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 ProteinsTransducin: 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.HistoryFatigue: The state of weariness following a period of exertion, mental or physical, characterized by a decreased capacity for work and reduced efficiency to respond to stimuli.Databases, Protein: Databases containing information about PROTEINS such as AMINO ACID SEQUENCE; PROTEIN CONFORMATION; and other properties.Sequence Analysis, Protein: A process that includes the determination of AMINO ACID SEQUENCE of a protein (or peptide, oligopeptide or peptide fragment) and the information analysis of the sequence.Systems Integration: The procedures involved in combining separately developed modules, components, or subsystems so that they work together as a complete system. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)Internet: A loose confederation of computer communication networks around the world. The networks that make up the Internet are connected through several backbone networks. The Internet grew out of the US Government ARPAnet project and was designed to facilitate information exchange.Sequence Alignment: The arrangement of two or more amino acid or base sequences from an organism or organisms in such a way as to align areas of the sequences sharing common properties. The degree of relatedness or homology between the sequences is predicted computationally or statistically based on weights assigned to the elements aligned between the sequences. This in turn can serve as a potential indicator of the genetic relatedness between the organisms.Melanesia: The collective name for the islands of the Pacific Ocean northeast of Australia, including NEW CALEDONIA; VANUATU; New Hebrides, Solomon Islands, Admiralty Islands, Bismarck Archipelago, FIJI, etc. Melanesia (from the Greek melas, black + nesos, island) is so called from the black color of the natives who are generally considered to be descended originally from the Negroid Papuans and the Polynesians or Malays. (From Webster's New Geographical Dictionary, 1988, p748 & Room, Brewer's Dictionary of Names, 1992, p344)Anopheles: A genus of mosquitoes (CULICIDAE) that are known vectors of MALARIA.Anopheles gambiae: A species of mosquito in the genus Anopheles and the principle vector of MALARIA in Africa.Algorithms: A procedure consisting of a sequence of algebraic formulas and/or logical steps to calculate or determine a given task.Entomology: A discipline or occupation concerned with the study of INSECTS, including the biology and the control of insects.Molecular Sequence Data: Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.Arrestins: Regulatory proteins that down-regulate phosphorylated G-protein membrane receptors, including rod and cone photoreceptors and adrenergic receptors.GTP-Binding Protein alpha Subunits, Gq-G11: A family of heterotrimeric GTP-binding protein alpha subunits that activate TYPE C PHOSPHOLIPASES dependent signaling pathways. The Gq-G11 part of the name is also spelled Gq/G11.Gene Amplification: A selective increase in the number of copies of a gene coding for a specific protein without a proportional increase in other genes. It occurs naturally via the excision of a copy of the repeating sequence from the chromosome and its extrachromosomal replication in a plasmid, or via the production of an RNA transcript of the entire repeating sequence of ribosomal RNA followed by the reverse transcription of the molecule to produce an additional copy of the original DNA sequence. Laboratory techniques have been introduced for inducing disproportional replication by unequal crossing over, uptake of DNA from lysed cells, or generation of extrachromosomal sequences from rolling circle replication.Organophosphates: Carbon-containing phosphoric acid derivatives. Included under this heading are compounds that have CARBON atoms bound to one or more OXYGEN atoms of the P(=O)(O)3 structure. Note that several specific classes of endogenous phosphorus-containing compounds such as NUCLEOTIDES; PHOSPHOLIPIDS; and PHOSPHOPROTEINS are listed elsewhere.Receptors, G-Protein-Coupled: The largest family of cell surface receptors involved in SIGNAL TRANSDUCTION. They share a common structure and signal through HETEROTRIMERIC G-PROTEINS.Signal Transduction: The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.Retina: The ten-layered nervous tissue membrane of the eye. It is continuous with the OPTIC NERVE and receives images of external objects and transmits visual impulses to the brain. Its outer surface is in contact with the CHOROID and the inner surface with the VITREOUS BODY. The outer-most layer is pigmented, whereas the inner nine layers are transparent.Hominidae: Family of the suborder HAPLORHINI (Anthropoidea) comprising bipedal primate MAMMALS. It includes modern man (HOMO SAPIENS) and the great apes: gorillas (GORILLA GORILLA), chimpanzees (PAN PANISCUS and PAN TROGLODYTES), and orangutans (PONGO PYGMAEUS).Cone Opsins: Photosensitive proteins expressed in the CONE PHOTORECEPTOR CELLS. They are the protein components of cone photopigments. Cone opsins are classified by their peak absorption wavelengths.Rhodopsin: A purplish-red, light-sensitive pigment found in RETINAL ROD CELLS of most vertebrates. It is a complex consisting of a molecule of ROD OPSIN and a molecule of 11-cis retinal (RETINALDEHYDE). Rhodopsin exhibits peak absorption wavelength at about 500 nm.G-Protein-Coupled Receptor Kinase 2: A ubiquitously expressed G-protein-coupled receptor kinase subtype that has specificity for the agonist-occupied form of BETA-ADRENERGIC RECEPTORS. It may play an essential role in regulating myocardial contractile response.Photoreceptor Cells: Specialized cells that detect and transduce light. They are classified into two types based on their light reception structure, the ciliary photoreceptors and the rhabdomeric photoreceptors with MICROVILLI. Ciliary photoreceptor cells use OPSINS that activate a PHOSPHODIESTERASE phosphodiesterase cascade. Rhabdomeric photoreceptor cells use opsins that activate a PHOSPHOLIPASE C cascade.Authorship: The profession of writing. Also the identity of the writer as the creator of a literary production.Knowledge Bases: Collections of facts, assumptions, beliefs, and heuristics that are used in combination with databases to achieve desired results, such as a diagnosis, an interpretation, or a solution to a problem (From McGraw Hill Dictionary of Scientific and Technical Terms, 6th ed).Editorial Policies: The guidelines and policy statements set forth by the editor(s) or editorial board of a publication.Scientific Misconduct: Intentional falsification of scientific data by presentation of fraudulent or incomplete or uncorroborated findings as scientific fact.Publishing: "The business or profession of the commercial production and issuance of literature" (Webster's 3d). It includes the publisher, publication processes, editing and editors. Production may be by conventional printing methods or by electronic publishing.Game Theory: Theoretical construct used in applied mathematics to analyze certain situations in which there is an interplay between parties that may have similar, opposed, or mixed interests. In a typical game, decision-making "players," who each have their own goals, try to gain advantage over the other parties by anticipating each other's decisions; the game is finally resolved as a consequence of the players' decisions.

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)

*Arrestin

... -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 between two GPCRs available ... Arrestin-4 was cloned by two groups and termed cone arrestin, after photoreceptor type that expresses it, and X-arrestin, after ...

*Arrestin 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- ... Beta-arrestin might also play a role as scaffold protein in the GPCR pathways.[citation needed] Arrestin beta 1 has been shown ... 1997). "Arrestin/clathrin interaction. Localization of the arrestin binding locus to the clathrin terminal domain". J. Biol. ... "Entrez Gene: ARRB1 arrestin, beta 1". Claing A, Chen W, Miller WE, Vitale N, Moss J, Premont RT, Lefkowitz RJ (November 2001 ...

*Arrestin 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, 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- ... a novel member of the arrestin/beta-arrestin gene family". The Journal of Biological Chemistry. 267 (25): 17882-90. PMID ...

*Arresto facto super bonis mercatorum alienigenorum

... (literally, "Stoppage made upon the goods of a foreign merchant"), in ...

*CLTC

1997). "Arrestin/clathrin interaction. Localization of the arrestin binding locus to the clathrin terminal domain". J. Biol. ...

*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 photoreceptor protein that is involved in desensitization of the ... Additionally, S-arrestin is highly antigenic, and is capable of inducing experimental autoimmune uveoretinitis. Mutations in ...

*Aruban general election, 1985

arresten.eu. "Politieke partijen en verkiezingen". Historia di Aruba (in Dutch). Retrieved 25 September 2017. ...

*Raymond 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- ...

*Domenico Raccuglia

... dopo gli arresti Archived July 22, 2011, at the Wayback Machine., Left, June 28, 2006 Changes in Mafia Leadership Reveal New ... Arresti e lavoro'. Intervista al magistrato De Lucia Archived 2008-10-05 at the Wayback Machine., Ateneonline, November 20, ...

*Pietro Tagliavia

Arresti e lavoro'. Intervista al magistrato De Lucia, Ateneonline, November 20, 2007 (in Italian) Mafia: Le signore omicidi, La ...

*Matteo Messina Denaro

In Sicily, the end of 'Pax Mafiosa'?, International Herald Tribune, April 13, 2006 (in Italian) 'Vincere Cosa nostra? Arresti e ...

*Κ-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 Zyklophin - selective peptide antagonist; dynorphin A analogue Found in numerous species of mint, ( ... β-arrestin antagonist Tifluadom - (atypical) benzodiazepine Nalfurafine (Remitch), which was introduced in 2009, is the first ... β-arrestin antagonist Amentoflavone - non-selective; naturally-occurring AT-076 - non-selective, likely long acting; JDTic ...

*Lorenzo Alejandro Laviosa Lopez

"Orden Judicial de Arresto". www.box.com. Retrieved 2017-04-29. "Policía de El Hatillo detuvo a cuatro extorsionadores - Sucesos ...

*Francesco Schettino

"Arresti domiciliari a Schettino". La Repubblica Firenze. 2012-01-17. Retrieved 2014-07-27. "Judge lifts Costa Concordia ...

*Herkinorin

Unlike most μ-opioid agonists, herkinorin does not promote the recruitment of β-arrestin-2 to the intracellular domain of the μ ... "An Opioid Agonist that Does Not Induce μ-Opioid Receptor-Arrestin Interactions or Receptor Internalization". Molecular ... "Herkinorin analogues with differential beta-arrestin-2 interactions". Journal of Medicinal Chemistry. 51 (8): 2421-31. doi: ...

*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 ...

*Trevena Inc

While it binds to the same receptors as opioid analgesics, TRV734 has very weak β-arrestin recruitment, unlike other available ... Trevena's developed TRV027 for acute heart failure, targets the angiotensin receptor utilizing beta-arrestin bias, an approach ... Violin, Jonathan D.; Lefkowitz, Robert J. (2007). "Β-Arrestin-biased ligands at seven-transmembrane receptors". Trends in ... ß-arrestin-biased ligand at the angiotensin II type I receptor, in healthy and heart failure canines: A novel therapeutic ...

*AP3B1

Kim YM, Barak LS, Caron MG, Benovic JL (May 2002). "Regulation of arrestin-3 phosphorylation by casein kinase II". The Journal ...

*Benelux Court of Justice

"Consultatie van de arresten en conclusies". Benelux Court of Justice (in Dutch). Retrieved 2 July 2014. "Judgement of the Court ...

*Androlepsy

Arresto facto super bonis mercatorum alienigenorum. ...

*Christian Thomsen Carl

Arresta und Gefangenschaften <...> Sonders beschwerlich und unjustificirlich vorgenommen worden. [s.i.] Therein: No. 331. Copia ...

*Via D'Amelio bombing

"Strage via D'Amelio, quattro nuovi arresti. 'Borsellino sapeva di trattative Stato-mafia'". ADN Kronos. Retrieved 23 May 2012. ...

*Leopoldo Fernández

"Leopoldo Fernández sale con arresto domiciliario". Opinión. 6 February 2013. Alanoca, Jesús (31 March 2016). "Leopoldo ' ...

*G 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 ...

*ARR3

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)". Human ARR3 genome location and ARR3 gene details page in the UCSC Genome ... "X-arrestin: a new retinal arrestin mapping to the X chromosome". FEBS Lett. 334 (2): 203-9. doi:10.1016/0014-5793(93)81712-9. ... 2002). "Mouse cone arrestin expression pattern: light induced translocation in cone photoreceptors". Mol. Vis. 8: 462-71. PMID ...
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 ...
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 ...
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
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
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 ...
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 ...
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 ...
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 ...
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.
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.
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 ...
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 ...
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 ...
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 ...
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, ...
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, ...
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 ...
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.. ...
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 ...
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 ...
By contrast, specific inhibition of endogenous GRK2 by dominant-negative mutants robustly inhibited OTR phosphorylation and internalization as well as arrestin/OTR interactions ...
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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 ...
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 ...
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 ...
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 ...
G protein-coupled receptors (GPCRs) at the plasma membrane bind to their ligands and couple to heterotrimeric G proteins, leading to the generation of second messengers such as cyclic adenosine monophosphate (cAMP). Phosphorylation of activated GPCRs leads to their desensitization and internalization, which is thought to result in signal termination, although β-arrestin-dependent signaling can also be initiated. However, aspects of the spatial and temporal regulation of GPCRs are still unclear. Calebiro et al. generated transgenic mice expressing a fluorescent resonance energy transfer-based sensor of cAMP and used fluorescence microscopy to examine signaling by the thyroid-stimulating hormone (TSH) receptor, a GPCR, in thyroid follicles in 3D culture. Although short-term stimulation with TSH led to transient cAMP generation, prolonged stimulation or stimulation with higher concentrations of TSH led to the accumulation of cAMP. Confocal microscopy experiments performed with a fluorescently ...
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 ...
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. ...
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 ...
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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 ...
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 ...
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 ...
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 ...
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, ...
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Our current findings raise a number of important new and unanswered questions. For example, is Ops5 an active photopigment? This question must be addressed directly in future studies, but our observation that Ops5 co-localizes, at least in part, with Ops1-2 in debris shed via LDS (Fig. 8) provides indirect evidence that it is. LDS is a clathrin-mediated endocytosis involving arrestin as an adaptor protein (Sacunas et al., 2002), and arrestin binding and clathrin-mediated endocytosis are hallmarks of activated G-protein-coupled receptors.. If Ops5 participates in phototransduction, of what functional significance is its co-expression with Ops1-2 in Limulus photoreceptors and what are the functional consequences of the observed diurnal change in the ratio of rhabdomeral Ops5 to Ops1-2? Can the influence of the clock on the night-time ratio of rhabdomeral Ops5 to Ops1-2 explain any of the clock-regulated changes in photoreceptor function? If Ops5 and Ops1-2 have different spectral properties, as ...
Chemokines orchestrate cell migration for development, immune surveillance, and disease by binding to cell surface heterotrimeric guanine nucleotide-binding protein (G protein)-coupled receptors (GPCRs). The array of interactions between the nearly 50 chemokines and their 20 GPCR targets generates an extensive signaling network to which promiscuity and biased agonism add further complexity. The receptor CXCR4 recognizes both monomeric and dimeric forms of the chemokine CXCL12, which is a distinct example of ligand bias in the chemokine family. We demonstrated that a constitutively monomeric CXCL12 variant reproduced the G protein-dependent and β-arrestin-dependent responses that are associated with normal CXCR4 signaling and lead to cell migration. In addition, monomeric CXCL12 made specific contacts with CXCR4 that are not present in the structure of the receptor in complex with a dimeric form of CXCL12, a biased agonist that stimulates only G protein-dependent signaling. We produced an ...
Research in my laboratory is aimed at understanding the mechanisms of signal dependent protein localization and transport in neurons. Dynamic protein localization within cells is often determined by environmental stimuli. In rod photoreceptors of the retina transitions between darkness and light result in the massive translocation of several key signal transduction proteins between two major compartments. The second and third most abundant proteins in rods, arrestin and transducin, respectively, move in opposite directions. Arrestin, a protein that has been identified to be important for regulation of heterotrimeric G protein coupled receptors, is found primarily in the inner segment compartment of dark adapted rods, but essentially its entire compliment is transported to the outer segment compartment upon exposure to light. Transducin, the G protein in rod visual transduction, is found in the rod outer segment in dark-adapted rods and moves to the inner segment with the onset of light. A third ...
Kurtz (Krz) is the only Drosophila homolog of mammalian beta-arrestins. We have already implicated Krz in regulation of Toll, receptor tyrosine kinase (RTK) and mitogen activated protein kinase (MAPK) pathways. As a multifunctional adaptor, how does Krz coordinate different signaling pathways and carry out well-orchestrated duties? I hypothesize that a possible strategy for Krz is to dynamically reorganize its core interaction complexes in response to the given physiological status. I systematically tested this hypothesis by analyzing in vivo Krz signaling networks dynamics. I also performed an in vivo structure-function analysis of Krz by biochemistry and genetic analysis. I successfully identified the in vivo core Krz interaction complexes, which include: Ulp1, Dos, shep, CG10289 and CG3797; my results suggested phosphoinositide binding elements (KRK motif) in Krz was important for normal fertility of flies, which may due to combined defects of RTK and Toll. As a case study, I also investigated
Dopamine is a neurotransmitter in circuits that convey reward and motivation, and abnormalities in dopamine signaling have been associated with mental illness. In particular, reduced function of the D2-type dopamine receptor (D2DR) is thought to contribute to schizophrenia, addiction, and mood disorders. Park et al. used a yeast two-hybrid screen to uncover prostate apoptosis response 4 (Par-4) as a binding partner for D2DR. In striatal neurons from mice that expressed a mutant form of Par-4 (in which the domain mediating the interaction with D2DR had been deleted), activation of signaling through cAMP was disrupted. Furthermore, behavioral tests of the mutant mice showed a depression-like phenotype, but no effects on measures of anxiety. Beaulieu et al. examined another signaling pathway emanating from D2DR, and they find that β-arrestin 2 is important in mediating the behavioral effects of dopamine. In wild-type mice, β-arrestin 2 was shown to associate with protein phosphatase 2a (PP2A) and ...
Polymerase chain reaction amplification of several polymorphic genes has been used to study the population biology of Plasmodium falciparum. S antigen is particularly suitable for such studies, but difficulties in the amplification of this gene have precluded its use. Here we describe a simple method for the amplification of S antigen and show why previous attempts may have been unsuccessful. Data are presented from both laboratory and field isolates.
Dr. Hubbells research is focused on understanding the relationship between the molecular structure of a protein and the conformational changes that control its function. Of particular interest are membrane proteins that behave as "molecular switches", i.e., proteins whose structures are switched to an active state by a physical or chemical signal. A primary example under study is light-activated rhodopsin, the visual pigment in photoreceptor cells of the retina. The goal is to elucidate the structure of rhodopsin, the mechanism of the molecular switch, and the regulation of this switch by associated proteins, transducin and arrestin. Recently, his research has broadened to include structure/function relationships in water-soluble proteins such as the lens protein a-crystallin and the family of retinoid carrying proteins that transport vitamin A throughout photoreceptor cells.. To investigate these proteins, Dr. Hubbells laboratory has developed the technique of site-directed spin labeling ...
ID A0A0V1PID2_9BILA Unreviewed; 735 AA. AC A0A0V1PID2; DT 16-MAR-2016, integrated into UniProtKB/TrEMBL. DT 16-MAR-2016, sequence version 1. DT 25-OCT-2017, entry version 10. DE SubName: Full=Cyclic nucleotide-gated olfactory channel {ECO:0000313,EMBL:KRZ95997.1}; GN Name=CNGA2 {ECO:0000313,EMBL:KRZ95997.1}; GN ORFNames=T08_6129 {ECO:0000313,EMBL:KRZ95997.1}; OS Trichinella sp. T8. OC Eukaryota; Metazoa; Ecdysozoa; Nematoda; Enoplea; Dorylaimia; OC Trichocephalida; Trichinellidae; Trichinella. OX NCBI_TaxID=92180 {ECO:0000313,EMBL:KRZ95997.1, ECO:0000313,Proteomes:UP000054924}; RN [1] {ECO:0000313,EMBL:KRZ95997.1, ECO:0000313,Proteomes:UP000054924} RP NUCLEOTIDE SEQUENCE [LARGE SCALE GENOMIC DNA]. RC STRAIN=ISS272 {ECO:0000313,EMBL:KRZ95997.1}; RA Korhonen P.K., Edoardo P., Giuseppe L.R., Gasser R.B.; RT "Evolution of Trichinella species and genotypes."; RL Submitted (JAN-2015) to the EMBL/GenBank/DDBJ databases. CC -!- CAUTION: The sequence shown here is derived from an CC EMBL/GenBank/DDBJ ...
Vision requires the photoreceptors in the eye to rapidly respond to changes in light intensity. These processes are accomplished within rod photoreceptors by the visual pigment rhodopsin that initiates a downstream signaling cascade called phototransduction. Rhodopsin is composed of an apoprotein opsin that is covalently bonded with light sensitive 11-cis retinal. Rhodopsin is activated when 11-cis retinal is photoisomerized into all-trans retinal. This isomerization initiates the phototransduction cascade that culminates in a change in current at the plasma membrane. Rhodopsin, once activated ("bleached"), can no longer absorb photons to activate phototransduction, and must be regenerated through the visual cycle. To enable the photoreceptors to respond to rapid changes in light intensities, phototransduction must terminate in a timely manner. Deactivation involves phosphorylation of activated rhodopsin by rhodopsin kinase, and then binding of visual arrestin. Exposing rods to daylight bleaches ...
Chen, Xiangting, Chinnery, Holly R., Kezic, Jelena, Sidhu, Manpreet, Bernard, Claude, Forrester, John V. and McMenamin, Paul G. 2012, In vivo imaging of experimental autoimmune uveitis disease progression in Cx3cr1-GFP and CD11c-YFP mice, in ARVO 2012 : Proceedings of the 2012 Association for Research in Vision and Opthalmology Conference, ARVO, [Fort Lauderdale, Flo.], pp. 1-1. ...
Interphotoreceptor retinoid-binding protein(668-687), the amino acid residues 668 to 687 of human interphotoreceptor retinoid binding protein (IRBP), induces uveitis ...
See related article, pp 972-981. Heart failure (HF) is a clinical syndrome that is the terminal stage for several cardiac conditions, such as hypertension, ischemic heart disease, and valvular heart disease. According to the National Health and Nutrition Examination Survey, ≈6.5 million Americans ≥20 years of age live with HF. The prevalence of HF is expected to increase by ≈50% by 2030, resulting in ,8 million Americans with HF.1 Mortality and morbidity rates associated with HF place a considerable burden on the healthcare system by being the second most prevalent cause of hospitalization.2 Hemodynamically, HF is defined as a failure of the heart to pump blood in the amounts that meet the metabolic needs of the body. Several mechanisms contribute to the development of HF2: (1) neurohumoral activation, (2) increased myocardial fibrosis, (3) cellular hypertrophy and susceptibility to cell death, (4) vicious circle of adrenergic stimulation that raises myocardial contractility in the setting ...
A biomedical breakthrough, published today in the journal Nature, reveals never-before-seen details of the human bodys cellular switchboard that regulates sensory and hormonal responses. The work is based on an X-ray laser experiment at the Department of Energys SLAC National Accelerator Laboratory. The much-anticipated discovery, a decade in the making, could have broad impacts on development of more highly targeted and effective drugs with fewer side effects to treat conditions including high blood pressure, diabetes, depression and even some types of cancer. The ultrabright X-rays of SLACs Linac Coherent Light Source (LCLS) enabled the research team to complete the first 3-D atomic-scale map of a key signaling protein called arrestin while it was docked with a cell receptor involved in vision. The receptor is a well-studied example from a family of hundreds of G protein-coupled receptors, or GPCRs, which are targeted by about 40 percent of drugs on the market. Its structure while coupled ...
Southern, Craig; Cook, Jennifer M.; Neetoo-Isseljee, Zaynab; Taylor, Debra L.; Kettleborough, Catherine A.; Merritt, Andy; Bassoni, Daniel L.; Raab, William J.; Quinn, Elizabeth; Wehrman, Tom S.; Davenport, Anthony P.; Brown, Andrew J.; Green, Andrew; Wigglesworth, Mark J.; Rees, Steve (2013). "Screening β-Arrestin Recruitment for the Identification of Natural Ligands for Orphan G-Protein-Coupled Receptors". Journal of biomolecular screening. SAGE Publications. 18 (5): 599-609. doi:10.1177/1087057113475480. ISSN 1087-0571. PMID 23396314 ...
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Our data demonstrate the novel finding that GRK5 activity attenuates atherosclerosis, and that it does so through distinct antiatherogenic mechanisms in ECs, SMCs, monocytes, and Mϕs. These cell-specific mechanisms encompass diverse signaling systems, including the receptor tyrosine kinases CSF-1R and PDGFRβ, the 7-transmembrane receptor CCR2, the innate immunity receptors TLR4 and TNFR1, and the transcription factor NF-κB. Thus, despite data from overexpression and model cell systems suggesting the possibility that GRK5 could mediate proatherogenic activities,9,11,13,14 net physiological GRK5 activity clearly appears to be antiatherogenic.. Because GRK5-mediated phosphorylation of 7-transmembrane receptors promotes receptor/β-arrestin association,1 it may seem paradoxical that whereas GRK5 activity is antiatherogenic, β-arrestin2 activity is proatherogenic.19 However, at least 2 possibilities may help reconcile these findings. First, GRK5-mediated receptor phosphorylation may promote the ...
1. Tang H, Inoki K, Lee M, Wright E, Khuong A, Khuong A. et al. mTORC1 Promotes Denervation-Induced Muscle Atrophy Through a Mechanism Involving the Activation of FoxO and E3 Ubiquitin Ligases. Sci Signal. 2014;7:ra18 2. Sartori R, Schirwis E, Blaauw B, Bortolanza S, Zhao J, Enzo E. et al. BMP signaling controls muscle mass. Nature genetics. 2013;45:1309-18 3. Sartorelli V, Fulco M. Molecular and cellular determinants of skeletal muscle atrophy and hypertrophy. Sciences STKE: signal transduction knowledge environment. 2004;2004:re11 4. Kim HK, Lee YS, Sivaprasad U, Malhotra A, Dutta A. Muscle-specific microRNA miR-206 promotes muscle differentiation. J Cell Biol. 2006;174:677-87 5. Lynch GS, Ryall JG. Role of beta-adrenoceptor signaling in skeletal muscle: implications for muscle wasting and disease. Physiol Rev. 2008;88:729-67 6. Claeys MC, Mulvaney DR, McCarthy FD, Gore MT, Marple DN, Sartin JL. Skeletal muscle protein synthesis and growth hormone secretion in young lambs treated with ...
PubMed Central Canada (PMC Canada) provides free access to a stable and permanent online digital archive of full-text, peer-reviewed health and life sciences research publications. It builds on PubMed Central (PMC), the U.S. National Institutes of Health (NIH) free digital archive of biomedical and life sciences journal literature and is a member of the broader PMC International (PMCI) network of e-repositories.
Principal Investigator:IWABUCHI Kazuya, Project Period (FY):2001 - 2002, Research Category:Grant-in-Aid for Scientific Research (C), Section:一般, Research Field:Ophthalmology
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Currently, go/no-go decision making in proof-of-concept (POC) multiple sclerosis (MS) trials for promising drug/dose selection are predominantly qualitative in nature. POC trials employ placebo corrected magnetic resonance imaging lesion counts (MRI-T2 counts) as endpoint, whereas, phase 3 trials employ annualized relapse rate at 24 months (ARR-24) as the efficacy endpoint. The objective of the current investigation is to provide a quantitative framework that can aid informed decision making in MS clinical drug development. Blinded summary level data on MRI-T2 lesions at 12 months and aggregate ARR-24 across six clinical development programs digitized from a Food and Drug Administration (FDA)s 2012 science day presentation were utilized to develop a pharmaco-statistical model linking the MRI-T2 lesions at 12 months with ARR-24. The developed MRI-T2-ARR-24 model was further evaluated by clinical trial simulations and was used to predict the probability of phase 3 clinical trial success given the ...
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βarrestin (βarr)-1 and -2 (βarrs) (or Arrestin-2 and -3, respectively) are universal G protein-coupled receptor (GPCR) adapter proteins expressed abundantly in extra-retinal tissues, including the myocardium. Both were discovered in the lab of the 2012 Nobel Prize in Chemistry co-laureate Robert Lefkowitz, initially as terminators of signaling from the β-adrenergic receptor (βAR), a process known as functional desensitization. They are now known to switch GPCR signaling from G protein-dependent to G protein-independent, which, in the case of βARs and angiotensin II type 1 receptor (AT1R), might be beneficial, e.g., anti-apoptotic, for the heart. However, the specific role(s) of each βarr isoform in cardiac GPCR signaling and function (or dysfunction in disease), remain unknown. The current consensus is that, whereas both βarr isoforms can desensitize and internalize cardiac GPCRs, they play quite different (even opposing in certain instances) roles in the G protein-independent signaling pathways
Authors: Aramant, R. , Seiler, M. , Ehinger, B. , Bergström, A. , Gustavii, B. , Brundin, P. , Adolph, A.R. Article Type: Research Article Abstract: Human embryonic retinas (postconceptional age 3-10 weeks) with or without retinal pigment epithelium were grafted to the retina of immuno-suppressed adult rat hosts. The development of the xenografts was followed up to 37 weeks of total age by histology and by immunohistochemistry for S-antigen. The donor tissue became rearranged in folded sheets with rosettes. The grafts developed approximately according to their intrinsic timetable, but with a developmental delay in the later stages. Occasionally, the grafts were well fused with the host retina. At 13 weeks of total age, the grafts contained areas of inner plexiform layer with presumptive ganglion cells, …one neuroblastic layer, and cone precursor cells around rosettes. At 19 weeks, an outer plexiform layer and inner segments of the cones started to form. At 20 weeks, the first immunoreactivity ...
Target-based classification of drugs [BR:br08310] G Protein-coupled receptors Rhodopsin family Histamine HRH1 [HSA:3269] [KO:K04149] D06021 Tecastemizole (USAN/INN ...
Killer dyes that can wipe out bacteria could help solve the superbug problems faced by surgical patients, scientists heard today at the Society for General Microbiologys Autumn meeting being held this week at Trinity College, ...
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Western blotting. Eyecups (including the retina) from dark-adapted mice were homogenized in 100 mm Tris/HCl, pH 7.4, and analyzed for protein content. Standard SDS-PAGE (7.5 or 10%) and Western blotting were performed. For immunodetection, polyclonal rabbit antisera directed against RPE65 (raised against amino acids 150-164 of human/bovine RPE65) (Redmond and Hamel, 2000), interphotoreceptor retinoid binding protein (IRBP) (Smith et al., 1997), cellular retinaldehyde-binding protein (CRALBP) (Crabb et al., 1991), transducin (Hamm et al., 1987), rhodopsin-kinase (Zhao et al., 1998), arrestin (Kueng-Hitz et al., 2000), and actin (Lessard, 1988) were applied. HRP-conjugated secondary antibodies were applied (catalog #sc 2004 and 2031; Santa Cruz Biotechnology, Santa Cruz, CA), and immunoreactivity was visualized using the Renaissance-Western blot detection kit (PerkinElmer Life Sciences, Emeryville, CA).. RT-PCR and Rpe65 sequence analysis. Total RNA was prepared from eyecups using the RNeasy kit ...
The role of carcinine in signaling at the Drosophila photoreceptor synapse. Gavin BA, Arruda SE, Dolph PJ. PLoS Genet. 2007 Dec;3(12):e206. PMID: 18069895 [PubMed - indexed for MEDLINE]. Accelerated accumulation of misfolded prion protein and spongiform degeneration in a Drosophila model of Gerstmann-Sträussler-Scheinker syndrome. Gavin BA, Dolph MJ, Deleault NR, Geoghegan JC, Khurana V, Feany MB, Dolph PJ, Supattapone S. J Neurosci. 2006 Nov 29;26(48):12408-14. PMID: 17135402 [PubMed - indexed for MEDLINE]. An essential role for endocytosis of rhodopsin through interaction of visual arrestin with the AP-2 adaptor. Orem NR, Xia L, Dolph PJ. J Cell Sci. 2006 Aug 1;119(Pt 15):3141-8. Epub 2006 Jul 11. PMID: 16835270 [PubMed - indexed for MEDLINE]. Molecular cloning of the pawn locus from Drosophila melanogaster. Arruda SE, Dolph PJ. Gene. 2003 May 22;310:169-73. PMID: 12801644 [PubMed - indexed for MEDLINE]. Post-transcriptional suppression of pathogenic prion protein expression in Drosophila ...
Receptor ligands, identified as antagonists, based on the absence of stimulation of signaling, can rarely stimulate receptor internalization. d-Tyr-Gly-[(Nle(28,31),d-Trp(30))CCK-26-32]-2-phenylethyl ester (d-Trp-OPE) is such a ligand that binds to the cholecystokinin (CCK) receptor and stimulates internalization. Here, the molecular basis of this trafficking event is explored, with the assumption that ligand binding initiates conformational change, exposing an epitope to direct endocytosis. Ligand-stimulated internalization was studied morphologically using fluorescent CCK and d-Trp-OPE. d-Trp-OPE occupation of Chinese hamster ovary cell receptors stimulated internalization into the same region as CCK. Arrestin-biased action was ruled out using morphological translocation of fluorescent arrestin 2 and arrestin 3, moving to the membrane in response to CCK, but not d-Trp-OPE. Possible roles of the carboxyl terminus were studied using truncated receptor constructs, eliminating the proline-rich distal tail
We are sometimes asked how one or two nutritional supplements can benefit patients with so many different gene defects," Dr. Berson said. "With respect to vitamin A, we and others have suggested that under daylight conditions rods give cones vitamin A via Müller cells. Interphotoreceptor retinoid binding protein (IRBP) transports vitamin A between these cells. Release of vitamin A from IRBP requires DHA present in oily fish. Rod degeneration leads to a deficiency of vitamin A and DHA. This could explain why vitamin A plus an oily fish diet benefits patients with RP. Patients are advised to take vitamin A to replace their rods and eat oily fish to enhance delivery of vitamin A to cones ...
TY - JOUR. T1 - Truncation and mutagenesis analysis of the human X-arrestin gene promoter. AU - Fujimaki, Takuro. AU - Huang, Zhen Yong. AU - Kitagawa, Hitoshi. AU - Sakuma, Hitoshi. AU - Murakami, Akira. AU - Kanai, Atsushi. AU - McLaren, Margaret J.. AU - Inana, George. PY - 2004/9/15. Y1 - 2004/9/15. N2 - X-arrestin (arrestin-3) is an arrestin present specifically in the outer segments of red-, green-, and blue-cone photoreceptors. The X-arrestin gene is on Xcen-q22, and consists of 17 exons with a promoter containing a TATA box and elements important for photoreceptor expression, including three CRX and one PCE-1-like element. In order to delineate the promoter structure necessary for the pan-cone-specific expression of X-arrestin, the expression of the gene in retinoblastoma cell lines was investigated, and a structure-function analysis of the promoter was conducted in the appropriate cellular substrate. Expression of X-arrestin was detected at a low level in the Y79 retinoblastoma cell ...
PubMed Central Canada (PMC Canada) provides free access to a stable and permanent online digital archive of full-text, peer-reviewed health and life sciences research publications. It builds on PubMed Central (PMC), the U.S. National Institutes of Health (NIH) free digital archive of biomedical and life sciences journal literature and is a member of the broader PMC International (PMCI) network of e-repositories.
History AND PURPOSE While maintaining cardiac performance, chronic -adrenoceptor activation ultimately exacerbates the development of cardiac remodelling and failure. from 7 to 10 weeks of age mainly prevented development of ventricular dilatation, maintained contractile function (fractional shortening 37 5% vs. 25 3%, ejection portion 52 5% vs. 32 4%, both Fingolimod 0.05), reduced cardiac fibrosis and suppressed matrix metalloproteinase activity. Summary AND IMPLICATIONS 2-adrenoceptor activation provoked NADPH oxidase-derived ROS creation in the center. Elevated ROS triggered p38 MAPK and added considerably to cardiac swelling, remodelling and failing. LINKED ARTICLE This short article is usually commented on by Di Lisa research recommended an anti-apoptotic actions opposing that of 1-adrenoceptors (Zhu research, including ours, possess revealed several nonclassical signalling molecules employed by 2-adrenoceptors, including -arrestin 1 (Drake systems, not really exposing the signalling ...
Objectives: The objective was to critically appraise and highlight methodologically superior medical education research specific to emergency medicine (EM) published in 2009.. Methods: A search of the English language literature in 2009 querying Ovid MEDLINE In-Process & Other Non-Indexed Citations, Ovid MEDLINE 1950 to Present, Web of Science, Education Resources Information Center (ERIC), and PsychInfo identified 36 EM studies that used hypothesis-testing or observational investigations of educational interventions. Six reviewers independently ranked all publications based on 10 criteria, including four related to methodology, that were chosen a priori to standardize evaluation by reviewers. This was a refinement of the methods used to appraise medical education published in 2008.. Results: Seven studies met the standards as determined by the averaged rankings and are highlighted and summarized here. This year, 16 of 36 (44%) identified studies had funding, compared to 11 of 30 (36%) ...
The family of G-protein-coupled receptors includes many well-studied members, such as the adrenergic and the muscarinic acetylcholine receptors. These receptors are regulated by multiple mechanisms that serve to adapt their expression and their function to a rapidly changing environment. One of the most intriguing and important regulatory mechanisms involves the phosphorylation of such receptors by a set of specific kinases, termed the G-protein-coupled receptor kinases (GRKs). This phosphorylation is followed by binding of specific arrestin proteins to the phosphorylated receptors, which uncouples the receptors from their G proteins and thus causes a loss of receptor function. Several isoforms of the GRKs and the arrestins are expressed in the heart. They may be involved in the loss of receptor function in response to drugs. Furthermore, increased expression of one of the GRKs, β-adrenergic receptor kinase-1, has been found in failing hearts, and its increased activity may contribute to the loss of β
The stress-related catecholamine hormones and the α- and β-adrenergic receptors (α- and β-AR) may affect carcinogenesis. The β-AR GRK/β-arrestin biased agonist carvedilol can induce β-AR-mediated transactivation of the epidermal growth factor receptor (EGFR). The initial purpose of this study was to determine whether carvedilol, through activation of EGFR, can promote cancer. Carvedilol failed to promote anchorage-independent growth of JB6 P+ cells, a skin cell model used to study tumor promotion. However, at non-toxic concentrations carvedilol dose-dependently inhibited EGF-induced malignant transformation of JB6 P+ cells suggesting that carvedilol has chemopreventive activity against skin cancer. Such effect was not observed for the β-AR agonist isoproterenol and the β-AR antagonist atenolol. Gene expression, receptor binding, and functional studies indicate that JB6 P+ cells only express β2-ARs. Carvedilol, but not atenolol, inhibited EGF-mediated activator protein-1 (AP-1) ...
This application note highlights the direct optic bottom reading performance of a HTS microplate reader in two different cell-based fluorescence intensity assays from Invitrogen. First, the intracellular calcium response to histamine was measured in HEK 293 cells using the Fluo-4 Direct™ Calcium Assay. Second, arrestin recruitment through activation of the dopamine D1 receptor with dopamine (D1 agonist) was measured using Tango™ D1-bla U2OS cells and a live cell FRET substrate.
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Cognitive dysfunction is a core feature of dementia and a prominent feature in psychiatric disease. As non-redundant regulators of intracellular cAMP gradients, phosphodiesterases (PDE) mediate fundamental aspects of brain function relevant to learning, memory, and higher cognitive functions. Phosphodiesterase-4B (PDE4B) is an important phosphodiesterase in the hippocampal formation, is a major Disrupted in Schizophrenia 1 (DISC1) binding partner and is itself a risk gene for psychiatric illness. To define the effects of specific inhibition of the PDE4B subtype, we generated mice with a catalytic domain mutant form of PDE4B (Y358C) that has decreased ability to hydrolyze cAMP. Structural modelling predictions of decreased function and impaired binding with DISC1 were confirmed in cell assays. Phenotypic characterization of the PDE4BY358C mice revealed facilitated phosphorylation of CREB, decreased binding to DISC1, and upregulation of DISC1 and β-Arrestin in hippocampus and amygdala. In ...
As tool compounds to study cardiac ischemia, the endogenous δ-opioid receptors (δOR) agonist Leu5-enkephalin and the more metabolically stable synthetic peptide (d-Ala2, d-Leu5)-enkephalin are frequently employed. However, both peptides have similar pharmacological profiles that restrict detailed investigation of the cellular mechanism of the δOR’s protective role during ischemic events. Thus, a need remains for δOR peptides with improved selectivity and unique signaling properties for investigating the specific roles for δOR signaling in cardiac ischemia. To this end, we explored substitution at the Phe4 position of Leu5-enkephalin for its ability to modulate receptor function and selectivity. Peptides were assessed for their affinity to bind to δORs and µ-opioid receptors (µORs) and potency to inhibit cAMP signaling and to recruit β-arrestin 2. Additionally, peptide stability was measured in rat plasma. Substitution of the meta-position of
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Arrestin-like, N-terminal (IPR011021) | InterPro | EMBL-EBIArrestin-like, N-terminal (IPR011021) | InterPro | EMBL-EBI

Arrestin-like, N-terminal (IPR011021). Short name: Arrestin-like_N Overlapping homologous superfamilies *Arrestin, N-terminal ( ... Beta-arrestin2, a novel member of the arrestin/beta-arrestin gene family.. J. Biol. Chem. 267 17882-90 1992 ... Cone photoreceptors C-arrestin (arrestin-X) [PMID: 7720881], which could bind to phosphorylated red/green opsins; and ... Arrestin-subtypes in insect antennae.. Cell. Signal. 5 69-80 1993. Attramadal H, Arriza JL, Aoki C, Dawson TM, Codina J, Kwatra ...
more infohttp://www.ebi.ac.uk/interpro/entry/IPR011021

Arrestin - WikipediaArrestin - Wikipedia

Arrestin-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 between two GPCRs available ... Arrestin-4 was cloned by two groups and termed cone arrestin, after photoreceptor type that expresses it, and X-arrestin, after ...
more infohttps://en.wikipedia.org/wiki/Arrestin

arrestin - definition and meaningarrestin - definition and meaning

You vont think o arrestin your own son for the money, and sendin him off to the Fleet, will you, you unnatral wagabone? ... In a human study, the same scientists found that beta-arrestin-1 levels were low in the blood cells of depressed patients but ... Boy takes a grab at yo money, an if deys any lef , you gives it to a policeman fo arrestin him. ... MCSO is not going to each house in a neighborhood, kicking down doors, and arrestin whomever they run into. ...
more infohttps://www.wordnik.com/words/arrestin

Arrestin C-terminal-like domain (IPR011022) | InterPro | EMBL-EBIArrestin C-terminal-like domain (IPR011022) | InterPro | EMBL-EBI

Beta-arrestin2, a novel member of the arrestin/beta-arrestin gene family.. J. Biol. Chem. 267 17882-90 1992 ... Cone photoreceptors C-arrestin (arrestin-X) [PMID: 7720881], which could bind to phosphorylated red/green opsins; and ... Arrestin-subtypes in insect antennae.. Cell. Signal. 5 69-80 1993. Attramadal H, Arriza JL, Aoki C, Dawson TM, Codina J, Kwatra ... S-Arrestin (retinal S-antigen) is a major protein of the retinal rod outer segments. It interacts with photo-activated ...
more infohttp://www.ebi.ac.uk/interpro/entry/IPR011022

Arrestin-related proteins mediate pH signaling in fungi | PNASArrestin-related proteins mediate pH signaling in fungi | PNAS

... human arrestin β1 (arrB), and bovine visual arrestin (arrV) and the consensi for arrestin N-terminal and C-terminal PFAM ... Here we show that PalF is a non-metazoan arrestin-related protein, as verified by (i) the presence of arrestin N- and C- ... Conservation of the PalF family arrestin N-terminal and C-terminal domains. Shown above are positions of the PalF PFAM arrestin ... for amino acid sequences are P08168 (bovine visual arrestin), P49407 (human β1 arrestin), P78612 and Q9P904 (A. nidulans PalF ...
more infohttps://www.pnas.org/content/102/34/12141?ijkey=53679b7e67d89082ee15588ee8e2cac11c21ecb0&keytype2=tf_ipsecsha

Diversifying Role for β-Arrestin | Science SignalingDiversifying Role for β-Arrestin | Science Signaling

E. F. Grady, β-Arrestin, a two-fisted terminator. Science 315, 605-606 (2007). [Summary] [Full Text] ...
more infohttps://stke.sciencemag.org/content/2007/372/tw41

Arrestin C domain-containing protein - Anopheles farautiArrestin C domain-containing protein - Anopheles farauti

IPR011021 Arrestin-like_N. IPR014752 Arrestin_C. IPR011022 Arrestin_C-like. IPR017864 Arrestin_CS. IPR014753 Arrestin_N. ... IPR011021 Arrestin-like_N. IPR014752 Arrestin_C. IPR011022 Arrestin_C-like. IPR017864 Arrestin_CS. IPR014753 Arrestin_N. ... Arrestin_C domain-containing proteinInterPro annotation. ,p>Information which has been generated by the UniProtKB automatic ... tr,A0A182QD30,A0A182QD30_9DIPT Arrestin_C domain-containing protein OS=Anopheles farauti OX=69004 PE=4 SV=1 ...
more infohttps://www.uniprot.org/uniprot/A0A182QD30

Arrestin
     Summary Report | CureHunterArrestin Summary Report | CureHunter

Arrestin quenches G-protein activation by binding to phosphorylated photolyzed rhodopsin. Arrestin causes experimental ... Arrestin: A 48-Kd protein of the outer segment of the retinal rods and a component of the phototransduction cascade. ... Arrestin. Subscribe to New Research on Arrestin A 48-Kd protein of the outer segment of the retinal rods and a component of the ... Arrestin quenches G-protein activation by binding to phosphorylated photolyzed rhodopsin. Arrestin causes experimental ...
more infohttp://www.curehunter.com/public/keywordSummaryD019393-Arrestin.do

RCSB PDB - Gene View 









 - ARRDC3 - arrestin domain containing 3RCSB PDB - Gene View - ARRDC3 - arrestin domain containing 3

The PDB archive contains information about experimentally-determined structures of proteins, nucleic acids, and complex assemblies. As a member of the wwPDB, the RCSB PDB curates and annotates PDB data according to agreed upon standards. The RCSB PDB also provides a variety of tools and resources. Users can perform simple and advanced searches based on annotations relating to sequence, structure and function. These molecules are visualized, downloaded, and analyzed by users who range from students to specialized scientists.
more infohttp://www.rcsb.org/pdb/gene/ARRDC3?chromosome=chr5&range=90678630&v=hg19

RCSB PDB - Gene View 









 - ARRDC3 - arrestin domain containing 3RCSB PDB - Gene View - ARRDC3 - arrestin domain containing 3

The PDB archive contains information about experimentally-determined structures of proteins, nucleic acids, and complex assemblies. As a member of the wwPDB, the RCSB PDB curates and annotates PDB data according to agreed upon standards. The RCSB PDB also provides a variety of tools and resources. Users can perform simple and advanced searches based on annotations relating to sequence, structure and function. These molecules are visualized, downloaded, and analyzed by users who range from students to specialized scientists.
more infohttp://www.rcsb.org/pdb/gene/ARRDC3?chromosome=chr5&range=90669501&v=hg19

Anti-beta Arrestin 1 antibody (ab31868) | AbcamAnti-beta Arrestin 1 antibody (ab31868) | Abcam

Rabbit polyclonal beta Arrestin 1 antibody validated for WB, IP, IHC, ICC/IF and tested in Mouse and Rat. Referenced in 2 ... Beta Arrestin 1 was immunoprecipitated using 0.5mg Mouse Brain tissue lysate, 5µg of Rabbit polyclonal to Beta Arrestin 1 and ... Anti-beta Arrestin 1 antibody. See all beta Arrestin 1 primary antibodies. ... Lanes 2-4 : Anti-beta Arrestin 1 antibody (ab31868) at 1 µg/ml. Lane 2 : Mouse Brain at 20 µg. Lane 3 : Mouse brain tissue ...
more infohttps://www.abcam.com/beta-arrestin-1-antibody-ab31868.html

Recombinant Human Arrestin C protein (ab116769) ProtocolsRecombinant Human Arrestin C protein (ab116769) Protocols

There are no specific protocols for Recombinant Human Arrestin C protein (ab116769). Please download our general protocols ...
more infohttp://www.abcam.com/recombinant-human-arrestin-c-protein-ab116769-protocols.html

Arrestin beta 1 - WikipediaArrestin beta 1 - Wikipedia

Arrestin, beta 1, also known as ARRB1, is a protein which in humans is encoded by the ARRB1 gene. Members of arrestin/beta- ... Beta-arrestin might also play a role as scaffold protein in the GPCR pathways.[citation needed] Arrestin beta 1 has been shown ... 1997). "Arrestin/clathrin interaction. Localization of the arrestin binding locus to the clathrin terminal domain". J. Biol. ... "Entrez Gene: ARRB1 arrestin, beta 1". Claing A, Chen W, Miller WE, Vitale N, Moss J, Premont RT, Lefkowitz RJ (November 2001 ...
more infohttps://en.wikipedia.org/wiki/Arrestin_beta_1

GPCRs - B-arrestinGPCRs - B-arrestin

PathHunter® β-Arrestin Assays Largest Portfolio of β-Arrestin Cell-based Assays and Reagents for Drug Discovery. β-Arrestins ... PathHunter β-Arrestin Principle for GPCR Applications. PathHunter GPCR β-Arrestin assays take advantage of DiscoverXs ... Ultimate Flexibility - Create Your Own GPCR β-Arrestin Cell-based Assays in Any Cell Type. Create your own GPCR β-arrestin cell ... DiscoverX provides a complete set of tools to analyze β-arrestin biology. The PathHunter β-arrestin assays and reagents offer a ...
more infohttps://discoverx.com/arrestin

GPCRs - B-arrestinGPCRs - B-arrestin

PathHunter® β-Arrestin Assays Largest Portfolio of β-Arrestin Cell-based Assays and Reagents for Drug Discovery. β-Arrestins ... PathHunter β-Arrestin Principle for GPCR Applications. PathHunter GPCR β-Arrestin assays take advantage of DiscoverXs ... Ultimate Flexibility - Create Your Own GPCR β-Arrestin Cell-based Assays in Any Cell Type. Create your own GPCR β-arrestin cell ... DiscoverX provides a complete set of tools to analyze β-arrestin biology. The PathHunter β-arrestin assays and reagents offer a ...
more infohttps://www.discoverx.com/arrestin

ARR3 - Arrestin-C - Homo sapiens (Human) - ARR3 gene & proteinARR3 - Arrestin-C - Homo sapiens (Human) - ARR3 gene & protein

IPR000698. Arrestin. IPR011021. Arrestin-like_N. IPR011022. Arrestin_C-like. IPR017864. Arrestin_CS. IPR014753. Arrestin_N. ... IPR000698. Arrestin. IPR011021. Arrestin-like_N. IPR011022. Arrestin_C-like. IPR017864. Arrestin_CS. IPR014753. Arrestin_N. ... Belongs to the arrestin family.Curated. Phylogenomic databases. evolutionary genealogy of genes: Non-supervised Orthologous ... sp,P36575,ARRC_HUMAN Arrestin-C OS=Homo sapiens GN=ARR3 PE=1 SV=2 MSKVFKKTSSNGKLSIYLGKRDFVDHVDTVEPIDGVVLVDPEYLKCRKLFVMLTCAFRYG ...
more infohttp://www.uniprot.org/uniprot/P36575

Cone Arrestin Expression and Induction in Retinoblastoma Cells | SpringerLinkCone Arrestin Expression and Induction in Retinoblastoma Cells | SpringerLink

The arrestin superfamily includes visual arrestins, beta-arrestins (βarrestins) and insect... ... also known as S-antigen or Arrestin 1) and cone arrestin (X-arrestin or Arresting. Rod arrestin was the first member to be ... A. Murakami, T. Yajima, H. Sakuma, M. J. McLaren, and G. Inana, X-arrestin: a new retinal arrestin mapping to the X chromosome ... a novel member of the arrestin/beta-arrestin gene family, J Biol Chem 267(25), 17882-17890 (1992).PubMedGoogle Scholar ...
more infohttps://link.springer.com/chapter/10.1007/978-1-4615-1355-1_33

anti-Arrestin 3 Primary Antibodiesanti-Arrestin 3 Primary Antibodies

Order monoclonal and polyclonal Arrestin 3 antibodies for many applications. Selected quality suppliers for anti-Arrestin 3 ... arrestin beta 2 , arrestin, beta 2 , arrestin 2 , beta-Arrestin 2 , arrestin beta-2 , beta-arrestin-2 , beta-arrestin-2-like , ... Arrestin 3 (ARRB2) Antigen Profile Antigen Summary Members of arrestin/beta-arrestin protein family are thought to participate ... Top referenced anti-Arrestin 3 Antibodies. Show all anti-Arrestin, beta 2 (ARRB2) Antibodies with Pubmed References. * Human ...
more infohttps://www.antibodies-online.com/intracellular-steroid-hormone-receptor-signaling-pathway-pathway-34/arrestin-3-antibody-2158/

arrestin beta 2 L homeolog ELISA Kits | Biocompare.comarrestin beta 2 L homeolog ELISA Kits | Biocompare.com

Compare arrestin beta 2 L homeolog ELISA Kits from leading suppliers on Biocompare. View specifications, prices, citations, ... arrestin beta 2 L homeolog ELISA Kits. The ELISA (enzyme-linked immunosorbent assay) is a widely used application for detecting ... Your search returned 5 arrestin beta 2 L homeolog ELISA ELISA Kit across 1 supplier. ...
more infohttps://www.biocompare.com/pfu/110627/soids/2-2319264/ELISA_Kit/ELISA_arrestin_beta_2_L_homeolog

β-Blockers alprenolol and carvedilol stimulate β-arrestin-mediated EGFR transactivation | PNASβ-Blockers alprenolol and carvedilol stimulate β-arrestin-mediated EGFR transactivation | PNAS

Both β-Arrestin 1 and β-Arrestin 2 Are Required for Alp- or Car-Induced ERK Activation.. To determine if Alp or Car stimulation ... In our experiments, we show that both Alp and Car use β-arrestin to induce β1AR-mediated EGFR transactivation. As β-arrestin is ... In contrast, ERK activation was significantly blocked in the presence of siRNA targeting β-arrestin 1, β-arrestin 2, or both ... but also β-arrestin-dependent signaling. One such β-arrestin-mediated pathway uses the β1-adrenergic receptor (β1AR) to ...
more infohttps://www.pnas.org/content/105/38/14555?ijkey=e7e32fc2e86e2fb7f3042136e1cfdac3084442bc&keytype2=tf_ipsecsha

Arrestin-S ELISA Kits from AMSBIO LLC | Biocompare.comArrestin-S ELISA Kits from AMSBIO LLC | Biocompare.com

Compare Arrestin-S ELISA Kits from AMSBIO LLC from leading suppliers on Biocompare. View specifications, prices, citations, ... Arrestin-S ELISA Kits from AMSBIO LLC. The ELISA (enzyme-linked immunosorbent assay) is a well-established antibody-based tool ...
more infohttps://www.biocompare.com/pfu/110627/soids/2-26863/Assay_Kit/ELISA_Arrestin-S?vids=103753

SMART: Pfam domain Arrestin NSMART: Pfam domain Arrestin N

Cone photoreceptors C-arrestin (arrestin-X) [(PUBMED:7720881)], which could bind to phosphorylated red/green opsins; and ... Arrestin_N. PFAM accession number:. PF00339. Interpro abstract (IPR011021):. G protein-coupled receptors are a large family of ... Arrestin (retinal S-antigen) is a major protein of the retinal rod outer segments. It interacts with photo-activated ... In mammals, arrestin is associated with autoimmune uveitis.. Arrestins comprise a family of closely-related proteins that ...
more infohttp://smart.embl.de/smart/do_annotation.pl?DOMAIN=Pfam:Arrestin_N&START=7&END=139&E_VALUE=8.5e-19&TYPE=PFAM&BLAST=FEIRLSQGRVVYGPGEPLAGTVHLRLGAPLPFRAIRVTCMGSCGVSTKANDGAWVVEESYFNSSLSLADKGSLPAGEHNFPFQFLLPATAPTSFEGPFGKIVHQVRASIDTPRFSKDHKCSLVFYILSPLNLN

Molecular mechanism of β-arrestin-biased agonism at seven-transmembrane receptors.  - PubMed - NCBIMolecular mechanism of β-arrestin-biased agonism at seven-transmembrane receptors. - PubMed - NCBI

Molecular mechanism of β-arrestin-biased agonism at seven-transmembrane receptors.. Reiter E1, Ahn S, Shukla AK, Lefkowitz RJ. ... Pluridimensionality of β-arrestin-dependent signaling at seven-transmembrane receptor (7TMRs). Some of the best-characterized β ... Relative activities of the nine ligands for G protein activation (G prot), β-arrestin recruitment (β-arr), and extracellular ... A general model for β-arrestin-biased ligand mechanism of action is proposed (, , ). GRK2/3 and GRK5/6 exert qualitatively ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/21942629?dopt=Abstract

Emerging paradigms of β-arrestin-dependent seven transmembrane receptor signaling.  - PubMed - NCBIEmerging paradigms of β-arrestin-dependent seven transmembrane receptor signaling. - PubMed - NCBI

The global scope of the β-arrestin interactome and β-arrestin dependent phosphorylation events. (a) Subcellular and (b) ... The protein highlighted in red and outlined in green were present in both, the β-arrestin interactome and the β-arrestin ... Recent global analyses of β-arrestin interactions and β-arrestin-dependent phosphorylation events have uncovered several ... b) Binding of an unbiased agonist to a β-arrestin biased receptor also induces a distinct conformation in the receptor which is ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/21764321?dopt=Abstract

WikiGenes - ARR3 - arrestin 3, retinal (X-arrestin)WikiGenes - ARR3 - arrestin 3, retinal (X-arrestin)

The promoter elements, common to both the X-arrestin and S-antigen genes, include the Ret-1/PCE-1 (PCE-1-like in X-arrestin), ... A gene for human C-arrestin was mapped to the X chromosome, making C-arrestin a candidate for several inherited X-linked ... The localization of C-arrestin to cone photoreceptors suggests that it, like others in the arrestin family, may bind to ... GRK1-dependent phosphorylation of S and M opsins and their binding to cone arrestin during cone phototransduction in the mouse ...
more infohttps://www.wikigenes.org/e/gene/e/407.html
  • The N-terminal domain consists of an immunoglobulin-like beta-sandwich structure and is found in arrestin and related proteins. (ebi.ac.uk)
  • For example he counts the accessory proteins arrestin and retinoid binding protein, but these can be completely absent in vertebrates with either no effect or mild night blindness eg. (wordnik.com)
  • Internalized arrestin-receptor complexes traffic to intracellular endosomes, where they remain uncoupled from G-proteins. (abcam.com)
  • βarrestins have an analogous function to rod arrestin in the termination of GPCR signaling by sterically inhibiting the coupling of phosphorylated receptors to their respective G proteins. (springer.com)
  • Additionally we are shipping Arrestin 3 Kits (40) and Arrestin 3 Proteins (8) and many more products for this protein. (antibodies-online.com)
  • Note that the majority of β-arrestin interaction partners are distributed in the cytoplasm but a significant fraction are nuclear proteins highlighting the potential nuclear roles of β-arrestins. (nih.gov)
  • The functional distribution of β-arrestin binding proteins highlights their major roles in cellular signaling, cellular organization and nucleic acid binding. (nih.gov)
  • Arrestins family contains four types of soluble cytoplasmic proteins that act as negative regulators of GPCR signaling, wherein, cognate ligand binding stimulates GPCR phosphorylation, followed by arrestin binding to phospho-GPCR leading to receptor internalization and ultimately, the desensitization of GPCR signaling. (novusbio.com)
  • S-arrestin is rod specific and constitutes major proteins of retinal rod outer segments and associate with photoactivated/phosphorylated rhodopsin, thereby preventing transducin-mediated phosphodiesterase activation. (novusbio.com)
  • These results reveal, at high resolution, a receptor-interacting interface on β-arrestin, and they indicate a potentially general molecular mechanism for activation of these multifunctional signalling and regulatory proteins. (nature.com)
  • 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. (ebi.ac.uk)
  • Class B receptors, like AVPR2, AGTR1, NTSR1, TRHR and TACR1 internalize as a complex with arrestin and traffic with it to endosomal vesicles, presumably as desensitized receptors, for extended periods of time. (abcam.com)
  • Arrestin beta 1 is a cytosolic protein and acts as a cofactor in the beta-adrenergic receptor kinase (BARK) mediated desensitization of beta-adrenergic receptors. (wikipedia.org)
  • Molecular mechanism of β-arrestin-biased agonism at seven-transmembrane receptors. (nih.gov)
  • It was first named β-arrestin simply because between two GPCRs available in purified form at the time, rhodopsin and β2-adrenergic receptor, it showed preference for the latter. (wikipedia.org)
  • The second non-visual arrestin cloned was first termed β-arrestin-2 (retroactively changing the name of β-arrestin into β-arrestin-1), even though by that time it was clear that non-visual arrestins interact with hundreds of different GPCRs, not just with β2-adrenergic receptor. (wikipedia.org)
  • First, arrestin binding to the cytoplasmic face of the receptor occludes the binding site for heterotrimeric G-protein, preventing its activation (desensitization). (wikipedia.org)
  • Second, arrestin links the receptor to elements of the internalization machinery, clathrin and clathrin adaptor AP2, which promotes receptor internalization via coated pits and subsequent transport to internal compartments, called endosomes. (wikipedia.org)
  • The strength of arrestin-receptor interaction plays a role in this choice: tighter complexes tend to increase the probability of receptor degradation (Class B), whereas more transient complexes favor recycling (Class A), although this "rule" is far from absolute. (wikipedia.org)
  • Receptor resensitization then requires that receptor-bound arrestin is removed so that the receptor can be dephosphorylated and returned to the plasma membrane. (abcam.com)
  • The PathHunter β-arrestin assays and reagents offer a powerful and universal screening and profiling platform that can be used for virtually any G i -, G s -, or G q -coupled receptor. (discoverx.com)
  • Recent evidence suggests that binding of agonist to its cognate receptor initiates not only classical G protein-mediated signaling, but also β-arrestin-dependent signaling. (pnas.org)
  • One such β-arrestin-mediated pathway uses the β 1 -adrenergic receptor (β 1 AR) to transactivate the EGFR. (pnas.org)
  • Pluridimensionality of β-arrestin-dependent signaling at seven-transmembrane receptor (7TMRs). (nih.gov)
  • Emerging paradigms of β-arrestin-dependent seven transmembrane receptor signaling. (nih.gov)
  • Here we report the crystal structure of β-arrestin-1 (also called arrestin-2) in complex with a fully phosphorylated 29-amino-acid carboxy-terminal peptide derived from the human V2 vasopressin receptor (V2Rpp). (nature.com)
  • For example, thioredoxin-interacting protein (TXNIP) matches the arrestin N domain [ PMID: 18664266 , PMID: 23519408 ]. (ebi.ac.uk)
  • The binding region for phosphorylated light-activated rhodopsin is located at the N-terminal domain, as indicated by the docking of the photoreceptor to the three-dimensional structure of arrestin. (ebi.ac.uk)
  • A 49-kilodalton phosphoprotein in the Drosophila photoreceptor is an arrestin homolog. (ebi.ac.uk)
  • This also turned out to be a misnomer: arrestin-1 expresses at comparable very high levels in both rod and cone photoreceptor cells. (wikipedia.org)
  • Arrestin-4 was cloned by two groups and termed cone arrestin, after photoreceptor type that expresses it, and X-arrestin, after the chromosome where its gene resides. (wikipedia.org)
  • Besides retinal rod photoreceptor cell outer segment, S-arrestin is also expressed in the pineal gland where its function is largely unknown. (novusbio.com)
  • Arrestin knockout mice develop photoreceptor cell degeneration because of continuous phototransduction upregulation, as a consequence of defective rhodopsin/opsin shut-off mechanism, and in human subjects, S-arrestin mutations have been linked to Oguchi disease and retinitis pigmentosa. (novusbio.com)
  • S-arrestin, also known as S-antigen, is a major soluble photoreceptor protein that is involved in desensitization of the photoactivated transduction cascade. (genetex.com)
  • Aspergillus nidulans PalF, a protein involved in the fungal ambient pH signaling pathway, contains arrestin N-terminal and C-terminal domains and binds strongly to two different regions within the C-terminal cytoplasmic tail of the 7TM, putative pH sensor PalH. (pnas.org)
  • On the origins of arrestin and rhodopsin. (ebi.ac.uk)
  • The systematic arrestin name (1-4) plus the most widely used aliases for each arrestin subtype are listed in bold below: Arrestin-1 was originally identified as the S-antigen (SAG) causing uveitis (autoimmune eye disease), then independently described as a 48 kDa protein that binds light-activated phosphorylated rhodopsin before it became clear that both are one and the same. (wikipedia.org)
  • Arrestin quenches G-protein activation by binding to phosphorylated photolyzed rhodopsin. (curehunter.com)
  • Two different modes of arrestin-mediated internalization occur. (abcam.com)
  • On www.antibodies-online.com are 98 Arrestin, beta 2 (ARRB2) Antibodies from 23 different suppliers available. (antibodies-online.com)
  • Additionally, S-arrestin is highly antigenic, and is capable of inducing experimental autoimmune uveoretinitis. (genetex.com)
  • Localization of the arrestin binding locus to the clathrin terminal domain, J Biol Chem 272 (23), 15017-15022(1997). (springer.com)
  • Alternatively spliced transcripts encoding different isoforms of arrestin beta 1 have been described, however, their exact functions are not known. (wikipedia.org)
  • We recently showed that β-arrestin can also mediate β 1 AR transactivation of the EGFR, resulting in a cardioprotective effect under conditions of chronic catecholamine stimulation ( 3 ). (pnas.org)
  • Mammals express four arrestin subtypes and each arrestin subtype is known by multiple aliases. (wikipedia.org)
  • The product comes with a complete set of retroparticles and reagents combined with an easy-to-follow protocol to help you generate your own β-arrestin cell-based assays. (discoverx.com)
  • Fungi have distant arrestin relatives involved in pH sensing. (wikipedia.org)
  • The β-arrestin recruitment assay followed by the second messenger (cAMP) assay were performed on the same cell line expressing human cholinergic muscarinic 2 (CHRM2) fused with PK. (discoverx.com)
  • Only using the β-arrestin recruitment assay (left) revealed the possible true partial agonist pharmacology for oxo-M due to the non-amplified signal nature of the β-arrestin pathway compared to the amplified G-protein dependent pathway (right). (discoverx.com)
  • β-Arrestin 1 and 2 (Barr1 and Barr2, respectively) are intracellular signaling molecules that regulate many important metabolic functions. (jci.org)
  • To determine whether β-adrenergic ligands that do not activate G protein signaling (i.e., β-blockers) can stabilize the β 1 AR in a signaling conformation, we screened 20 β-blockers for their ability to stimulate β-arrestin-mediated EGFR transactivation. (pnas.org)
  • This review focuses on one particular class of biased ligands that has the ability to alter the balance between G protein-dependent and β-arrestin-dependent signal transduction. (nih.gov)
  • Arrestin-subtypes in insect antennae. (ebi.ac.uk)