW
Chatsworth house winds up with 1000 guinea pigs after taking in survivors - The Daily
|table border=0 cellpadding=2 cellspacing=7 style=vertical-align:top;||tr||td width=80 align=center valign=top||font style=font-size:85%;font-family:arial,sans-serif||a href=http://news.google.com/news/url?sa=t&fd=R&ct2=us&usg=AFQjCNHnTfhYiw26vV_kRZ6gDyEnPfYc9Q&clid=c3a7d30bb8a4878e06b80cf16b898331&cid=52779784971174&ei=6dxwWsjcA8GzWaCim_AC&url=https://www.dailybreeze.com/2018/01/30/chatsworth-house-winds-up-with-1000-guinea-pigs-after-taking-in-survivors/||img
https://www.guineapigcages.com/forum/threads/118315-Chatsworth-house-winds-up-with-1000-guinea-pigs-after-taking-in-survivors-The-Daily?p=999119
ArrestinArrestin
... -3. The second non-visual arrestin cloned was first termed β-arrestin-2 (retroactively changing the name of β-arrestin ... In mammals, arrestin-1 and arrestin-4 are largely confined to photoreceptors, whereas arrestin-2 and arrestin-3 are ubiquitous ... Arrestin-2 was the first non-visual arrestin cloned. It was first named β-arrestin simply because of the two GPCRs available in ... Arrestin-4 was cloned by two groups and termed cone arrestin, after photoreceptor type that expresses it, and X-arrestin, after ...
https://en.wikipedia.org/wiki/Arrestin
Alpha ArrestinAlpha Arrestin
... β-arrestins (also referred to as visual and non-visual arrestins) and Vps26-like arrestins proteins. The α-Arrestins are an ... The arrestin family of proteins is subdivided into α-arrestins (also referred to as arrestin-related trafficking adaptors (ARTs ... It is unclear if α-arrestins lack each of these structural features thought to distinguish the β-arrestins from the α-arrestins ... β-arrestins contain a polar core flanked on both sides by the arrestin N- and C-terminal fold domains. They also contain ...
https://en.wikipedia.org/wiki/Alpha_Arrestin
Arrestin beta 2Arrestin beta 2
Beta-arrestin-2, also known as arrestin beta-2, is an intracellular protein that in humans is encoded by the ARRB2 gene. ... Arrestin beta 2 is crucial for the development of tolerance to morphine and other opioids. Arrestin beta 2 has been shown to ... Arrestin beta 2, like arrestin beta 1, was shown to inhibit beta-adrenergic receptor function in vitro. It is expressed at high ... Members of arrestin/beta-arrestin protein family are thought to participate in agonist-mediated desensitization of G protein- ...
https://en.wikipedia.org/wiki/Arrestin_beta_2
Arrestin beta 1Arrestin beta 1
Arrestin, beta 1, also known as ARRB1, is a protein which in humans is encoded by the ARRB1 gene. Members of arrestin/beta- ... "Entrez Gene: ARRB1 arrestin, beta 1". Peterson YK, Luttrell LM (July 2017). "The Diverse Roles of Arrestin Scaffolds in G ... "Substance P-induced trafficking of beta-arrestins. The role of beta-arrestins in endocytosis of the neurokinin-1 receptor". The ... Beta-arrestin has been shown to play a role as a scaffold that binds intermediates and may direct G-protein signaling by ...
https://en.wikipedia.org/wiki/Arrestin_beta_1
SAG (gene)SAG (gene)
S-arrestin is a protein that in humans is encoded by the SAG gene. Members of arrestin/beta-arrestin protein family are thought ... 1995). "Chromosome mapping of the human arrestin (SAG), beta-arrestin 2 (ARRB2), and beta-adrenergic receptor kinase 2 (ADRBK2 ... S-arrestin, also known as S-antigen, is a major soluble protein in photoreceptor cells that is involved in desensitization of ... Additionally, S-arrestin is highly antigenic, and is capable of inducing experimental autoimmune uveoretinitis. Mutations in ...
https://en.wikipedia.org/wiki/SAG_(gene)
Raymond C. StevensRaymond C. Stevens
Crystal structure of rhodopsin bound to arrestin determined by femtosecond X-ray laser Nature 526: 561-567 T. Hua, K. Vemuri, M ... and the human Rhodopsin-Arrestin complex. 2016: The marijuana receptor-human Cannabinoid receptor type 1 (CB1) and the human C- ...
https://en.wikipedia.org/wiki/Raymond_C._Stevens
Κ-opioid receptorΚ-opioid receptor
Bruchas MR, Macey TA, Lowe JD, Chavkin C (June 2006). "Kappa opioid receptor activation of p38 MAPK is GRK3- and arrestin- ... β-arrestin antagonist Amentoflavone - non-selective; naturally-occurring AT-076 - non-selective, likely long acting; JDTic ... β-arrestin antagonist Zyklophin - selective peptide antagonist; dynorphin A analogue Aticaprant - selective Found in numerous ... β-arrestin antagonist Salvinorin A - naturally-occurring 2-Methoxymethyl salvinorin B - and its ethoxymethyl and ...
https://en.wikipedia.org/wiki/Κ-opioid_receptor
Denis BaylorDenis Baylor
"Prolonged photoresponses in transgenic mouse rods lacking arrestin". Nature. 389 (6650): 505-509. Bibcode:1997Natur.389..505X. ...
https://en.wikipedia.org/wiki/Denis_Baylor
HerkinorinHerkinorin
Unlike most μ-opioid receptor agonists, herkinorin does not promote the recruitment of β-arrestin 2 to the intracellular domain ... April 2008). "Herkinorin analogues with differential beta-arrestin-2 interactions". Journal of Medicinal Chemistry. 51 (8): ... arrestin interactions or receptor internalization". Molecular Pharmacology. 71 (2): 549-57. doi:10.1124/mol.106.028258. PMC ... and some other analogues related to herkinorin can recruit β-arrestins. Kurkinorin Salvinorin B methoxymethyl ether RB-64 ...
https://en.wikipedia.org/wiki/Herkinorin
Retinal degeneration (rhodopsin mutation)Retinal degeneration (rhodopsin mutation)
2006). "Stable rhodopsin/arrestin complex leads to retinal degeneration in a transgenic mouse model of autosomal dominant ... In this research null mutations in the rhodopsin kinase and arrestin genes, each of which plays a role in terminating rhodopsin ... Besides this, the stable rhodopsin and arrestin complexes are shown to mislocalize and accumulate in the inner segments of rod ... The R135 mutant rhodopsin is noted to form stable complex with arrestin and undergo endocytosis resulting in aberrant endocytic ...
https://en.wikipedia.org/wiki/Retinal_degeneration_(rhodopsin_mutation)
5-HT7 receptor5-HT7 receptor
Kim Y, Kim H, Lee J, Lee JK, Min SJ, Seong J, Rhim H, Tae J, Lee HJ, Choo H (August 2018). "Discovery of β-Arrestin Biased ... beta-arrestin recruitment, and receptor internalization. Inactivating antagonists all likely interact with the 5-HT7 receptor ... role of G protein-coupled receptor kinases and arrestins in receptor desensitization and resensitization". Receptors & Channels ...
https://en.wikipedia.org/wiki/5-HT7_receptor
Raul GainetdinovRaul Gainetdinov
He is the author of fundamental scientific works in pharmacology of dopamine, β-Arrestins and NMDA receptors. He is a pioneer ... Beaulieu JM, Sotnikova TD, Marion S, Lefkowitz RJ, Gainetdinov RR, Caron MG (2005-07-29). "An Akt/β-Arrestin 2/PP2A Signaling ... "Enhanced Morphine Analgesia in Mice Lacking β-Arrestin 2". Science. 286 (5449): 2495-2498. doi:10.1126/science.286.5449.2495. ...
https://en.wikipedia.org/wiki/Raul_Gainetdinov
AP3B1AP3B1
Kim YM, Barak LS, Caron MG, Benovic JL (May 2002). "Regulation of arrestin-3 phosphorylation by casein kinase II". The Journal ...
https://en.wikipedia.org/wiki/AP3B1
Martin J. LohseMartin J. Lohse
Lohse, Martin J.; Benovic, Jeffrey L.; Codina, Juan; Caron, Marc G.; Lefkowitz, Robert J. (22 June 1990). "β-Arrestin: a ... While working with Robert Lefkowitz at Duke University he discovered beta-arrestins, proteins that regulate the function of ...
https://en.wikipedia.org/wiki/Martin_J._Lohse
G protein-coupled receptorG protein-coupled receptor
In many cases, arrestin's binding to the receptor is a prerequisite for translocation. For example, beta-arrestin bound to β2- ... Arrestin linking: The phosphorylated receptor can be linked to arrestin molecules that prevent it from binding (and activating ... Upon GRK phosphorylation, the GPCR's affinity for β-arrestin (β-arrestin-1/2 in most tissues) is increased, at which point β- ... Once β-arrestin is bound to a GPCR, it undergoes a conformational change allowing it to serve as a scaffolding protein for an ...
https://en.wikipedia.org/wiki/G_protein-coupled_receptor
Arun Kumar ShuklaArun Kumar Shukla
Reiter, Eric; Ahn, Seungkirl; Shukla, Arun K.; Lefkowitz, Robert J. (11 January 2012). "Molecular Mechanism of β-Arrestin- ... India portal Biology portal Cell signaling Arrestin Membrane proteins Please see Selected bibliography section "Arun K. Shukla ... "Functional specialization of β-arrestin interactions revealed by proteomic analysis". Proceedings of the National Academy of ... "Global phosphorylation analysis of β-arrestin-mediated signaling downstream of a seven transmembrane receptor (7TMR)". ...
https://en.wikipedia.org/wiki/Arun_Kumar_Shukla
Signal transductionSignal transduction
... via protein kinase phosphorylation or b-arrestin-dependent internalization. A study was conducted where a point mutation was ...
https://en.wikipedia.org/wiki/Signal_transduction
N-2′-IndolylnaltrexamineN-2′-Indolylnaltrexamine
van Koppen, C. J.; Jakobs, K. H. Arrestin-Independent Internalization of G Protein-Coupled Receptors. Molecular Pharmacology ... of β-arrestin and the activation of the p38 MAPK and other secondary signaling cascades that are dependent on β-arrestin. INTA ... to form a conformation to block the recruitment of a protein family known as the β-arrestins. These proteins are responsible ...
https://en.wikipedia.org/wiki/N-2′-Indolylnaltrexamine
Thyrotropin-releasing hormone receptorThyrotropin-releasing hormone receptor
Differential regulation of beta-arrestins 1 and 2". The Journal of Biological Chemistry. 277 (52): 50422-30. doi:10.1074/jbc. ...
https://en.wikipedia.org/wiki/Thyrotropin-releasing_hormone_receptor
Visual phototransductionVisual phototransduction
It is this pathway, where Metarhodopsin II is phosphorylated and bound to arrestin and thus deactivated, which is thought to be ... Finally, arrestin, another protein, binds the phosphorylated metarhodopsin II, completely deactivating it. Thus, finally, ... Arrestin then completely deactivates the phosphorylated-metarhodopsin II, terminating the phototransduction cascade (restoring ...
https://en.wikipedia.org/wiki/Visual_phototransduction
Receptor-mediated endocytosisReceptor-mediated endocytosis
August 2016). "GPCR-G Protein-β-Arrestin Super-Complex Mediates Sustained G Protein Signaling". Cell. 166 (4): 907-919. doi: ... "Absence of a stable secondary structure is not a limitation for photoswitchable inhibitors of β-arrestin/β-Adaptin 2 protein- ...
https://en.wikipedia.org/wiki/Receptor-mediated_endocytosis
VPS26AVPS26A
... which has been observed for arrestins. Moreover, Vps26 does not have similar sequences as arrestins for GPCR and phospholipid ... Both Vps26 and arrestins are composed of two structurally related β-sheet domains forming extensive interfaces with each other ... Vps26 is a 38-kDa subunit that has a two-lobed structure with a polar core that resembles the arrestin family of trafficking ... Shi H, Rojas R, Bonifacino JS, Hurley JH (2006). "The retromer subunit Vps26 has an arrestin fold and binds Vps35 through its C ...
https://en.wikipedia.org/wiki/VPS26A
Vasopressin receptorVasopressin receptor
The V2R continues to activate Gs after being internalized by β-arrestin rather than being desensitized. This internalized Gs ... "GPCR-G Protein-β-Arrestin Super-Complex Mediates Sustained G Protein Signaling". Cell. 166 (4): 907-19. doi:10.1016/j.cell. ... signaling by V2R is explained by the receptors ability to form "mega-complexes" consisting of a single V2R, β-arrestin, and ...
https://en.wikipedia.org/wiki/Vasopressin_receptor
ARR3ARR3
Arrestin-C, also known as retinal cone arrestin-3, is a protein that in humans is encoded by the ARR3 gene. Arrestin GRCh38: ... "Entrez Gene: ARR3 arrestin 3, retinal (X-arrestin)". Craft CM, Whitmore DH, Wiechmann AF (1994). "Cone arrestin identified by ... Murakami A, Yajima T, Sakuma H, McLaren MJ, Inana G (Dec 1993). "X-arrestin: a new retinal arrestin mapping to the X chromosome ... 2002). "Mouse cone arrestin expression pattern: light induced translocation in cone photoreceptors". Mol. Vis. 8: 462-71. PMID ...
https://en.wikipedia.org/wiki/ARR3
SmoothenedSmoothened
"Activity-dependent internalization of smoothened mediated by beta-arrestin 2 and GRK2". Science. 306 (5705): 2257-60. Bibcode: ...
https://en.wikipedia.org/wiki/Smoothened
Oguchi diseaseOguchi disease
These include mutations in the arrestin gene or the rhodopsin kinase gene. The condition is more frequent in individuals of ...
https://en.wikipedia.org/wiki/Oguchi_disease
GRK4GRK4
Arrestin binding to a phosphorylated, active receptor also enables receptor signaling through arrestin partner proteins. Thus ... which promotes the binding of an arrestin protein to the receptor. Arrestin binding to a phosphorylated, active receptor ... Gurevich VV, Gurevich EV (2019). "GPCR Signaling Regulation: The Role of GRKs and Arrestins". Front Pharmacol. 10: 125. doi: ... the GRK/arrestin system serves as a signaling switch for G protein-coupled receptors. GRK4 is most expressed in the testes, ...
https://en.wikipedia.org/wiki/GRK4
G protein-coupled receptor kinase 2G protein-coupled receptor kinase 2
Arrestin binding to phosphorylated, active receptor also enables receptor signaling through arrestin partner proteins. Thus the ... which promotes the binding of an arrestin protein to the receptor. Arrestin binding to phosphorylated, active receptor prevents ... Arrestin binding also directs receptors to specific cellular internalization pathways, removing the receptors from the cell ... Gurevich VV, Gurevich EV (2019). "GPCR Signaling Regulation: The Role of GRKs and Arrestins". Front Pharmacol. 10: 125. doi: ...
https://en.wikipedia.org/wiki/G_protein-coupled_receptor_kinase_2
GRK5GRK5
Arrestin binding to phosphorylated, active receptor also enables receptor signaling through arrestin partner proteins. Thus the ... which promotes the binding of an arrestin protein to the receptor. Arrestin binding to phosphorylated, active receptor prevents ... Arrestin binding also directs receptors to specific cellular internalization pathways, removing the receptors from the cell ... GRK5 and the closely related GRK6 phosphorylate receptors at sites that encourage arrestin-mediated signaling rather than ...
https://en.wikipedia.org/wiki/GRK5
G protein-coupled receptor kinase 3G protein-coupled receptor kinase 3
Arrestin binding to phosphorylated, active receptor also enables receptor signaling through arrestin partner proteins. Thus the ... which promotes the binding of an arrestin protein to the receptor. Arrestin binding to phosphorylated, active receptor prevents ... "Chromosome mapping of the human arrestin (SAG), beta-arrestin 2 (ARRB2), and beta-adrenergic receptor kinase 2 (ADRBK2) genes ... Feng YH, Wang L, Wang Q, Li X, Zeng R, Gorodeski GI (June 2005). "ATP stimulates GRK-3 phosphorylation and beta-arrestin-2- ...
https://en.wikipedia.org/wiki/G_protein-coupled_receptor_kinase_3
GPCR Signaling Regulation: The Role of GRKs and ArrestinsGPCR Signaling Regulation: The Role of GRKs and Arrestins
... Front Pharmacol. 2019 Feb 19;10:125. doi: 10.3389/fphar.2019.00125. ... In addition, GRKs and arrestins play a role in multiple signaling pathways in the cell, both GPCR-initiated and receptor- ... Here we focus on the mechanisms of GRK- and arrestin-mediated regulation of GPCR signaling, which includes homologous ... and subsequent binding of arrestin proteins, that selectively recognize active phosphorylated receptors. ...
https://pubmed.ncbi.nlm.nih.gov/30837883/?dopt=Abstract
Functionally Biased D2R Antagonists: Targeting the β-Arrestin Pathway to Improve Antipsychotic Treatment. | Broad InstituteFunctionally Biased D2R Antagonists: Targeting the β-Arrestin Pathway to Improve Antipsychotic Treatment. | Broad Institute
Animals, Antipsychotic Agents, beta-Arrestins, Diagnostic Imaging, GTP-Binding Proteins, Humans, Locomotion, Mice, Receptors, ... At D2R, antipsychotic drugs antagonize both G-protein dependent (Gα) signaling and G-protein independent (β-arrestin) signaling ... Recent evidence from mouse genetic and pharmacological studies point to β-arrestin signaling as the major driver of ... Here, we characterize BRD5814, a highly brain penetrant β-arrestin biased D2R antagonist. BRD5814 demonstrated good target ...
https://www.broadinstitute.org/publications/broad432026
Beta Arrestin 1 Antibody,Beta Arrestin 1 Peptide Suppliers & ManufacturersBeta Arrestin 1 Antibody,Beta Arrestin 1 Peptide Suppliers & Manufacturers
Comprehensive supplier list for Beta Arrestin 1 Antibody,Beta Arrestin 1 Peptide ... Beta Arrestin 1 Antibody (2 suppliers). Beta Arrestin 1 Peptide (2 suppliers). Beta Carotene (3 suppliers). Beta Catenin ...
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Human Arrestin, beta 1 (ARRB1) Protein (Myc-DYKDDDDK Tag), Recombinant | ABIN2714946Human Arrestin, beta 1 (ARRB1) Protein (Myc-DYKDDDDK Tag), Recombinant | ABIN2714946
Recombinant Arrestin, beta 1 (ARRB1) Protein (Myc-DYKDDDDK Tag). Spezies: Human. Quelle: HEK-293 Cells. Jetzt Produkt ... arrestin, beta 1, arrestin beta 1 L homeolog, beta-arrestin 1, putative beta-arrestin 1, ARRB1, arrb1, arrb1.L, CpipJ_ ... beta Arrestin 1 (ARRB1) (Arrestin, beta 1 (ARRB1)) Andere Bezeichnung Arrestin beta-1,arrb1 (ARRB1 Produkte) Synonyme arrb1, ... Target Alle beta Arrestin 1 (ARRB1) Proteine anzeigen beta Arrestin 1 (ARRB1) (Arrestin, beta 1 (ARRB1)) Protein-Typ ...
https://www.antikoerper-online.de/protein/2714946/Arrestin,+beta+1+ARRB1+Transcript+Variant+2+protein+Myc-DYKDDDDK+Tag/
Beta-arrestin-2 regulates the development of allergic asthma. | Scholars@DukeBeta-arrestin-2 regulates the development of allergic asthma. | [email protected]
Beta-arrestin-2 regulates the development of allergic asthma. ... Beta-arrestin-2 regulates the development of allergic asthma. ... is fully functional in mice lacking beta-arrestin-2. beta-arrestin-2-deficient mice demonstrate OVA-specific IgE responses, but ... Because beta-arrestin-2 regulates the development of allergic inflammation at a proximal step in the inflammatory cascade, ... Here we show that allergen-sensitized mice having a targeted deletion of the beta-arrestin-2 gene do not accumulate T ...
https://scholars.duke.edu/display/pub645100
Figures and data in ß-arrestin 2 germline knockout does not attenuate opioid respiratory depression | eLifeFigures and data in ß-arrestin 2 germline knockout does not attenuate opioid respiratory depression | eLife
The key mechanism for opioid-like biased agonists to provide analgesia but not respiratory depression does not involve ß-arrestin 2.
https://elifesciences.org/articles/62552/figures
Unique Properties of PathHunter® β-Arrestin Assays for GPCR Antagonist Discovery and CharacterizatioUnique Properties of PathHunter® β-Arrestin Assays for GPCR Antagonist Discovery and Characterizatio
The PathHunter® Arrestin assay is unique among arrestin assays in that it preserves the one-to-one nature of arrestin binding ... The work presented here focuses on how this property of the PathHunter® Arrestin platform makes it ideal for the discovery and ... A common feature of 7TM receptors is that upon activation, the receptors are bound by cellular Arrestin proteins. DiscoveRx has ... Tools & Resources / Document Resource Library / Documents / Unique Properties of PathHunter® β-Arrestin Assays for GPCR ...
https://discoverx.com/tools-resources/document-resource-library/documents/unique-properties-of-pathhunter-%CE%B2-arrestin-assays
Monitoring of beta-arrestin recruitment to chemokine receptor heteromers,</em>...
Monitoring of beta-arrestin recruitment to chemokine receptor heteromers,. Ruth Seeber, Ethan See, Martina Kocan, Karin Eidne, ... Monitoring of beta-arrestin recruitment to chemokine receptor heteromers, / Seeber, Ruth; See, Ethan; Kocan, Martina et al. ... Seeber, R., See, E., Kocan, M., Eidne, K., & Pfleger, K. (2010). Monitoring of beta-arrestin recruitment to chemokine receptor ... Seeber, R, See, E, Kocan, M, Eidne, K & Pfleger, K 2010, Monitoring of beta-arrestin recruitment to chemokine receptor ...
https://research-repository.uwa.edu.au/en/publications/monitoring-of-beta-arrestin-recruitment-to-chemokine-receptor-het
beta-Arrestin Promotes Wnt-induced Low Density Lipoprotein Receptor-related Protein 6 (Lrp6) Phosphorylation via Increased...beta-Arrestin Promotes Wnt-induced Low Density Lipoprotein Receptor-related Protein 6 (Lrp6) Phosphorylation via Increased...
beta-Arrestin is a scaffold protein that regulates signal transduction by seven transmembrane-spanning receptors. Among other ... In the present study we provide for the first time a mechanistic basis for the beta-arrestin function in Wnt/beta-catenin ... beta-Arrestin regulates Lrp6 phosphorylation via a novel interaction with phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P-2 ... beta-Arrestin Promotes Wnt-induced Low Density Lipoprotein Receptor-related Protein 6 (Lrp6) Phosphorylation via Increased ...
https://www.med.muni.cz/en/research-and-development/research-and-development/publishing-activity/publikace-lf-mu/1173918
Beta Arrestin 1 Mouse anti-Human, Unconjugated, Clone: 1H8E4, Proteintech 150 μL Products | Fisher ScientificBeta Arrestin 1 Mouse anti-Human, Unconjugated, Clone: 1H8E4, Proteintech 150 μL Products | Fisher Scientific
Mouse Monoclonal Antibody Shop Beta Arrestin 1 Mouse anti-Human, Unconjugated, Clone: 1H8E4, Proteintech ... Beta Arrestin 1 Mouse anti-Human, Unconjugated, Clone: 1H8E4, Proteintech - ... The Beta Arrestin 1 antibody from Proteintech is a mouse monoclonal antibody generated with recombinant protein of human Beta ... The Beta Arrestin 1 antibody has been validated for the following applications: WB, ELISA analysis. ...
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Reactome | Lysosome Destined Cargo:AP-1:beta-Arrestin-1:Vamp Complex [Golgi membrane]Reactome | Lysosome Destined Cargo:AP-1:beta-Arrestin-1:Vamp Complex [Golgi membrane]
Lysosome Destined Cargo:AP-1:Beta-arrestin:Vamp:Clathrin Triskelion:Dynamin:Endophilin Complex [Golgi membrane] (Homo sapiens) ... Lysosome Destined Cargo:AP-1:Beta-arrestin:Vamp:Clathrin Triskelion:Dynamin:Endophilin Complex [Golgi membrane] (Homo sapiens) ... Lysosome Destined Cargo:AP-1:beta-Arrestin-1:Vamp Complex [Golgi membrane] Stable Identifier ... Lysosome Destined Cargo:AP-1:Beta-arrestin:Vamp:Clathrin Triskelion:Dynamin:Endophilin Complex [Golgi membrane] (Homo sapiens) ...
https://www.reactome.org/content/detail/R-HSA-432687
Arrestins | NIH 3D Print ExchangeArrestins | NIH 3D Print Exchange
G PROTEIN-COUPLED RECEPTOR, Lysozyme, fusion, transducer, Adrenergic, G-Proteins, Arrestins, Adrenaline, Alprenolol, ...
https://3dprint.nih.gov/discover/arrestins
Gentraget - Arrestin (Arr)
Arrestins. Arrestins (abbreviated Arr) are a family of proteins which are important in the regulation of signal transduction G- ...
http://arrestins.com/products/3008-gentraget
DI-fusion Usage statistics: The Bul1/2 Alpha-Arrestins Promote...
The Bul1/2 Alpha-Arrestins Promote Ubiquitylation and Endocytosis of the Can1 Permease upon Cycloheximide-Induced TORC1- ...
https://difusion.ulb.ac.be/vufind/Record/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/336742/Stats
Recombinant Human B Arrestin 1 ARRB1Recombinant Human B Arrestin 1 ARRB1
Recombinant Human B Arrestin 1_ARRB1 is available at Genprice in USA and Gentaur in Europe. ... The Tech File of Recombinant Human B-Arrestin 1_ARRB1 is here. ...
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Agonist-independent interactions between beta-arrestins and mutant vasopressin type II receptors associated with nephrogenic...
... we demonstrate that both V2R-R137C and V2R-R137L mutants interact with beta-arrestins in an agonist-independent manner ... Animals, Arginine Vasopressin, Arrestins, Cell Line, Diabetes Insipidus, Nephrogenic, Humans, Hyponatremia, Inappropriate ADH ... Agonist-independent interactions between beta-arrestins and mutant vasopressin type II receptors associated with nephrogenic ... Agonist-independent interactions between beta-arrestins and mutant vasopressin type II receptors associated with nephrogenic ...
https://www.imm.ox.ac.uk/publications/734393
LinkLight™ U2-OS CCR6 / β-arrestin Cell Line | Bon Opus BiosciencesLinkLight™ U2-OS CCR6 / β-arrestin Cell Line | Bon Opus Biosciences
... targeting Human CCR6 pathway via b-arrestin. The proprietary LinkLight™ technology uses a standard Luciferase Assay as the ... β-arrestin Cell Line is a stable monoclonal cell line in U2-OS cells, ...
https://www.bonopusbio.com/product-page/linklight-u2-os-ccr6-%CE%B2-arrestin-cell-line
No arrest in Quincy Christmas Day stabbingNo arrest in Quincy Christmas Day stabbing
Mutation in the intracellular chloride channel CLCC1 associated with autosomal recessive retinitis pigmentosa | PLOS GeneticsMutation in the intracellular chloride channel CLCC1 associated with autosomal recessive retinitis pigmentosa | PLOS Genetics
c-h) Immunostaining of cone arrestin in WT (c-e) and heterozygous Clcc1 knockout (f-h) mice. The WT mice exhibit normal cone ... Dropout of cone cells is confirmed in Fig 9c-9h, where immunohistochemistry to cone arrestin displays ~half the cone density of ... Immunofluorescence assessment of mouse retinal cones by cone arrestin staining. Wax embedded tissue sections were kept at 37 °C ... Sections were incubated with cone arrestin (1:1000; Millipore, Germany) primary antibody reconstituted 1 × PBS containing 1% ...
https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1007504
β-arrestin - Not just for G protein-coupled receptors<...β-arrestin - Not just for G protein-coupled receptors<...
β-arrestin - Not just for G protein-coupled receptors. / Spiegel, Allen.. In: Science, Vol. 301, No. 5638, 05.09.2003, p. 1338- ... β-arrestin - Not just for G protein-coupled receptors. Science. 2003 Sep 5;301(5638):1338-1339. doi: 10.1126/science.1089552 ... β-arrestin - Not just for G protein-coupled receptors. In: Science. 2003 ; Vol. 301, No. 5638. pp. 1338-1339. ... Spiegel, A. (2003). β-arrestin - Not just for G protein-coupled receptors. Science, 301(5638), 1338-1339. https://doi.org/ ...
https://einstein.pure.elsevier.com/en/publications/%CE%B2-arrestin-not-just-for-g-protein-coupled-receptors-2
Involvement of Beta-arrestin 1 and Beta-arrestin 2 in store operated calcium entryInvolvement of Beta-arrestin 1 and Beta-arrestin 2 in store operated calcium entry
... Autre titre : Implication de Beta-arrestin ... On the other hand, calcium imaging experiment in knocked down β-arrestin 1 or β-arrestin 2 in HEK 293 cells as well as HEK 293 ... En plus de Gα12 et Gα13, les protéines de désensibilisation des GPCR β -arrestin 1 et / ou β-arrestin 2 peuvent aussi activer ... The purpose of our study is to investigate the involvement of the proteins Gα12/13 and β-arrestin 1/β-arrestin 2 in the ...
https://savoirs.usherbrooke.ca/handle/11143/9499?locale-attribute=fr
Inhibition of chemoattractant N-formyl peptide receptor trafficking by active arrestins.Inhibition of chemoattractant N-formyl peptide receptor trafficking by active arrestins.
Furthermore, expression of arrestin-2 I386A/V387A/F388A but not arrestin-2 [1-382] inhibited recycling of the N-formyl peptide ... truncated arrestin-2 [1-382], and arrestin-2 I386A, V387A, F388A). Complexes between the N-formyl peptide receptor and active ... Inhibition of chemoattractant N-formyl peptide receptor trafficking by active arrestins. Academic Article * ... Recent studies have highlighted the emergence of a class of G protein-coupled receptors that are internalized in an arrestin- ...
https://vivo.health.unm.edu/display/n1079236922
Research Highlights | NeuropsychopharmacologyResearch Highlights | Neuropsychopharmacology
Opioid overdose and tolerance: is the recruitment of β-arrestin to the µ-receptor involved? *Alexander Gillis ...
https://www.nature.com/npp/articles?type=research-highlight&error=cookies_not_supported&code=35661d9f-e5c9-4f88-9bba-988de8defce9
PubPeer - Involvement of PKA/DARPP-32/PP1α and β- arrestin/Akt/GSK-3β...PubPeer - Involvement of PKA/DARPP-32/PP1α and β- arrestin/Akt/GSK-3β...
... arrestin/Akt/GSK-3β Signaling in Cadmium-Induced DA-D2 Receptor-Mediated Motor Dysfunctions: Protective Role of Quercetin (2018 ... Involvement of PKA/DARPP-32/PP1α and β- arrestin/Akt/GSK-3β Signaling in Cadmium-Induced DA-D2 Receptor-Mediated Motor ...
https://pubpeer.com/publications/F1BF100F3AB61590305110CD719519
UW students raise money to put AED in residence hall to save someone in cardiac arrest - In A HeartbeatUW students raise money to put AED in residence hall to save someone in cardiac arrest - In A Heartbeat
MADISON, Wis. - The University of Wisconsin - Madison student organization Cardiac on Campus has raised $1,200 to buy an Automatic External Defibrillator, or AED, to keep in the Witte Residence Hall.. Read the full story here.. - Channel 3000 ...
https://inaheartbeat.org/uw-students-raise-money-to-put-aed-in-residence-hall-to-save-someone-in-cardiac-arrest/
MDR - P2Y12 inhibitor Clinical Implications and Adverse EffectsMDR - P2Y12 inhibitor Clinical Implications and Adverse Effects
arrestin recruits Src, that leads to MMP activation and HB-EGF launch and subsequent EGFR transactivation (50) -arrestin ...
https://tsfaq.info/category/mdr/
CXCR7: a β-arrestin-biased receptor that potentiates cell migration and recruits β-arrestin2 exclusively through Gβγ subunits...
CXCR7, also known as ACKR3, binds to only two chemokines, SDF-1α and I-TAC, and recruits β-arrestins. SDF-1α also binds to its ... CXCR7, also known as ACKR3, binds to only two chemokines, SDF-1α and I-TAC, and recruits β-arrestins. SDF-1α also binds to its ... CXCR7, also known as ACKR3, binds to only two chemokines, SDF-1α and I-TAC, and recruits β-arrestins. SDF-1α also binds to its ... CXCR7, also known as ACKR3, binds to only two chemokines, SDF-1α and I-TAC, and recruits β-arrestins. SDF-1α also binds to its ...
https://koreauniv.pure.elsevier.com/en/publications/cxcr7-a-%CE%B2-arrestin-biased-receptor-that-potentiates-cell-migratio
Structural snapshots uncover a lock-and-key type conserved activation mechanism of β-arrestins by GPCRs | ScietyStructural snapshots uncover a lock-and-key type conserved activation mechanism of β-arrestins by GPCRs | Sciety
Structural snapshots uncover a lock-and-key type conserved activation mechanism of β-arrestins by GPCRs. *Jagannath Maharana ... is a key determinant for the binding and activation of multifunctional regulatory proteins known as β-arrestins (βarrs). ...
https://sciety.org/articles/activity/10.1101/2022.10.10.511556
Florida Police Arrest Woman For Domestic Nut Punching Incident | The Smoking GunFlorida Police Arrest Woman For Domestic Nut Punching Incident | The Smoking Gun
Neonatal Intensive Care Drug Therapy Update: A Bibliography | Article | NursingCenterNeonatal Intensive Care Drug Therapy Update: A Bibliography | Article | NursingCenter
Hypoxia/ischemia modulates G protein-coupled receptor kinase 2 and beta-arrestin-1 levels in the neonatal rat brain. Stroke. ...
https://www.nursingcenter.com/journalarticle?Article_ID=519136&Journal_ID=54008&Issue_ID=519112
ReceptorsProteinsARRB2ReceptorGPCRENDOCYTOSISKinasesPhosphorylationArrb1AntibodyInternalizationBindsActivationInteractionDownstreamCellsRoleBetaUniqueAlphaMouseRecruitmentGPCRsPathwayPathwaysKinaseBinding to phosphorylatedInteractionsActivateTranslocationPlasma membranePolyclonal antibodySignalingBovineInhibitMediatesMiceGRK2DopamineProteaseMoleculeBecoming phosphorylatedGeneBoundRegulationOverexpressionDistinctCompoundsExpressionAgonists
Receptors10
  • A common feature of 7TM receptors is that upon activation, the receptors are bound by cellular Arrestin proteins. (discoverx.com)
  • beta-Arrestin is a scaffold protein that regulates signal transduction by seven transmembrane-spanning receptors. (muni.cz)
  • Arrestins (abbreviated Arr) are a family of proteins which are important in the regulation of signal transduction G-protein coupled receptors, which at first was discovered, as part of a conserved two step mechanism for regulating the activity of G protein-coupled receptors (GPCR) in rhodopsin visual system by Ursula Kuhn found Scott court, and β-called Global Martin J. Lohse system and kidney and colleagues. (arrestins.com)
  • Agonist-independent interactions between beta-arrestins and mutant vasopressin type II receptors associated with nephrogenic syndrome of inappropriate antidiuresis. (ox.ac.uk)
  • Spiegel, A 2003, ' β-arrestin - Not just for G protein-coupled receptors ', Science , vol. 301, no. 5638, pp. 1338-1339. (elsevier.com)
  • Recent studies have highlighted the emergence of a class of G protein-coupled receptors that are internalized in an arrestin-independent manner. (unm.edu)
  • These results indicate not only that a functional interaction between receptor and arrestin is required for recycling of certain G protein-coupled receptors, such as the N-formyl peptide receptor, but that the pattern of receptor phosphorylation further regulates this process. (unm.edu)
  • Agonist-induced phosphorylation of G protein-coupled receptors (GPCRs) is a key determinant for the binding and activation of multifunctional regulatory proteins known as β-arrestins (βarrs). (sciety.org)
  • Furthermore, molecular dynamics simulations suggest that tiotropium binds transiently to an allosteric site en route to the binding pocket of both receptors. (nature.com)
  • A beta-arrestin that functions similarly to BETA-ARRESTIN 1 in regulating signaling by G-PROTEIN-COUPLED RECEPTORS. (bvsalud.org)
Proteins3
  • The signaling of most GPCRs via G proteins is terminated by the phosphorylation of active receptor by specific kinases (GPCR kinases, or GRKs) and subsequent binding of arrestin proteins, that selectively recognize active phosphorylated receptors. (nih.gov)
  • A study from Nationwide Children's Hospital suggests that a newly identified group of proteins, alpha arrestins, may play a role in cell signaling that is crucial to new drug development. (news-medical.net)
  • Lack of beta-arrestin signaling in the absence of active G proteins. (nih.gov)
ARRB22
  • The present study explored the potential roles of G protein-coupled receptor kinase 6 (GRK6) and β-arrestin 2 (ARRB2) that are involved in the trafficking of DRD2 in patients with DSP. (dovepress.com)
  • Arrestin 2 (ARRB2) Polymorphism is Associated With Adverse Consequences of Chronic Heroin Use. (cdc.gov)
Receptor13
  • In addition, GRKs and arrestins play a role in multiple signaling pathways in the cell, both GPCR-initiated and receptor-independent. (nih.gov)
  • GPCRs are known to undergo desensitization involving phosphorylation of the receptor and the subsequent binding of beta(arrestins), which prevents further receptor-G-protein coupling. (duke.edu)
  • Inhibition of chemoattractant N-formyl peptide receptor trafficking by active arrestins. (unm.edu)
  • In addition to demonstrating that the N-formyl peptide receptor belongs in this family, we have recently shown that recycling of the receptor requires the presence of arrestins. (unm.edu)
  • To further elucidate mechanisms of arrestin-dependent regulation of G protein-coupled receptor processing, we examined the effects of altering the receptor-arrestin complex on ternary complex formation and cellular trafficking of the N-formyl peptide receptor by studying two active arrestin-2 mutants (truncated arrestin-2 [1-382], and arrestin-2 I386A, V387A, F388A). (unm.edu)
  • Complexes between the N-formyl peptide receptor and active arrestins exhibited higher affinity in vitro than the complex between the N-formyl peptide receptor and wild-type arrestin and furthermore were observed in vivo by colocalization studies using confocal microscopy. (unm.edu)
  • To assess the effects of these altered interactions on receptor trafficking, we demonstrated that active, but not wild-type, arrestin expression retards N-formyl peptide receptor internalization. (unm.edu)
  • Furthermore, expression of arrestin-2 I386A/V387A/F388A but not arrestin-2 [1-382] inhibited recycling of the N-formyl peptide receptor, reflecting an expanded role for arrestins in G protein-coupled receptor processing and trafficking. (unm.edu)
  • [ 89 ] Exposure to bacterial LPS decreases membrane expression of CCR8 on DCs possibly by receptor internalization through β-arrestin. (medscape.com)
  • Receptor interaction with b-arrestin is an important regulatory key element in the termination of G-protein-dependent receptor signalling. (uniklinikum-jena.de)
  • The interaction of a GPCR and β-arrestin is regulated by ligand binding and receptor phosphorylation by specific receptor kinases. (uniklinikum-jena.de)
  • Since β-arrestins not only turn off G-protein-dependent-signalling but represent starting points for novel signalling cascades, we are also interested to investigate receptor ligands which are able to discriminate between G-protein and β-arrestin mediated receptor signalling. (uniklinikum-jena.de)
  • The antidepressant-like activity of chiral xanthone derivatives may be mediated by 5-HT1A receptor and β-arrestin signalling. (krakow.pl)
GPCR5
  • Here we focus on the mechanisms of GRK- and arrestin-mediated regulation of GPCR signaling, which includes homologous desensitization and redirection of signaling to additional pathways by bound arrestins. (nih.gov)
  • DiscoveRx has pioneered the PathHunter ® β-Arrestin assay platform for monitoring these events using enzyme fragment complementation (EFC) and applied this technique to develop assays for more than 170 human GPCR targets. (discoverx.com)
  • Unlike second messenger assays that are amplified through downstream signaling events, each arrestin protein binds to a single activated GPCR. (discoverx.com)
  • The work presented here focuses on how this property of the PathHunter ® Arrestin platform makes it ideal for the discovery and characterization of GPCR antagonists. (discoverx.com)
  • En plus de Gα12 et Gα13, les protéines de désensibilisation des GPCR β -arrestin 1 et / ou β-arrestin 2 peuvent aussi activer RhoA. (usherbrooke.ca)
ENDOCYTOSIS1
  • The Bul1/2 Alpha-Arrestins Promote Ubiquitylation and Endocytosis of the Can1 Permease upon Cycloheximide-Induced TORC1-Hyperactivation. (ac.be)
Kinases2
  • Finally, we show that beta-arrestin interacts with PtdIns kinases PI4KII alpha and PIP5KI beta. (muni.cz)
  • We propose that beta-arrestins via their scaffolding function facilitate Amer1 interaction with PtdIns(4,5)P-2, which is produced locally upon Wnt3a stimulation by beta-arrestin- and Dishevelled-associated kinases. (muni.cz)
Phosphorylation3
  • We demonstrate that beta-arrestin is required for efficient Wnt3a-induced Lrp6 phosphorylation, a key event in downstream signaling. (muni.cz)
  • beta-Arrestin regulates Lrp6 phosphorylation via a novel interaction with phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P-2)-binding protein Amer1/WTX/Fam123b. (muni.cz)
  • In summary, our data show that beta-arrestins regulate Wnt3a-induced Lrp6 phosphorylation by the regulation of the membrane dynamics of Amer1. (muni.cz)
Arrb12
  • Recombinant human Arrestin beta-1 / ARRB1 (transcript variant 2) protein expressed in HEK293 cells. (antikoerper-online.de)
  • Recombinant Human B Arrestin 1_ARRB1 is available at Genprice in USA and Gentaur in Europe. (genprice.shop)
Antibody2
  • The Beta Arrestin 1 antibody from Proteintech is a mouse monoclonal antibody generated with recombinant protein of human Beta Arrestin 1. (fishersci.no)
  • The Beta Arrestin 1 antibody has been validated for the following applications: WB, ELISA analysis. (fishersci.no)
Internalization1
  • Using bioluminescence resonance energy transfer and confocal microscopy, we demonstrate that both V2R-R137C and V2R-R137L mutants interact with beta-arrestins in an agonist-independent manner resulting in dynamin-dependent internalization. (ox.ac.uk)
Binds1
  • CXCR7, also known as ACKR3, binds to only two chemokines, SDF-1α and I-TAC, and recruits β-arrestins. (elsevier.com)
Activation1
  • Upon T cell activation of human peripheral blood T cells, we found that the majority of cAMP was generated in T cell lipid rafts followed by activation of protein kinase A. However, upon TCR and CD28 coligation, beta-arrestin in complex with cAMP-specific phosphodiesterase 4 (PDE4) was recruited to lipid rafts which down-regulated cAMP levels. (ox.ac.uk)
Interaction1
  • Des études de co-immunoprécipitation démontrent une interaction entre la β-arrestin 1 et STIM1, alors qu'aucune interaction n'a été observée entre les β-arrestin 1 et Orai1. (usherbrooke.ca)
Downstream1
  • Using fluorescence recovery after photobleaching we show here that beta-arrestin is required for the Wnt3a-induced Amer1 membrane dynamics and downstream signaling. (muni.cz)
Cells1
  • Importantly, cells lacking beta-arrestin showed higher steady-state levels of the relevant PtdInsP and were unable to increase levels of these PtdInsP in response to Wnt3a. (muni.cz)
Role1
  • Beneficial metabolic role of β-arrestin-1 expressed by AgRP neurons. (nih.gov)
Beta7
  • Dieses beta Arrestin 1 Protein ist gelabelt mit Myc-DYKDDDDK Tag. (antikoerper-online.de)
  • In the present study we provide for the first time a mechanistic basis for the beta-arrestin function in Wnt/beta-catenin signaling. (muni.cz)
  • Enhanced rewarding properties of morphine, but not cocaine, in beta(arrestin)-2 knock-out mice. (duke.edu)
  • Mice lacking beta(arrestin)-2 (beta(arr2)) display enhanced sensitivity to morphine in tests of pain perception attributable to impaired desensitization of muOR. (duke.edu)
  • arrestin, and mitragynines no This distinction is important because beta-arrestin activity is associated with the dangerous side effects of opioids, including slow, shallow breathing that cannot sustain life. (justicenewsflash.com)
  • Beta-arrestina que funciona de forma similar a la BETA-ARRESTINA 1 en la regulación de la señalización mediante RECEPTORES ACOPLADOS A PROTEÍNAS G. Se expresión es alta en el sistema nervioso central donde puede regular la señalización mediante RECEPTORES SINÁPTICOS. (bvsalud.org)
  • Conversely, overexpression of either PDE4 or beta-arrestin augmented TCR/CD28-stimulated cytokine production. (ox.ac.uk)
Unique1
  • The PathHunter ® Arrestin assay is unique among arrestin assays in that it preserves the one-to-one nature of arrestin binding and directly translates the binding events to signal generation. (discoverx.com)
Alpha1
  • DI-fusion Usage statistics: The Bul1/2 Alpha-Arrestins Promote. (ac.be)
Mouse1
  • Recent evidence from mouse genetic and pharmacological studies point to β-arrestin signaling as the major driver of antipsychotic efficacy and suggest that a β-arrestin biased D2R antagonist could achieve an additional level of selectivity at D2R, increasing the therapeutic index of next generation antipsychotics. (broadinstitute.org)
Recruitment11
  • For GPCRs, ligand-induced β-arrestin recruitment activates signaling cascades independent of G-protein signaling to provide a nonamplified signal which is ideal for antagonist mode screening, ligand pharmacology analysis, and GPCR deorphanization. (discoverx.com)
  • The recruitment of arrestins to activated 7TMRs results in the activation of alternative signaling pathways, quenching of G-protein activation, and coupling to clathrin-mediated endocytosis. (discoverx.com)
  • This chapter discusses the utility and methods involved in using the PathHunter β-galactosidase complementation system to monitor arrestin recruitment and the advantages of exploiting this pathway in the characterization of 7TMR function. (discoverx.com)
  • Here, we evaluate μOR trafficking in response to activation by a novel μ-selective agonist derived from the naturally occurring plant product, salvinorin A. It is interesting that this compound, termed herkinorin , does not promote the recruitment of β-arrestin-2 to the μOR and does not lead to receptor internalization. (aspetjournals.org)
  • Administration of a single isolated serine protease from Alternaria, Alternaria alkaline serine protease (AASP), was sufficient to fully activate PAR 2 signaling and induce β-arrestin-2 / -dependent eosinophil and lymphocyte recruitment in vivo. (arizona.edu)
  • MRAP2 inhibits β-arrestin recruitment to the ghrelin receptor by preventing GHSR1a phosphorylation. (wjgnet.com)
  • The latter is often assumed to be nonbiased, or balanced, and usually produces efficient activation of the most measured signaling outputs, normally G protein activation and arrestin recruitment. (aspetjournals.org)
  • G protein by Ca 2+ flux and β-arrestin recruitment, hence allowing biased activity studies. (innoprot.com)
  • Functional [small beta]-arrestin recruitment assays were used to determine equilibrium dissociation constants (Kb) and showed that all of the tested SF5 and CF3 compounds are CB1 neutral antagonists. (sinapse.ac.uk)
  • 346 - Formation and release of arrestin domain-containing protein 1-mediated microvesicles (ARMMs) at plasma membrane by recruitment of TSG101 protein - Proc. (nih.gov)
  • This compound was confirmed to be selective for the μ opioid receptor and preferentially activated the G-protein signaling with little β-arrestin recruitment. (nih.gov)
GPCRs7
  • Arrestins play a key role in controlling the activity and signal transduction of GPCRs inside the cells of the body. (technologynetworks.com)
  • The researchers' close observation of the interactions between arrestins and GPCRs yielded crucial conclusions. (technologynetworks.com)
  • Different arrestins (visual arrestin (or Arrestin 1), beta-arrestin 1 (or Arrestin 2) and beta-arrestin 2 (or Arrestin 3) can reduce the activity of their target GPCRs in several different ways. (chemeurope.com)
  • Structure-inspired design of β-arrestin-biased ligands for aminergic GPCRs. (nih.gov)
  • This strategy may facilitate the structure-guided design of arrestin-biased ligands at other GPCRs, including polypharmacological biased ligands. (nih.gov)
  • In addition, GPCRs have also been found to signal through arrestin-mediated cascades. (frontiersin.org)
  • MPX NOMAD Cells are cell lines stably co-expressing tag-free GPCRs and two Nomad Biosensors to monitor G-protein and β-arrestin modulation. (innoprot.com)
Pathway10
  • This study aimed to elucidate the regulation of β-arrestin 1/2 on podocyte apoptosis through the Wnt/b-catenin pathway. (medscimonit.com)
  • Up-regulated β-arrestin 1/2 promoted podocyte apoptosis and p53 pathway by increasing Bax, cleaved caspase-3, and p-p53 levels in high-glucose-induced podocytes. (medscimonit.com)
  • Expression of β-catenin was increased in the β-arrestin 1/2 up-regulated group, which indicated that the Wnt/b-catenin pathway was activated. (medscimonit.com)
  • Wnt/b-catenin pathway inhibitor (Dkk1) distinctly suppressed the apoptosis induced by β-arrestin 1/2 overexpression and high glucose. (medscimonit.com)
  • These results provide a molecular pathomechanism of β-arrestin 1/2 and Wnt/β-catenin pathway on podocyte apoptosis and provide new ideas for the treatment of diabetic nephropathy, which paves the way for the future study of diabetic nephropathy and podocytes. (medscimonit.com)
  • 15. KISS1R signals independently of Gαq/11 and triggers LH secretion via the β-arrestin pathway in the male mouse. (nih.gov)
  • One emerging strategy to address the opioid crisis is the development of mu opioid receptor (MOR) ligands that preferentially signal the G-protein vs. β-arrestin pathway. (rti.org)
  • These effects of Istradefylline were reduced by the knockdown of A2AR but independent of A2AR-mediated G protein- or β-arrestin-dependent signal pathway. (nih.gov)
  • The authors of this study hypothesized that if a molecule could interact with the μ opioid receptor and activate the G-protein but not the β-arrestin pathway it would provide the pain relief of opioids, without the negative side effects. (nih.gov)
  • The authors then synthesized modified versions of some of these compounds to enhance binding to the μ opioid receptor and arrived at a compound that strongly bound the μ opioid receptor (but not the κ opioid receptor) and activated the G-protein signaling pathway but not the β-arrestin pathway. (nih.gov)
Pathways4
  • Arrestins can also activate numerous signaling pathways. (nih.gov)
  • Some of the side effects that occur with certain medicines (such as morphine-based drugs) are the result of arrestin-dependent signaling pathways. (technologynetworks.com)
  • C-X-C Motif Chemokine Receptor 3 Splice Variants Differentially Activate Beta-Arrestins to Regulate Downstream Signaling Pathways. (harvard.edu)
  • 8. Distinct beta-arrestin- and G protein-dependent pathways for parathyroid hormone receptor-stimulated ERK1/2 activation. (nih.gov)
Kinase7
  • Using permanent and primary human bronchial epithelial (HBE) cells at air-liquid interface, we show that DEPs activate the human MMP-1 gene via RAS and subsequent activation of RAF-MEK-ERK1/2 mitogen-activated protein kinase signaling, which can be scaffolded by β-arrestins. (nih.gov)
  • The function of beta-arrestin in the nucleus is not yet well understood, even if some data indicate clearly that beta-arrestin enters and exit the nucleus to take out from there some of its partners like the kinase JNK3 or the ubiquitin ligase Mdm2. (chemeurope.com)
  • Beta-arrestin 2, for example, is responsible for the downregulation of β-Adrenergic receptor which is phosphorylated by the β-adrenergic receptor kinase, thyrotropin releasing hormone receptor (TRHR), C5a Receptor (C5aR), AngiotensinII receptor. (chemeurope.com)
  • Recent in vitro studies highlighted G protein-coupled receptor kinase (GRK)2 and β-arrestins as important players in driving somatostatin receptor (SSTR) desensitization and trafficking. (elsevier.com)
  • 6. Expression and regulation of G protein-coupled receptor kinase 5 and beta-arrestin-1 in rat thyroid FRTL5 cells. (nih.gov)
  • The interaction can be triggered by protein activation/inactivation and is the basis of several DiscoveRx cell based assays including the Arrestin and the Kinase assays. (discoverx.com)
  • Genetic association between G protein-coupled receptor kinase 6/ß-arrestin 2 and dopamine supersensitivity psychosis in schizophrenia. (cdc.gov)
Binding to phosphorylated1
  • Arrestin quenches G-protein activation by binding to phosphorylated photolyzed rhodopsin. (nih.gov)
Interactions2
  • Our approach provides a template for generating arrestin-biased ligands by modifying predicted ligand interactions that block TM5 interactions and promote EL2 interactions. (nih.gov)
  • Such projects include investigating receptor structure/function/pharmacology relationships, receptor-effector coupling mechanisms, G protein and beta-arrestin interactions, and molecular mechanisms of receptor desensitization and intracellular trafficking. (nih.gov)
Activate3
  • Therefore, drugs that can activate the receptor without recruiting the arrestins may be a promising step in the development of opiate analgesics that distinguish between agonist activity and receptor regulation and may ultimately lead to therapeutics designed to provide pain relief without the adverse side effects normally associated with the opiate narcotics. (aspetjournals.org)
  • In most cases agonists regarded as nonbiased can efficiently activate both G protein- and arrestin-dependent signaling. (aspetjournals.org)
  • Relative to this, biased agonists preferentially activate either G protein- or arrestin-dependent signaling as shown in bold arrows. (aspetjournals.org)
Translocation5
  • In this study, the involvement of microtubules and microfilaments in the light-driven translocation of arrestin and transducin was investigated. (arvojournals.org)
  • Quantitative confocal imaging was used to assess the impact of these treatments on arrestin and transducin translocation. (arvojournals.org)
  • Perturbation of the microtubule cytoskeleton with thiabendazole slowed the translocation of both arrestin and transducin, but only in moving from the outer to the inner segments. (arvojournals.org)
  • Transgenic Xenopus expressing fusions of green fluorescent protein (GFP) with portions of arrestin implicates the C terminus of arrestin as an important portion of the molecule for promoting translocation. (arvojournals.org)
  • The results show that disruption of the cytoskeletal network in rod photoreceptors has specific effects on the translocation of arrestin and transducin. (arvojournals.org)
Plasma membrane1
  • Previous studies show that β-arrestin signaling and receptor endocytosis are modulated by the plasma membrane phosphoinositide lipid phosphatidylinositol-(4, 5)-bisphosphate (PI(4,5)P 2 ). (pnas.org)
Polyclonal antibody1
  • Arrestin antibody LS-C752710 is an unconjugated rabbit polyclonal antibody to human Arrestin (SAG). (lsbio.com)
Signaling12
  • The nearly ubiquitous involvement of arrestin in 7TMR signaling has spurred the development of several methods for monitoring this interaction in mammalian cells. (discoverx.com)
  • We identified specific amino acid-ligand contacts at transmembrane helix 5 (TM5) and extracellular loop 2 (EL2) responsible for Gi/o and β-arrestin signaling, respectively, and targeted those residues to develop biased ligands. (nih.gov)
  • A unique aspect of arrestin-3 is its ability to support both receptor-dependent and receptor-independent signaling. (elsevier.com)
  • These switch regions may work with the inter-domain twist to initiate and direct arrestin-mediated signaling. (elsevier.com)
  • We sought to determine whether Alternaria-induced PAR 2 signaling contributed to asthma symptoms via a PAR 2 /β-arrestin signaling axis, identify the protease activity responsible for PAR 2 signaling, and determine whether protease activity was sufficient for Alternaria-induced asthma symptoms in animal models. (arizona.edu)
  • We initially used in vitro models to demonstrate Alternaria-induced PAR 2 /β-arrestin-2 signaling. (arizona.edu)
  • In conclusion, Alternaria filtrates induce airway inflammation and mucus hyper-plasia largely via AASP using the PAR 2 /β-arrestin signaling axis. (arizona.edu)
  • 21: Deubiquitinases and Their Emerging Roles in β-Arrestin-mediated Signaling. (gale.com)
  • 2. β-Arrestin 1 in Thyrotropin Receptor Signaling in Bone: Studies in Osteoblast-Like Cells. (nih.gov)
  • 10. Distinct and shared roles of β-arrestin-1 and β-arrestin-2 on the regulation of C3a receptor signaling in human mast cells. (nih.gov)
  • β-Arrestin-1 inhibits glucocorticoid receptor turnover and alters glucocorticoid signaling. (nih.gov)
  • Research focused on the mapping of a receptor/G protein interface and a receptor dimer interface, and the investigation of the physiological roles of G protein-dependent versus β-arrestin-dependent signaling in hepatocytes. (nih.gov)
Bovine1
  • In the same issue of Nature , a team led by researchers in Germany published the structure of another arrestin from the bovine eye called arrestin p44. (nih.gov)
Inhibit2
  • We demonstrate that β-arrestins interact directly with FAK and inhibit its autophosphorylation in resting cells. (inserm.fr)
  • Arrestin beta 2, like arrestin beta 1, was shown to inhibit beta-adrenergic receptor function in vitro. (anticorps-enligne.fr)
Mediates1
  • 1. β-Arrestin-1 mediates thyrotropin-enhanced osteoblast differentiation. (nih.gov)
Mice4
  • Studies in mice have shown that β-arrestin-2 plays an important role in the development of morphine-induced tolerance, constipation, and respiratory depression. (aspetjournals.org)
  • Alternaria filtrates were then used to sensitize and challenge wild-type, PAR 2 / and β-arrestin-2 / mice in vivo. (arizona.edu)
  • Intranasal administration of Alternaria filtrate resulted in a protease-dependent increase of airway inflammation and mucin production in wild-type but not PAR 2 / or β-arrestin-2 / mice. (arizona.edu)
  • Degroot G , Lepage V, Parmentier M, Springael J. The Atypical Chemerin Receptor GPR1 Displays Different Modes of Interaction with β-Arrestins in Humans and Mice with Important Consequences on Subcellular Localization and Trafficking. (wjgnet.com)
GRK25
  • Our aim was to characterize GRK2 and β-arrestins expression in different pituitary adenomas and to investigate their potential role in the response to somatostatin analog (SSA) treatment in GH-secreting adenomas (GHomas). (elsevier.com)
  • 0001). SSA treatment did not affect GRK2 and β-arrestin expression in GHomas or in cultured rat pituitary tumor GH3 cells. (elsevier.com)
  • 05). In conclusion, for the first time, we characterized GRK2, β-arrestin 1, and β-arrestin 2 expression in a representative number of pituitary adenomas. (elsevier.com)
  • β-Arrestin 1 and GRK2 seem to have a role in modulating GH secretion during SSA treatment. (elsevier.com)
  • 19. GRK2 and beta-arrestin 1 as negative regulators of thyrotropin receptor-stimulated response. (nih.gov)
Dopamine2
  • Beta-arrestin promotes the release of dopamine. (nih.gov)
  • When beta-arrestin is too active, the brain eventually produces too much dopamine. (nih.gov)
Protease1
  • This parental cell line stably expresses a beta-arrestin/TEV protease fusion protein and the beta-lactamase ( bla ) reporter gene under the control of a UAS response element. (thermofisher.com)
Molecule1
  • Using single-molecule fluorescence resonance energy transfer imaging, we show that β-arrestin is strongly autoinhibited in its basal state. (nih.gov)
Becoming phosphorylated1
  • In another branch, the receptor becomes desensitized by becoming phosphorylated, bound to β-arrestin, and internalized by clathrin-coated pits. (pnas.org)
Gene2
  • In the nucleus, it has also been described that beta arrestins are also able to modify gene expression, by enhancing transcription of some specific genes. (chemeurope.com)
  • Possible association of beta-arrestin 2 gene with methamphetamine use disorder, but not schizophrenia. (cdc.gov)
Bound2
  • They thus searched for a synthetic antibody fragment that could stabilize β-arrestin-1 in its active state bound to a segment of the receptor. (nih.gov)
  • Once arrestin is bound to the receptor it is unable to signal further. (chemeurope.com)
Regulation2
  • Although β-arrestins (ARRBs) regulate diverse physiological and pathophysiological processes, their functions and regulation in Parkinson's disease (PD) remain poorly defined. (elsevier.com)
  • Nevertheless, the potential mechanism of β-arrestins on the regulation of podocyte apoptosis has rarely been discussed. (medscimonit.com)
Overexpression1
  • β-arrestin 1/2 overexpression inhibited the expression of nephrin and podocin protein. (medscimonit.com)
Distinct2
  • Importantly, we show that effector-binding sites on arrestins have distinct conformations in the basal and activated states, acting as switch regions. (elsevier.com)
  • Its engagement with a phosphopeptide mimicking phosphorylated receptor tail efficiently releases the β-arrestin tail from its N domain to assume distinct conformations. (nih.gov)
Compounds2
  • NCATS researchers used their expertise in drug screening to search through roughly 40,000 compounds to test their ability to interfere with beta-arrestin activity. (nih.gov)
  • They identified compounds that blocked beta-arrestin but also turned on the G protein's activity. (nih.gov)
Expression4
  • β-Arrestin 1 expression was low in all 3 adenoma histotypes. (elsevier.com)
  • This study structured β-arrestin 1/2 down-regulated and up-regulated expression by plasmid transfection. (medscimonit.com)
  • β-arrestin 1/2 expression levels of podocytes were up-regulated in high-glucose-induced podocytes. (medscimonit.com)
  • 13. Expression of beta-arrestins in toxic and cold thyroid nodules. (nih.gov)
Agonists1
  • This led to the key concept-which has dominated the opioid field now for almost 20 years-that the analgesic effects of μ -receptor agonists are G protein-mediated, and the adverse effects (constipation and respiratory depression) as well as tolerance, are mediated in the main by arrestin-3. (aspetjournals.org)
Arresto Calatabiano Archives - QdS
Arresto Calatabiano Archives - QdS (qds.it)
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Arresto Padre Nuvola, le intercettazioni (palermotoday.it)
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Guatemala | Democracy Now! (democracynow.org)
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Sfilate, Giorgio Armani Privé: abiti gioiosi per momenti speciali (tgcom24.mediaset.it)
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Marche: ultime notizie di spettacolo - ANSA (ansamed.info)
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CARABINIERI-DI-PALERMO | La Sicilia (lasicilia.it)
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