Arrestins. Medical search

Regulatory proteins that down-regulate phosphorylated G-protein membrane receptors, including rod and cone photoreceptors and adrenergic receptors.

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.

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.

A family of serine-threonine kinases that are specific for G-PROTEIN-COUPLED RECEPTORS. They are regulatory proteins that play a role in G-protein-coupled receptor densensitization.

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.

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.

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.

The largest family of cell surface receptors involved in SIGNAL TRANSDUCTION. They share a common structure and signal through HETEROTRIMERIC G-PROTEINS.

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.

A family of high molecular weight GTP phosphohydrolases that play a direct role in vesicle transport. They associate with microtubule bundles (MICROTUBULES) and are believed to produce mechanical force via a process linked to GTP hydrolysis. This enzyme was formerly listed as EC 3.6.1.50.

Cellular uptake of extracellular materials within membrane-limited vacuoles or microvesicles. ENDOSOMES play a central role in endocytosis.

Small oviparous fishes in the family Cyprinodontidae, usually striped or barred black. They are much used in mosquito control.

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.

The main structural coat protein of COATED VESICLES which play a key role in the intracellular transport between membranous organelles. Each molecule of clathrin consists of three light chains (CLATHRIN LIGHT CHAINS) and three heavy chains (CLATHRIN HEAVY CHAINS) that form a structure called a triskelion. Clathrin also interacts with cytoskeletal proteins.

A family of G-protein-coupled receptors that was originally identified by its ability to bind N-formyl peptides such as N-FORMYLMETHIONINE LEUCYL-PHENYLALANINE. Since N-formyl peptides are found in MITOCHONDRIA and BACTERIA, this class of receptors is believed to play a role in mediating cellular responses to cellular damage and bacterial invasion. However, non-formylated peptide ligands have also been found for this receptor class.

A G-protein-coupled receptor kinase subtype that is primarily expressed in the MYOCARDIUM and may play a role in the regulation of cardiac functions.

Eye proteins are the biological molecules that make up the various structures of the eye and are essential for its proper function.

CELL LINES derived from the CV-1 cell line by transformation with a replication origin defective mutant of SV40 VIRUS, which codes for wild type large T antigen (ANTIGENS, POLYOMAVIRUS TRANSFORMING). They are used for transfection and cloning. (The CV-1 cell line was derived from the kidney of an adult male African green monkey (CERCOPITHECUS AETHIOPS).)

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.

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.

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.

One of the two major classes of cholinergic receptors. Muscarinic receptors were originally defined by their preference for MUSCARINE over NICOTINE. There are several subtypes (usually M1, M2, M3....) that are characterized by their cellular actions, pharmacology, and molecular biology.

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.

The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.

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.

The process in which light signals are transformed by the PHOTORECEPTOR CELLS into electrical signals which can then be transmitted to the brain.

The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.

Established cell cultures that have the potential to propagate indefinitely.

The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.

Regulatory proteins that act as molecular switches. They control a wide range of biological processes including: receptor signaling, intracellular signal transduction pathways, and protein synthesis. Their activity is regulated by factors that control their ability to bind to and hydrolyze GTP to GDP. EC 3.6.1.-.

Substances that are recognized by the immune system and induce an immune reaction.

Specialized PHOTOTRANSDUCTION neurons in the vertebrates, such as the RETINAL ROD CELLS and the RETINAL CONE CELLS. Non-visual photoreceptor neurons have been reported in the deep brain, the PINEAL GLAND and organs of the circadian system.

A species of CERCOPITHECUS containing three subspecies: C. tantalus, C. pygerythrus, and C. sabeus. They are found in the forests and savannah of Africa. The African green monkey (C. pygerythrus) is the natural host of SIMIAN IMMUNODEFICIENCY VIRUS and is used in AIDS research.

The degree of similarity between sequences of amino acids. This information is useful for the analyzing genetic relatedness of proteins and species.

A form of fluorescent antibody technique commonly used to detect serum antibodies and immune complexes in tissues and microorganisms in specimens from patients with infectious diseases. The technique involves formation of an antigen-antibody complex which is labeled with fluorescein-conjugated anti-immunoglobulin antibody. (From Bennington, Saunders Dictionary & Encyclopedia of Laboratory Medicine and Technology, 1984)

Microscopy of specimens stained with fluorescent dye (usually fluorescein isothiocyanate) or of naturally fluorescent materials, which emit light when exposed to ultraviolet or blue light. Immunofluorescence microscopy utilizes antibodies that are labeled with fluorescent dye.

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.

Phosphoproteins are proteins that have been modified by the attachment of a phosphate group, which can regulate their activity and function in various cellular processes.

Recombinant proteins produced by the GENETIC TRANSLATION of fused genes formed by the combination of NUCLEIC ACID REGULATORY SEQUENCES of one or more genes with the protein coding sequences of one or more genes.

An E3 UBIQUITIN LIGASE that interacts with and inhibits TUMOR SUPPRESSOR PROTEIN P53. Its ability to ubiquitinate p53 is regulated by TUMOR SUPPRESSOR PROTEIN P14ARF.

The level of protein structure in which combinations of secondary protein structures (alpha helices, beta sheets, loop regions, and motifs) pack together to form folded shapes called domains. Disulfide bridges between cysteines in two different parts of the polypeptide chain along with other interactions between the chains play a role in the formation and stabilization of tertiary structure. Small proteins usually consist of only one domain but larger proteins may contain a number of domains connected by segments of polypeptide chain which lack regular secondary structure.

The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. PROTEIN STRUCTURE, QUATERNARY describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain).

Protein analogs and derivatives of the Aequorea victoria green fluorescent protein that emit light (FLUORESCENCE) when excited with ULTRAVIOLET RAYS. They are used in REPORTER GENES in doing GENETIC TECHNIQUES. Numerous mutants have been made to emit other colors or be sensitive to pH.

Commonly observed structural components of proteins formed by simple combinations of adjacent secondary structures. A commonly observed structure may be composed of a CONSERVED SEQUENCE which can be represented by a CONSENSUS SEQUENCE.

Genetically engineered MUTAGENESIS at a specific site in the DNA molecule that introduces a base substitution, or an insertion or deletion.

The parts of a macromolecule that directly participate in its specific combination with another molecule.

Cell surface proteins that bind signalling molecules external to the cell with high affinity and convert this extracellular event into one or more intracellular signals that alter the behavior of the target cell (From Alberts, Molecular Biology of the Cell, 2nd ed, pp693-5). Cell surface receptors, unlike enzymes, do not chemically alter their ligands.

Arrestin function in G protein-coupled receptor endocytosis requires phosphoinositide binding. (1/1016)

Internalization of agonist-activated G protein-coupled receptors is mediated by non-visual arrestins, which also bind to clathrin and are therefore thought to act as adaptors in the endocytosis process. Phosphoinositides have been implicated in the regulation of intracellular receptor trafficking, and are known to bind to other coat components including AP-2, AP180 and COPI coatomer. Given these observations, we explored the possibility that phosphoinositides play a role in arrestin's function as an adaptor. High-affinity binding sites for phosphoinositides in beta-arrestin (arrestin2) and arrestin3 (beta-arrestin2) were identified, and dissimilar effects of phosphoinositide and inositol phosphate on arrestin interactions with clathrin and receptor were characterized. Alteration of three basic residues in arrestin3 abolished phosphoinositide binding with complete retention of clathrin and receptor binding. Unlike native protein, upon agonist activation, this mutant arrestin3 expressed in COS1 cells neither supported beta2-adrenergic receptor internalization nor did it concentrate in coated pits, although it was recruited to the plasma membrane. These findings indicate that phosphoinositide binding plays a critical regulatory role in delivery of the receptor-arrestin complex to coated pits, perhaps by providing, with activated receptor, a multi-point attachment of arrestin to the plasma membrane. (+info)

Targeted construction of phosphorylation-independent beta-arrestin mutants with constitutive activity in cells. (2/1016)

Arrestin proteins play a key role in the desensitization of G protein-coupled receptors (GPCRs). Recently we proposed a molecular mechanism whereby arrestin preferentially binds to the activated and phosphorylated form of its cognate GPCR. To test the model, we introduced two different types of mutations into beta-arrestin that were expected to disrupt two crucial elements that make beta-arrestin binding to receptors phosphorylation-dependent. We found that two beta-arrestin mutants (Arg169 --> Glu and Asp383 --> Ter) (Ter, stop codon) are indeed "constitutively active." In vitro these mutants bind to the agonist-activated beta2-adrenergic receptor (beta2AR) regardless of its phosphorylation status. When expressed in Xenopus oocytes these beta-arrestin mutants effectively desensitize beta2AR in a phosphorylation-independent manner. Constitutively active beta-arrestin mutants also effectively desensitize delta opioid receptor (DOR) and restore the agonist-induced desensitization of a truncated DOR lacking the critical G protein-coupled receptor kinase (GRK) phosphorylation sites. The kinetics of the desensitization induced by phosphorylation-independent mutants in the absence of receptor phosphorylation appears identical to that induced by wild type beta-arrestin + GRK3. Either of the mutations could have occurred naturally and made receptor kinases redundant, raising the question of why a more complex two-step mechanism (receptor phosphorylation followed by arrestin binding) is universally used. (+info)

Real-time visualization of the cellular redistribution of G protein-coupled receptor kinase 2 and beta-arrestin 2 during homologous desensitization of the substance P receptor. (3/1016)

The substance P receptor (SPR) is a G protein-coupled receptor (GPCR) that plays a key role in pain regulation. The SPR desensitizes in the continued presence of agonist, presumably via mechanisms that implicate G protein-coupled receptor kinases (GRKs) and beta-arrestins. The temporal relationship of these proposed biochemical events has never been established for any GPCR other than rhodopsin beyond the resolution provided by biochemical assays. We investigate the real-time activation and desensitization of the human SPR in live HEK293 cells using green fluorescent protein conjugates of protein kinase C, GRK2, and beta-arrestin 2. The translocation of protein kinase C betaII-green fluorescent protein to and from the plasma membrane in response to substance P indicates that the human SPR becomes activated within seconds of agonist exposure, and the response desensitizes within 30 s. This desensitization process coincides with a redistribution of GRK2 from the cytosol to the plasma membrane, followed by a robust redistribution of beta-arrestin 2 and a profound change in cell morphology that occurs after 1 min of SPR stimulation. These data establish a role for GRKs and beta-arrestins in homologous desensitization of the SPR and provide the first visual and temporal resolution of the sequence of events underlying homologous desensitization of a GPCR in living cells. (+info)

Internalization of the TXA2 receptor alpha and beta isoforms. Role of the differentially spliced cooh terminus in agonist-promoted receptor internalization. (4/1016)

Thromboxane A2 (TXA2) potently stimulates platelet aggregation and smooth muscle constriction and is thought to play a role in myocardial infarction, atherosclerosis, and bronchial asthma. The TXA2 receptor (TXA2R) is a member of the G protein-coupled receptor family and is found as two alternatively spliced isoforms, alpha (343 residues) and beta (407 residues), which share the first 328 residues. In the present report, we demonstrate by enzyme-linked immunosorbent assay and immunofluorescence microscopy that the TXA2Rbeta, but not the TXA2Ralpha, undergoes agonist-induced internalization when expressed in HEK293 cells as well as several other cell types. Various dominant negative mutants were used to demonstrate that the internalization of the TXA2Rbeta is dynamin-, GRK-, and arrestin-dependent in HEK293 cells, suggesting the involvement of receptor phosphorylation and clathrin-coated pits in this process. Interestingly, the agonist-stimulated internalization of both the alpha and beta isoforms, but not of a mutant truncated after residue 328, can be promoted by overexpression of arrestin-3, identifying the C-tails of both receptors as necessary in arrestin-3 interaction. Simultaneous mutation of two dileucine motifs in the C-tail of TXA2Rbeta did not affect agonist-promoted internalization. Analysis of various C-tail deletion mutants revealed that a region between residues 355 and 366 of the TXA2Rbeta is essential for agonist-promoted internalization. These data demonstrate that alternative splicing of the TXA2R plays a critical role in regulating arrestin binding and subsequent receptor internalization. (+info)

The absence of a direct correlation between the loss of [D-Ala2, MePhe4,Gly5-ol]Enkephalin inhibition of adenylyl cyclase activity and agonist-induced mu-opioid receptor phosphorylation. (5/1016)

Chronic activation of the mu-opioid receptor (MOR1TAG) results in the loss of agonist response that has been attributed to desensitization and down-regulation of the receptor. It has been suggested that opioid receptor phosphorylation is the mechanism by which this desensitization and down-regulation occurs. When MOR1TAG was stably expressed in both neuroblastoma neuro2A and human embryonic kidney HEK293 cells, the opioid agonist [D-Ala2,MePhe4, Gly5-ol]enkephalin (DAMGO) induced a time- and concentration-dependent phosphorylation of the receptor, in both cell lines, that could be reversed by the antagonist naloxone. Protein kinase C can phosphorylate the receptor, but is not involved in DAMGO-induced MOR1TAG phosphorylation. The rapid rate of receptor phosphorylation, occurring within minutes, did not correlate with the rate of the loss of agonist-mediated inhibition of adenylyl cyclase, which occurs in hours. This lack of correlation between receptor phosphorylation and the loss of response was further demonstrated when receptor phosphorylation was increased by either calyculin A or overexpression of the G-protein receptor kinases. Calyculin A increased the magnitude of MOR1TAG phosphorylation without altering the DAMGO-induced loss of the adenylyl cyclase response. Similarly, when mu- and delta-opioid (DOR1TAG) receptors were expressed in the same system, overexpression of beta-adrenergic receptor kinase 2 elevated agonist-induced phosphorylation for both receptors. However, in the same cell lines under the same conditions, overexpression of beta-adrenergic receptor kinase 2 and beta-arrestin 2 accelerated the rate of DPDPE- but not DAMGO-induced receptor desensitization. Thus, these data show that phosphorylation of MOR1TAG is not an obligatory event for the DAMGO-induced loss in the adenylyl cyclase regulation by the receptor. (+info)

Decreased expression and activity of G-protein-coupled receptor kinases in peripheral blood mononuclear cells of patients with rheumatoid arthritis. (6/1016)

Beta2-Adrenergic and chemokine receptor antagonists delay the onset and reduce the severity of joint injury in rheumatoid arthritis. beta2-Adrenergic and chemokine receptors belong to the G-protein-coupled receptor family whose responsiveness is turned off by the G-protein-coupled receptor kinase family (GRK-1 to 6). GRKs phosphorylate receptors in an agonist-dependent manner resulting in receptor/G-protein uncoupling via subsequent binding of arrestin proteins. We assessed the activity of GRKs in lymphocytes of rheumatoid arthritis (RA) patients by rhodopsin phosphorylation. We found a significant decrease in GRK activity in RA subjects that is mirrored by a decrease in GRK-2 protein expression. Moreover, GRK-6 protein expression is reduced in RA patients whereas GRK-5 protein levels were unchanged. In search of an underlying mechanism, we demonstrated that proinflammatory cytokines induce a decrease in GRK-2 protein levels in leukocytes from healthy donors. Since proinflammatory cytokines are abundantly expressed in RA, it may provide an explanation for the decrease in GRK-2 expression and activity in patients. No changes in beta2-adrenergic receptor number and Kd were detected. However, RA patients showed a significantly increased cAMP production and inhibition of TNF-alpha production by beta2-adrenergic stimulation, suggesting that reduced GRK activity is associated with increased sensitivity to beta2-adrenergic activation. (+info)

The beta2-adrenergic receptor/betaarrestin complex recruits the clathrin adaptor AP-2 during endocytosis. (7/1016)

betaarrestins mediate the desensitization of the beta2-adrenergic receptor (beta2AR) and many other G protein-coupled receptors (GPCRs). Additionally, betaarrestins initiate the endocytosis of these receptors via clathrin coated-pits and interact directly with clathrin. Consequently, it has been proposed that betaarrestins serve as clathrin adaptors for the GPCR family by linking these receptors to clathrin lattices. AP-2, the heterotetrameric clathrin adaptor protein, has been demonstrated to mediate the internalization of many types of plasma membrane proteins other than GPCRs. AP-2 interacts with the clathrin heavy chain and cytoplasmic domains of receptors such as those for epidermal growth factor and transferrin. In the present study we demonstrate the formation of an agonist-induced multimeric complex containing a GPCR, betaarrestin 2, and the beta2-adaptin subunit of AP-2. beta2-Adaptin binds betaarrestin 2 in a yeast two-hybrid assay and coimmunoprecipitates with betaarrestins and beta2AR in an agonist-dependent manner in HEK-293 cells. Moreover, beta2-adaptin translocates from the cytosol to the plasma membrane in response to the beta2AR agonist isoproterenol and colocalizes with beta2AR in clathrin-coated pits. Finally, expression of betaarrestin 2 minigene constructs containing the beta2-adaptin interacting region inhibits beta2AR endocytosis. These findings point to a role for AP-2 in GPCR endocytosis, and they suggest that AP-2 functions as a clathrin adaptor for the endocytosis of diverse classes of membrane receptors. (+info)

Identification of NSF as a beta-arrestin1-binding protein. Implications for beta2-adrenergic receptor regulation. (8/1016)

Previous studies have demonstrated that beta-arrestin1 serves to target G protein-coupled receptors for internalization via clathrin-coated pits and that its endocytic function is regulated by dephosphorylation at the plasma membrane. Using the yeast two-hybrid system, we have identified a novel beta-arrestin1-binding protein, NSF (N-ethylmaleimide-sensitive fusion protein), an ATPase essential for many intracellular transport reactions. We demonstrate that purified recombinant beta-arrestin1 and NSF interact in vitro and that these proteins can be coimmunoprecipitated from cells. beta-Arrestin1-NSF complex formation exhibits a conformational dependence with beta-arrestin1 preferentially interacting with the ATP bound form of NSF. In contrast to the beta-arrestin1-clathrin interaction, however, the phosphorylation state of beta-arrestin1 does not affect NSF binding. Functionally, overexpression of NSF in HEK 293 cells significantly enhances agonist-mediated beta2-adrenergic receptor (beta2-AR) internalization. Furthermore, when coexpressed with a beta-arrestin1 mutant (betaarr1S412D) that mimics a constitutively phosphorylated form of beta-arrestin1 and that acts as a dominant negative with regards to beta2-AR internalization, NSF rescues the betaarr1S412D-mediated inhibition of beta2-AR internalization. The demonstration of beta-arrestin1-NSF complex formation and the functional consequences of NSF overexpression suggest a hitherto unappreciated role for NSF in facilitating clathrin coat-mediated G protein-coupled receptor internalization. (+info)

Arrestins are a family of proteins that play a role in regulating the activity of G protein-coupled receptors (GPCRs) in the cell. They are named for their ability to "arrest" or stop the activity of GPCRs after they have been activated by a signaling molecule such as a hormone or neurotransmitter. When a GPCR is activated, it triggers a signaling cascade that can lead to a variety of cellular responses. Arrestins bind to the activated GPCR and prevent it from interacting with other signaling molecules, effectively turning off the signaling cascade. This allows the cell to quickly reset the receptor and prepare for the next signaling event. Arrestins also play a role in the internalization of GPCRs, which is the process by which the receptors are removed from the cell surface and transported to the cell's interior. This can help to regulate the availability of GPCRs on the cell surface and prevent overstimulation of the receptor. Arrestins are found in a variety of organisms, including humans, and are involved in a wide range of physiological processes, including vision, metabolism, and the immune response. They are also the targets of several drugs, including some used to treat conditions such as diabetes and obesity.

Arrestin is a protein that plays a role in regulating the activity of certain receptors in the cell. It is involved in the process of desensitization, which is the decrease in the responsiveness of a receptor to its ligand (the molecule that binds to the receptor and triggers a response). Arrestin helps to internalize and degrade receptors that have been activated by their ligands, which prevents them from continuing to respond to the ligand. This process is important for maintaining the proper functioning of cells and for preventing overstimulation of receptors. Arrestins are found in a variety of cells and are involved in regulating the activity of a number of different receptors, including those for hormones, neurotransmitters, and sensory stimuli.

Mitogen-Activated Protein Kinase 10 (MAPK10), also known as p38γ, is a protein kinase enzyme that plays a role in cellular signaling pathways. It is a member of the mitogen-activated protein kinase (MAPK) family, which is involved in regulating various cellular processes such as cell growth, differentiation, and apoptosis. MAPK10 is activated by various extracellular stimuli, including cytokines, growth factors, and stress signals. Once activated, it phosphorylates and regulates the activity of downstream target proteins, including transcription factors and other signaling molecules. In the medical field, MAPK10 has been implicated in various diseases and conditions, including cancer, inflammatory disorders, and neurodegenerative diseases. For example, dysregulation of MAPK10 signaling has been observed in several types of cancer, including breast, lung, and colon cancer, and may contribute to tumor growth and progression. Additionally, MAPK10 has been shown to play a role in the regulation of immune responses and may be involved in the pathogenesis of inflammatory disorders such as rheumatoid arthritis and psoriasis. Finally, MAPK10 has been implicated in the development of neurodegenerative diseases such as Alzheimer's and Parkinson's disease, and may contribute to the progression of these conditions by regulating the activity of proteins involved in neuronal function and survival.

G-protein-coupled receptor kinases (GRKs) are a family of enzymes that play a critical role in regulating the function of G-protein-coupled receptors (GPCRs) in the human body. GPCRs are a large group of cell surface receptors that are activated by a variety of extracellular signals, including hormones, neurotransmitters, and sensory stimuli. When a GPCR is activated, it triggers a signaling cascade that ultimately leads to a cellular response. GRKs are activated by phosphorylation, which allows them to bind to and phosphorylate activated GPCRs. This phosphorylation event leads to the internalization of the receptor from the cell surface, which in turn terminates the signaling cascade and desensitizes the receptor to further activation. This process is an important mechanism for regulating the activity of GPCRs and preventing overstimulation of the cell. GRKs are involved in a wide range of physiological processes, including vision, hearing, smell, taste, and the regulation of blood pressure, heart rate, and other cardiovascular functions. Mutations in GRK genes have been linked to a number of human diseases, including cardiovascular disease, diabetes, and certain types of cancer.

Rhodopsin is a protein found in the retina of the eye that is responsible for the process of vision in low light conditions. It is a type of photopigment that is sensitive to light in the short-wavelength region of the visible spectrum, which corresponds to blue and violet light. When light strikes the rhodopsin molecules, it causes a chemical change in the protein that triggers a series of events that ultimately leads to the transmission of visual information to the brain. Rhodopsin is essential for night vision and plays a critical role in the early stages of the visual process.

Receptors, Adrenergic, beta-2 (β2-adrenergic receptors) are a type of protein found on the surface of cells in the body that bind to and respond to the hormone adrenaline (also known as epinephrine). These receptors are part of the adrenergic receptor family, which also includes alpha-adrenergic receptors (α-adrenergic receptors). β2-adrenergic receptors are found in many different tissues throughout the body, including the lungs, heart, and blood vessels. When adrenaline binds to these receptors, it triggers a series of chemical reactions within the cell that can have a variety of effects, depending on the tissue type and the specific receptor subtype. In the lungs, activation of β2-adrenergic receptors can cause bronchodilation, which is the widening of the airways and can help to improve breathing. In the heart, activation of these receptors can increase heart rate and contractility, which can help to improve blood flow. In the blood vessels, activation of β2-adrenergic receptors can cause vasodilation, which is the widening of blood vessels and can help to lower blood pressure. β2-adrenergic receptors are also important in the body's response to stress. When the body is under stress, the adrenal gland releases adrenaline, which binds to these receptors and triggers the body's "fight or flight" response. This response can help the body to prepare for physical activity and to respond to potential threats. In the medical field, β2-adrenergic receptors are the target of many medications, including bronchodilators used to treat asthma and other respiratory conditions, and beta blockers used to treat high blood pressure and other cardiovascular conditions.

G-Protein-Coupled Receptor Kinase 3 (GRK3) is a protein that plays a role in regulating the activity of G-protein-coupled receptors (GPCRs) in the body. GPCRs are a large family of cell surface receptors that are activated by a variety of extracellular signals, such as hormones, neurotransmitters, and sensory stimuli. When a GPCR is activated, it triggers a cascade of intracellular events that ultimately lead to a cellular response. GRK3 is a type of protein kinase that phosphorylates activated GPCRs, which in turn leads to the internalization of the receptor and its degradation. This process is an important mechanism for regulating the activity of GPCRs and preventing overstimulation of the cell. Dysregulation of GRK3 activity has been implicated in a number of diseases, including cardiovascular disease, neurological disorders, and cancer.

Receptors, G-Protein-Coupled (GPCRs) are a large family of membrane proteins that play a crucial role in transmitting signals from the outside of a cell to the inside. They are found in almost all types of cells and are involved in a wide range of physiological processes, including sensory perception, neurotransmission, and hormone signaling. GPCRs are activated by a variety of molecules, including neurotransmitters, hormones, and sensory stimuli such as light, sound, and odor. When a molecule binds to a GPCR, it causes a conformational change in the protein that activates a G protein, a small molecule that acts as a molecular switch. The activated G protein then triggers a cascade of intracellular signaling events that ultimately lead to a cellular response. Because GPCRs are involved in so many different physiological processes, they are an important target for drug discovery. Many drugs, including those used to treat conditions such as hypertension, depression, and allergies, work by binding to specific GPCRs and modulating their activity.

G-Protein-Coupled Receptor Kinase 2 (GRK2) is a protein that plays a role in regulating the activity of G-protein-coupled receptors (GPCRs) in the human body. GPCRs are a large family of cell surface receptors that are activated by a variety of extracellular signals, such as hormones, neurotransmitters, and sensory stimuli. When a GPCR is activated, it triggers a cascade of intracellular signaling events that ultimately lead to changes in cell behavior. GRK2 is a type of protein kinase that phosphorylates activated GPCRs, which in turn leads to the internalization of the receptor from the cell surface. This process is an important mechanism for regulating the activity of GPCRs and preventing overstimulation of the cell. Dysregulation of GRK2 activity has been implicated in a number of diseases, including cardiovascular disease, diabetes, and certain types of cancer.

Dynamins are a family of GTPases that play important roles in various cellular processes, including endocytosis, exocytosis, vesicle trafficking, and intracellular signaling. They are characterized by their ability to hydrolyze GTP (guanosine triphosphate) and are involved in the regulation of membrane dynamics and the formation of vesicles. In the medical field, dynamins are of interest because they have been implicated in a number of diseases, including neurodegenerative disorders such as Alzheimer's and Parkinson's disease, as well as certain types of cancer.

G-Protein-Coupled Receptor Kinase 1 (GRK1) is a protein that plays a role in regulating the activity of G-protein-coupled receptors (GPCRs) in the human body. GPCRs are a large family of cell surface receptors that are activated by a variety of extracellular signals, such as hormones, neurotransmitters, and sensory stimuli. When a GPCR is activated, it triggers a cascade of intracellular events that ultimately lead to a cellular response. GRK1 is a member of a family of enzymes called G-protein-coupled receptor kinases (GRKs) that phosphorylate activated GPCRs, which in turn leads to the internalization and degradation of the receptor. This process helps to regulate the activity of GPCRs and prevent overstimulation of the cell. GRK1 has been implicated in a number of physiological processes, including vision, hearing, and the regulation of blood pressure. It has also been linked to a number of diseases, including cardiovascular disease, diabetes, and certain types of cancer.

Clathrin is a protein that plays a crucial role in the process of endocytosis, which is the process by which cells take in substances from their environment. Clathrin forms a lattice-like structure that surrounds and helps to shape the plasma membrane as it buds inward to form a vesicle. This vesicle then pinches off from the plasma membrane and is transported into the cell, where it can be processed and used by the cell. Clathrin is also involved in the transport of certain molecules within the cell, such as the transport of proteins from the Golgi apparatus to the plasma membrane. In the medical field, clathrin is often studied in relation to diseases such as cancer, where it has been implicated in the formation of abnormal blood vessels and the spread of cancer cells.

Receptors, Formyl Peptide are a type of protein receptors found on the surface of immune cells, such as neutrophils and macrophages. These receptors are activated by the presence of formylated peptides, which are a type of amino acid sequence found on the N-terminus of certain bacterial proteins. Activation of these receptors triggers a signaling cascade that leads to the recruitment and activation of immune cells at the site of infection, helping to mount an immune response against the invading bacteria.

G-Protein-Coupled Receptor Kinase 5 (GRK5) is a protein that plays a role in regulating the activity of G-protein-coupled receptors (GPCRs) in the body. GPCRs are a large family of cell surface receptors that are activated by a variety of extracellular signals, such as hormones, neurotransmitters, and sensory stimuli. When a GPCR is activated, it triggers a cascade of intracellular events that ultimately lead to a cellular response. GRK5 is a member of a family of enzymes called G-protein-coupled receptor kinases (GRKs) that phosphorylate activated GPCRs, which in turn leads to the internalization and degradation of the receptor. This process helps to regulate the activity of GPCRs and prevent overstimulation of the cell. GRK5 has been implicated in a number of physiological processes, including the regulation of cardiovascular function, the control of blood pressure, and the modulation of pain perception. It has also been linked to a number of diseases, including hypertension, heart failure, and chronic pain.

Eye proteins are proteins that are found in the eye and play important roles in maintaining the structure and function of the eye. These proteins can be found in various parts of the eye, including the cornea, lens, retina, and vitreous humor. Some examples of eye proteins include: 1. Collagen: This is a protein that provides strength and support to the cornea and lens. 2. Alpha-crystallin: This protein is found in the lens and helps to maintain its shape and transparency. 3. Rhodopsin: This protein is found in the retina and is responsible for vision in low light conditions. 4. Vitreous humor proteins: These proteins are found in the vitreous humor, a clear gel-like substance that fills the space between the lens and the retina. They help to maintain the shape of the eye and provide support to the retina. Disruptions in the production or function of these proteins can lead to various eye diseases and conditions, such as cataracts, glaucoma, and age-related macular degeneration. Therefore, understanding the structure and function of eye proteins is important for the development of effective treatments for these conditions.

Receptors, Muscarinic are a type of cell surface receptors that are activated by the neurotransmitter acetylcholine. They are found in various tissues throughout the body, including the heart, lungs, digestive system, and central nervous system. There are five subtypes of muscarinic receptors, designated M1 through M5, each with different properties and functions. Activation of muscarinic receptors can produce a wide range of effects, including contraction of smooth muscle, stimulation of glandular secretion, and modulation of neurotransmitter release. In the medical field, muscarinic receptors are important targets for the treatment of various conditions, including asthma, irritable bowel syndrome, and certain types of heart disease. Drugs that interact with muscarinic receptors are often referred to as muscarinic agonists or antagonists, depending on whether they stimulate or block the activity of the receptors.

GTP-binding proteins, also known as G proteins, are a family of proteins that play a crucial role in signal transduction in cells. They are involved in a wide range of cellular processes, including cell growth, differentiation, and metabolism. G proteins are composed of three subunits: an alpha subunit, a beta subunit, and a gamma subunit. The alpha subunit is the one that binds to guanosine triphosphate (GTP), a molecule that is involved in regulating the activity of the protein. When GTP binds to the alpha subunit, it causes a conformational change in the protein, which in turn activates or inhibits downstream signaling pathways. G proteins are activated by a variety of extracellular signals, such as hormones, neurotransmitters, and growth factors. Once activated, they can interact with other proteins in the cell, such as enzymes or ion channels, to transmit the signal and initiate a cellular response. G proteins are found in all eukaryotic cells and play a critical role in many physiological processes. They are also involved in a number of diseases, including cancer, neurological disorders, and cardiovascular diseases.

Phosphoproteins are proteins that have been modified by the addition of a phosphate group to one or more of their amino acid residues. This modification is known as phosphorylation, and it is a common post-translational modification that plays a critical role in regulating many cellular processes, including signal transduction, metabolism, and gene expression. Phosphoproteins are involved in a wide range of biological functions, including cell growth and division, cell migration and differentiation, and the regulation of gene expression. They are also involved in many diseases, including cancer, diabetes, and cardiovascular disease. Phosphoproteins can be detected and studied using a variety of techniques, including mass spectrometry, Western blotting, and immunoprecipitation. These techniques allow researchers to identify and quantify the phosphorylation status of specific proteins in cells and tissues, and to study the effects of changes in phosphorylation on protein function and cellular processes.

Recombinant fusion proteins are proteins that are produced by combining two or more genes in a single molecule. These proteins are typically created using genetic engineering techniques, such as recombinant DNA technology, to insert one or more genes into a host organism, such as bacteria or yeast, which then produces the fusion protein. Fusion proteins are often used in medical research and drug development because they can have unique properties that are not present in the individual proteins that make up the fusion. For example, a fusion protein might be designed to have increased stability, improved solubility, or enhanced targeting to specific cells or tissues. Recombinant fusion proteins have a wide range of applications in medicine, including as therapeutic agents, diagnostic tools, and research reagents. Some examples of recombinant fusion proteins used in medicine include antibodies, growth factors, and cytokines.

Proto-oncogene proteins c-mdm2 are a family of proteins that play a role in regulating the activity of the tumor suppressor protein p53. p53 is a transcription factor that is activated in response to cellular stress, such as DNA damage or oncogene activation, and helps to prevent the development of cancer by promoting cell cycle arrest, apoptosis (programmed cell death), and DNA repair. Proto-oncogene proteins c-mdm2 can bind to and inhibit the activity of p53, thereby preventing it from carrying out its tumor suppressor functions. This can contribute to the development of cancer by allowing cells with damaged DNA to continue to divide and proliferate. Proto-oncogene proteins c-mdm2 are therefore considered to be oncogenes, which are genes that have the potential to cause cancer.

Green Fluorescent Proteins (GFPs) are a class of proteins that emit green light when excited by blue or ultraviolet light. They were first discovered in the jellyfish Aequorea victoria and have since been widely used as a tool in the field of molecular biology and bioimaging. In the medical field, GFPs are often used as a marker to track the movement and behavior of cells and proteins within living organisms. For example, scientists can insert a gene for GFP into a cell or organism, allowing them to visualize the cell or protein in real-time using a fluorescent microscope. This can be particularly useful in studying the development and function of cells, as well as in the diagnosis and treatment of diseases. GFPs have also been used to develop biosensors, which can detect the presence of specific molecules or changes in cellular environment. For example, researchers have developed GFP-based sensors that can detect the presence of certain drugs or toxins, or changes in pH or calcium levels within cells. Overall, GFPs have become a valuable tool in the medical field, allowing researchers to study cellular processes and diseases in new and innovative ways.

Receptors, cell surface are proteins that are located on the surface of cells and are responsible for receiving signals from the environment. These signals can be chemical, electrical, or mechanical in nature and can trigger a variety of cellular responses. There are many different types of cell surface receptors, including ion channels, G-protein coupled receptors, and enzyme-linked receptors. These receptors play a critical role in many physiological processes, including sensation, communication, and regulation of cellular activity. In the medical field, understanding the function and regulation of cell surface receptors is important for developing new treatments for a wide range of diseases and conditions.

... -3. The second non-visual arrestin cloned was first termed β-arrestin-2 (retroactively changing the name of β-arrestin ... In mammals, arrestin-1 and arrestin-4 are largely confined to photoreceptors, whereas arrestin-2 and arrestin-3 are ubiquitous ... Arrestin-2 was the first non-visual arrestin cloned. It was first named β-arrestin simply because of the two GPCRs available in ... Arrestin-4 was cloned by two groups and termed cone arrestin, after photoreceptor type that expresses it, and X-arrestin, after ...

https://en.wikipedia.org/wiki/Arrestin

... β-arrestins (also referred to as visual and non-visual arrestins) and Vps26-like arrestins proteins. The α-Arrestins are an ... The arrestin family of proteins is subdivided into α-arrestins (also referred to as arrestin-related trafficking adaptors (ARTs ... It is unclear if α-arrestins lack each of these structural features thought to distinguish the β-arrestins from the α-arrestins ... β-arrestins contain a polar core flanked on both sides by the arrestin N- and C-terminal fold domains. They also contain ...

https://en.wikipedia.org/wiki/Alpha_Arrestin

Beta-arrestin-2, also known as arrestin beta-2, is an intracellular protein that in humans is encoded by the ARRB2 gene. ... Arrestin beta 2 is crucial for the development of tolerance to morphine and other opioids. Arrestin beta 2 has been shown to ... Arrestin beta 2, like arrestin beta 1, was shown to inhibit beta-adrenergic receptor function in vitro. It is expressed at high ... Members of arrestin/beta-arrestin protein family are thought to participate in agonist-mediated desensitization of G protein- ...

https://en.wikipedia.org/wiki/Arrestin_beta_2

Arrestin, beta 1, also known as ARRB1, is a protein which in humans is encoded by the ARRB1 gene. Members of arrestin/beta- ... "Entrez Gene: ARRB1 arrestin, beta 1". Peterson YK, Luttrell LM (July 2017). "The Diverse Roles of Arrestin Scaffolds in G ... "Substance P-induced trafficking of beta-arrestins. The role of beta-arrestins in endocytosis of the neurokinin-1 receptor". The ... Beta-arrestin has been shown to play a role as a scaffold that binds intermediates and may direct G-protein signaling by ...

https://en.wikipedia.org/wiki/Arrestin_beta_1

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

https://en.wikipedia.org/wiki/CLTC

Differential regulation of beta-arrestins 1 and 2". The Journal of Biological Chemistry. 277 (52): 50422-30. doi:10.1074/jbc. ...

https://en.wikipedia.org/wiki/Thyrotropin-releasing_hormone_receptor

S-arrestin is a protein that in humans is encoded by the SAG gene. Members of arrestin/beta-arrestin protein family are thought ... 1995). "Chromosome mapping of the human arrestin (SAG), beta-arrestin 2 (ARRB2), and beta-adrenergic receptor kinase 2 (ADRBK2 ... S-arrestin, also known as S-antigen, is a major soluble protein in photoreceptor cells that is involved in desensitization of ... Additionally, S-arrestin is highly antigenic, and is capable of inducing experimental autoimmune uveoretinitis. Mutations in ...

https://en.wikipedia.org/wiki/SAG_(gene)

Moreover Arrestin binding to a phosphorylated, active receptor also enables receptor signaling through arrestin partner ... which promotes the binding of an arrestin protein to the receptor. Arrestin binding to a phosphorylated, active receptor ... Consequently the GRK/arrestin system serves as a signaling switch for G protein-coupled receptors. GRK4 is most highly ... Gurevich VV, Gurevich EV (2019). "GPCR Signaling Regulation: The Role of GRKs and Arrestins". Front Pharmacol. 10: 125. doi: ...

https://en.wikipedia.org/wiki/GRK4

Arrestin binding to phosphorylated, active receptor also enables receptor signaling through arrestin partner proteins. Thus the ... which promotes the binding of an arrestin protein to the receptor. Arrestin binding to phosphorylated, active receptor prevents ... Arrestin binding also directs receptors to specific cellular internalization pathways, removing the receptors from the cell ... Gurevich VV, Gurevich EV (2019). "GPCR Signaling Regulation: The Role of GRKs and Arrestins". Front Pharmacol. 10: 125. doi: ...

https://en.wikipedia.org/wiki/G_protein-coupled_receptor_kinase_2

Arrestin binding to phosphorylated, active receptor also enables receptor signaling through arrestin partner proteins. Thus the ... which promotes the binding of an arrestin protein to the receptor. Arrestin binding to phosphorylated, active receptor prevents ... Arrestin binding also directs receptors to specific cellular internalization pathways, removing the receptors from the cell ... GRK5 and the closely related GRK6 phosphorylate receptors at sites that encourage arrestin-mediated signaling rather than ...

https://en.wikipedia.org/wiki/GRK5

Arrestin binding to phosphorylated, active receptor also enables receptor signaling through arrestin partner proteins. As a ... which promotes the binding of an arrestin protein to the receptor. Arrestin binding to phosphorylated, active receptor prevents ... "Chromosome mapping of the human arrestin (SAG), beta-arrestin 2 (ARRB2), and beta-adrenergic receptor kinase 2 (ADRBK2) genes ... Feng YH, Wang L, Wang Q, Li X, Zeng R, Gorodeski GI (June 2005). "ATP stimulates GRK-3 phosphorylation and beta-arrestin-2- ...

https://en.wikipedia.org/wiki/G_protein-coupled_receptor_kinase_3

Arrestin binding to phosphorylated, active receptor also enables receptor signaling through arrestin partner proteins. Thus the ... Phosphorylated serine and threonine residues in GPCRs act as binding sites for and activators of arrestin proteins. Arrestin ... also known as arrestin-4 or X-arrestin. GRK2 was first identified as an enzyme that phosphorylated the beta-2 adrenergic ... Arrestin binding also directs receptors to specific cellular internalization pathways, removing the receptors from the cell ...

https://en.wikipedia.org/wiki/G_protein-coupled_receptor_kinase

https://en.wikipedia.org/wiki/GRK6

Crystal structure of rhodopsin bound to arrestin determined by femtosecond X-ray laser Nature 526: 561-567 T. Hua, K. Vemuri, M ... and the human Rhodopsin-Arrestin complex. 2016: The marijuana receptor-human Cannabinoid receptor type 1 (CB1) and the human C- ...

https://en.wikipedia.org/wiki/Raymond_C._Stevens

Bruchas MR, Macey TA, Lowe JD, Chavkin C (June 2006). "Kappa opioid receptor activation of p38 MAPK is GRK3- and arrestin- ... β-arrestin antagonist Nalfurafine (Remitch), which was introduced in 2009, is the first selective KOR agonist to enter clinical ... β-arrestin antagonist Zyklophin - selective peptide antagonist; dynorphin A analogue KSC-12-192 - selective, biased ligand: G ... β-arrestin antagonist Amentoflavone - non-selective; naturally-occurring AT-076 - non-selective, likely long acting; JDTic ...

https://en.wikipedia.org/wiki/Κ-opioid_receptor

... which has been observed for arrestins. Moreover, Vps26 does not have similar sequences as arrestins for GPCR and phospholipid ... Both Vps26 and arrestins are composed of two structurally related β-sheet domains forming extensive interfaces with each other ... Vps26 is a 38-kDa subunit that has a two-lobed structure with a polar core that resembles the arrestin family of trafficking ... Shi H, Rojas R, Bonifacino JS, Hurley JH (2006). "The retromer subunit Vps26 has an arrestin fold and binds Vps35 through its C ...

https://en.wikipedia.org/wiki/VPS26A

"Prolonged photoresponses in transgenic mouse rods lacking arrestin". Nature. 389 (6650): 505-509. Bibcode:1997Natur.389..505X. ...

https://en.wikipedia.org/wiki/Denis_Baylor

Unlike most μ-opioid receptor agonists, herkinorin does not promote the recruitment of β-arrestin 2 to the intracellular domain ... April 2008). "Herkinorin analogues with differential beta-arrestin-2 interactions". Journal of Medicinal Chemistry. 51 (8): ... arrestin interactions or receptor internalization". Molecular Pharmacology. 71 (2): 549-57. doi:10.1124/mol.106.028258. PMC ... and some other analogues related to herkinorin can recruit β-arrestins. Kurkinorin Salvinorin B methoxymethyl ether RB-64 ...

https://en.wikipedia.org/wiki/Herkinorin

2006). "Stable rhodopsin/arrestin complex leads to retinal degeneration in a transgenic mouse model of autosomal dominant ... In this research null mutations in the rhodopsin kinase and arrestin genes, each of which plays a role in terminating rhodopsin ... Besides this, the stable rhodopsin and arrestin complexes are shown to mislocalize and accumulate in the inner segments of rod ... The R135 mutant rhodopsin is noted to form stable complex with arrestin and undergo endocytosis resulting in aberrant endocytic ...

https://en.wikipedia.org/wiki/Retinal_degeneration_(rhodopsin_mutation)

While it binds to the same receptors as opioid analgesics, TRV734 has very weak β-arrestin recruitment, unlike other available ... 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 ... but Trevena hopes to avoid this with TRV250 by bypassing the β-arrestin pathway. TRV734 is an oral follow-up to the injected ...

https://en.wikipedia.org/wiki/Trevena_Inc

"S-Nitrosylation of β-Arrestins Biases Receptor Signaling and Confers Ligand Independence". Mol Cell. 70 (3): 473-487. doi: ...

https://en.wikipedia.org/wiki/Jonathan_Stamler

DeGraff JL, Gagnon AW, Benovic JL, Orsini MJ (1999). "Role of arrestins in endocytosis and signaling of alpha2-adrenergic ...

https://en.wikipedia.org/wiki/Alpha-2C_adrenergic_receptor

"Spatial regulation of GPR64/ADGRG2 signaling by β-arrestins and GPCR kinases". Annals of the New York Academy of Sciences. 1456 ...

https://en.wikipedia.org/wiki/GPR64

Kim Y, Kim H, Lee J, Lee JK, Min SJ, Seong J, Rhim H, Tae J, Lee HJ, Choo H (August 2018). "Discovery of β-Arrestin Biased ... beta-arrestin recruitment, and receptor internalization. Inactivating antagonists all likely interact with the 5-HT7 receptor ... role of G protein-coupled receptor kinases and arrestins in receptor desensitization and resensitization". Receptors & Channels ...

https://en.wikipedia.org/wiki/5-HT7_receptor

He is the author of fundamental scientific works in pharmacology of dopamine, β-Arrestins and NMDA receptors. He is a pioneer ... Beaulieu JM, Sotnikova TD, Marion S, Lefkowitz RJ, Gainetdinov RR, Caron MG (2005-07-29). "An Akt/β-Arrestin 2/PP2A Signaling ... "Enhanced Morphine Analgesia in Mice Lacking β-Arrestin 2". Science. 286 (5449): 2495-2498. doi:10.1126/science.286.5449.2495. ...

https://en.wikipedia.org/wiki/Raul_Gainetdinov

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

https://en.wikipedia.org/wiki/AP3B1

... has been shown to interact with: Arrestin beta 1, Arrestin beta 2, HRAS, KRAS, MRAS, RAP1A, RAP2A, RAPGEF2, and RRAS. ... "Beta-arrestins regulate a Ral-GDS Ral effector pathway that mediates cytoskeletal reorganization". Nat. Cell Biol. 4 (8): 547- ...

https://en.wikipedia.org/wiki/RALGDS

Lohse, Martin J.; Benovic, Jeffrey L.; Codina, Juan; Caron, Marc G.; Lefkowitz, Robert J. (22 June 1990). "β-Arrestin: a ... While working with Robert Lefkowitz at Duke University he discovered beta-arrestins, proteins that regulate the function of ...

https://en.wikipedia.org/wiki/Martin_J._Lohse

In many cases, arrestin's binding to the receptor is a prerequisite for translocation. For example, beta-arrestin bound to β2- ... Arrestin linking: The phosphorylated receptor can be linked to arrestin molecules that prevent it from binding (and activating ... Upon GRK phosphorylation, the GPCR's affinity for β-arrestin (β-arrestin-1/2 in most tissues) is increased, at which point β- ... Once β-arrestin is bound to a GPCR, it undergoes a conformational change allowing it to serve as a scaffolding protein for an ...

https://en.wikipedia.org/wiki/G_protein-coupled_receptor

Reiter, Eric; Ahn, Seungkirl; Shukla, Arun K.; Lefkowitz, Robert J. (11 January 2012). "Molecular Mechanism of β-Arrestin- ... India portal Biology portal Cell signaling Arrestin Membrane proteins Please see Selected bibliography section "Arun K. Shukla ... "Functional specialization of β-arrestin interactions revealed by proteomic analysis". Proceedings of the National Academy of ... "Global phosphorylation analysis of β-arrestin-mediated signaling downstream of a seven transmembrane receptor (7TMR)". ...

https://en.wikipedia.org/wiki/Arun_Kumar_Shukla

... requires arrestin (Arr1), it has been controversial whether the same requirement holds for cone … ... Arrestins are proteins that arrest the activity of G protein-coupled receptors (GPCRs). While it is well established that ... Arrestin-independent inactivation is 70-fold more rapid in cones than in rods, however. Dual arrestin expression in cones could ... Mouse cones require an arrestin for normal inactivation of phototransduction Neuron. 2008 Aug 14;59(3):462-74. doi: 10.1016/j. ...

https://pubmed.ncbi.nlm.nih.gov/18701071/

Home / Cell Line Starter Packs / PathHunter® CHO-K1 EDG4 β-Arrestin Cell Line Starter Pack. ... Youre viewing: PathHunter® CHO-K1 EDG4 β-Arrestin Cell Line Starter Pack $1,369.00 ...

https://www.discoverx.com/product/pathhunter-cho-k1-edg4-%CE%B2-arrestin-cell-line-starter-pack/

Alemayehu, Mistre, "P-ARRESTIN REGULATES LYSOPHOSPHATIDIC ACID-INDUCED HUMAN BREAST CANCER CELL INVASIVENESS VIA RAP1 AND ... P-ARRESTIN REGULATES LYSOPHOSPHATIDIC ACID-INDUCED HUMAN BREAST CANCER CELL INVASIVENESS VIA RAP1 AND IQGAP1 ...

https://ir.lib.uwo.ca/digitizedtheses/3720/

The arrestin clan now comprises ARTs, -arrestins, visual-arrestins and the Vps26 families in eukaryotes, and the Spo0M family ... arrestins include clathrin and AP2-interacting motifs, whereas those of -arrestins include PY motifs; -arrestins are usually ... It really is interesting in this respect that a accurate mammalian arrestin, -arrestin 2, has been proven to do something as ... It really is interesting in this respect that a accurate mammalian arrestin, -arrestin 2, has been demonstrated to do ...

http://bioskinrevive.com/2019/11/29/in-another-recent-survey-by-lin-2008-arrestin-related-transport-adaptors-were/

Arrestins. Arrestins (abbreviated Arr) are a family of proteins which are important in the regulation of signal transduction G- ...

http://arrestins.com/contact-data

However, β-arrestins do not consistently act as oncogenes or tumor suppressors. In certain cancer types, only one β-arrestin ... potentially affecting the composition and prevalence of GPCR-β-arrestin-effector complexes. By comparing β-arrestin expression ... β-Arrestins facilitate this process by interacting with adapter protein 2 (AP-2) and clathrin. The diversity in GPCR signaling ... β-arrestins exhibit interactions with over 100 diverse proteins, presenting an array of effectors that could be recruited to ...

https://www.ecosystem.drgpcr.com/post/decoding-%CE%B2-arrestins-from-structure-to-function

... β-arrestin 2, and AT1R knockout mice. Our data reveal β-arrestin 1, β-arrestin 2, and AT1R as key regulatory molecules in the ... Using invasive hemodynamics, we found that mice lacking β-arrestin 1, β-arrestin 2, or AT1R were unable to generate a Frank- ... "β-Arrestin mediates the Frank-Starling mechanism of cardiac contractility." Proc Natl Acad Sci U S A, vol. 113, no. 50, Dec. ... "β-Arrestin mediates the Frank-Starling mechanism of cardiac contractility." Proc Natl Acad Sci U S A 113, no. 50 (December 13, ...

https://scholars.duke.edu/publication/1162194

Call Us 24/7: (772) 489- ...

https://www.fort-pierce-criminal-lawyer.com/what-should-i-do-after-a-drug-arrest/drug-arrest-in-fort-pierce/

By attaching a fluorescent label, such as GFP, to beta-arrestin, the location of the receptor arrestin complex can be monitored ... Cell Meter™ Beta-Arrestin translocation GPCR Signaling Kit provides a powerful functional assay to screen activities of target ... The binding of beta-arrestin, a cytoplasmic protein, to an activated receptor deactivates the GPCR signaling and initiates the ... beta-arrestin-GFP DNA stock solution. Add 10 µL of ddH2O to the vial of beta-arrestin-GFP DNA (Component A), mix well to have ...

https://www.aatbio.com/products/cell-meter-beta-arrestin-translocation-gpcr-signaling-kit

A beta-arrestin 2 signaling complex mediates lithium action on behavior. Cell. 2008 Jan 11. 132(1):125-36. [QxMD MEDLINE Link] ... Glycogen synthase kinase-3 is essential for ß-arrestin-2 complex formation and lithium-sensitive behaviors in mice. J Clin ...

https://emedicine.medscape.com/article/2004136-overview

Mechanistically, FSH, via binding to hepatic FSHRs, activates the Gi2α/β-arrestin-2/Akt pathway and subsequently inhibits the ... 8f, g). β-arrestins, including β-arrestin1 (ARRB1) and β-arrestin 2 (ARRB2), were ubiquitously expressed and participated in ... which specifically did not express the respective protein of β-arrestin-1 or β-arrestin-2. The sequences of the sgRNAs are ... An Akt/β-arrestin 2/PP2A signaling complex mediates dopaminergic neurotransmission and behavior. Cell 122, 261-273 (2005). ...

https://www.nature.com/articles/s41422-018-0123-6?error=cookies_not_supported&code=e9d347f0-9546-4d3f-bf70-683dad0d250d

The movie shows the movement of GFP-beta-arrestin after TRH addition. When TRH binds to its receptor, the receptor changes ... the phospho-receptor binds to beta-arrestin. The movie covers about 10 min. ...

https://www.urmc.rochester.edu/labs/hinkle.aspx

Arrestin development: emerging roles for beta-arrestins in developmental signaling pathways. Dev Cell. 2009;17(4):443-458. ... GRK-mediated phosphorylation of ligand-occupied receptors leads to binding of β-arrestins, which in turn promotes GPCR ...

https://www.jci.org/articles/31768

Isolation and expression of an arrestin CDNA from the horseshoe crab lateral eye Submitted by admin_notgoodus... on Mon, 12/17/ ... Isolation and expression of an arrestin CDNA from the horseshoe crab lateral eye . Journal of Neurochemistry 64:1-13. ... Read more about Isolation and expression of an arrestin CDNA from the horseshoe crab lateral eye ...

https://www.horseshoecrab.org/research/search/Physiology?keys=&nid=&page=72&sort_by=field_main_author_value&sort_order=ASC

Former President Donald Trump turned himself in Thursday for arrest and processing at Atlantas Fulton County jail after being indicted along with 18 others for attempting to overturn the 2020 election results in Georgia.

https://uk.news.yahoo.com/trump-legal-brief-trump-turns-himself-in-for-arrest-in-atlanta-234157945.html

abc.net.au/news/victoria-police-reviewing-woman-mask-arrest-in-melbourne/12548866 ...

https://www.abc.net.au/news/2020-08-12/victoria-police-reviewing-woman-mask-arrest-in-melbourne/12548866

Chemokine-guided migration of cortical interneurons depends on CXCR7 phosphorylation but not on ß-Arrestins. Ralf Stumm, Jena/ ...

https://www.uni-muenster.de/Cells-in-Motion/de/events/lecture-series/index.html

β-arrestin-1. 25-G10. •. •. •. •. β-Tubulin. TU27/Tubulin. •. •. •. β2-microglobulin. 2M2. •. •. ...

https://www.biolegend.com/de-de/cross-reactivity

New Mexico investigators say they have ample evidence to prove Muhammad Syeds guilt, though they have yet to uncover the motive.

https://www.katc.com/news/national/new-mexicos-muslim-community-reels-from-arrest-in-killings

The Arlington County Police Department's Homicide/Robbery Unit is announcing the arrest of a suspect wanted for robbery of a convenience store in the Shirlington neighborhood.

https://www.arlingtonva.us/About-Arlington/Newsroom/Articles/2020/Police-Announce-Arrest-in-Convenience-Store-Robbery?OC_EA_EmergencyAnnouncementList_Dismiss=d22be84e-56e1-4cbd-beb6-0d3ec7e22855&lang_update=638311175153262273

birdsong, behavior, GPCRs, Arrestin, psychostimulants. jdunning. 2013‑02‑27. Bao H. Duong (Info). Scripps Institute. pq. 2015‑ ...

https://neurotree.org/neurotree/peoplelist.php?searchinst=Scripps%20Research%20Institute,%20La%20Jolla

Another member of Tehrans Bahai community was arrested after summons to a meeting.. The Ministry of Intelligence had previously summoned Namya Haghar, a Bahai from Tehran, to arrive at the Vali-Asr Square office on February 1, 2009, for questioning. Shortly after arriving at this location, Mr. Haghar was arrested to transferred to an undisclosed location. No further information is available about Mr. Haghars fate or reason for arrest.. A related report has revealed that two of the recent Bahai prisoners in Mashhad, Sima Eshraghi and Jalayer Vahdat, have contacted their families on Friday, January 30, 2009, and informed them of their continued detention.. [Source: HRA Iran at http://hrairan.org/index.php?option=com_content&view=article&id=442%3A987&catid=66%3A304&Itemid=293] ...

https://iranpresswatch.org/post/996/another-arrest-in-tehran/

Wang Lixiong and I arrived in Beijing from Inner Mongolia and got to our door at around 6:00 in the evening. At 7:00 State Security arrived. They said they would be taking up their posts for the next two days and that we were forbidden to go out. I asked for the reason and they said that it was confidential. But I know that its because the day before yesterday an American Embassy official had called me on my mobile phone and invited me this evening to the embassy residence. Knowing that I was on the road and couldnt participate, theyd set the date for the next day. I didnt know whom Id meet, but regardless of whom I would have met I was already prevented from doing so by State Security ...

https://highpeakspureearth.com/woeser-and-wang-lixiong-under-house-arrest-in-beijing/

Mexican Soap Opera Star Pablo Lyle is out on house arrest after his bond was set at $50,000 in a fatal punch case in Miami.

https://www.nbcmiami.com/on-air/as-seen-on/mexican-soap-star-on-house-arrest-in-miami_miami/79774/

The big gay rainbow crosswalk was just unveiled last weekend and was immediately vandalized. There has been an arrest! #LoveWins

https://www.wrmf.com/arrest-in-rainbow-crosswalk-vandalism-in-delray-beach/

In December 2007, Lee County law enforcement dove into the retention pond at Montego Bay apartments, looking for the body of Rupinder Goraya, who disappeared two months earlier. Rupinders co-workers at Southwest Regional Hospital reported her missing on October 19, 2007, but her body was never located. Even without a body today, Fort Myers police say they finally have enough evidence to charge her husband, Kultar Goroya, with murder. "Its a great feeling. we do this for the victims families. They had to go 7 years without knowing what happened to their sister, their daughter, relative, and now they are able to have closure for her disappearing," said Sergeant Brian OReilly, of the Fort Myers Police Department. Detectives got a break in the case when investigators with the television program "Cold Justice," came to Fort Myers to help. The team worked closely with Fort Myers detectives to investigate the case over a two week period in November of 2014, while filming an episode for the program. ...

https://winknews.com/2015/01/06/man-under-arrest-in-fort-myers-cold-case/

Platelet P2Y1 receptor exhibits constitutive G protein signaling and β-arrestin 2 recruitment Purinergic P2Y1 and P2Y12 ...

https://bmcbiol.biomedcentral.com/articles?searchType=journalSearch&sort=PubDate&page=4

Damn, Im only 29!" were the first words out of Danish playmaker Christian Eriksens mouth the moment regained consciousness after succumbing to a sudden cardiac arrest (SCA) during the opening week of matches at the ongoing Euros. While occurrences are rare, young and fit athletes are not immune to heart problems and breaking down the risks of cardiac arrest in sport - Datuk Dr Ramlan Aziz, Founding CEO National Sports Institute Malaysia, 6-time Olympic Medical Officer - joins us on the programme this episode ...

https://bfm.my/podcast/night-shift/bar-none/bar-none-perils-of-cardiac-arrest-in-sport

At issue is the arrest last week of Indias deputy consul general in New York. She is accused of using false documents to get a work visa for her Manhattan housekeeper. India is calling her arrest despicable and barbaric, and announced retaliatory steps against U.S. diplomats in the country.

https://www.wunc.org/npr-blogs/2013-12-17/india-u-s-row-over-diplomats-arrest-in-new-york-escalates

Several New York police officers have brutally beaten a man they were holding on the floor during his arrest in a Brooklyn store. A crowd of customers who

https://rinf.com/alt-news/multimedia/video-nypd-brutally-punch-man-pin-him-to-floor-during-arrest-in-brooklyn/

Arrestins are proteins that arrest the activity of G protein-coupled receptors (GPCRs). (nih.gov)
The two β -arrestins, β -arrestin-1 and -2 (systematic names: arrestin-2 and -3, respectively), are multifunctional intracellular proteins that regulate the activity of a very large number of cellular signaling pathways and physiologic functions. (aspetjournals.org)
Recent structural, biophysical, and biochemical studies have provided novel insights into how β -arrestins bind to activated GPCRs and downstream effector proteins. (aspetjournals.org)
Significance Statement The two β-arrestins, structurally closely related intracellular proteins that are evolutionarily highly conserved, have emerged as multifunctional proteins able to regulate a vast array of cellular and physiological functions. (aspetjournals.org)
In another recent survey by Lin (2008), arrestin-related transport adaptors were also found to target specific plasma-membrane proteins for endocytic downregulation by recruiting the ubiquitin E3 ligase Rsp5. (bioskinrevive.com)
This resulted in the identification of the yeast proteins category of arrestin-related trafficking adaptors (ARTs)which includes nine members which have conserved arrestin and PY motifs, seven which are predicted to really have the arrestin foldand hence Cvs7 was renamed Artwork1. (bioskinrevive.com)
It is concluded that PTH stimulates ERK1/2 through several distinct signal transduction pathways: an early G protein-dependent pathway meditated by PKA and PKC and a late pathway independent of G proteins mediated through beta-arrestins. (duke.edu)
Arrestins (abbreviated Arr) are a family of proteins which are important in the regulation of signal transduction G-protein coupled receptors, which at first was discovered, as part of a conserved two step mechanism for regulating the activity of G protein-coupled receptors (GPCR) in rhodopsin visual system by Ursula Kuhn found Scott court, and β-called Global Martin J. Lohse system and kidney and colleagues. (arrestins.com)

Scholars@Duke publication: Distinct beta-arrestin- and G protein-dependent pathways for parathyroid hormone receptor-stimulated ERK1/2 activation. (duke.edu)
This later phase of ERK1/2 activation at 30-60 min was blocked by depletion of cellular beta-arrestin 2 and beta-arrestin 1 by small interfering RNA. (duke.edu)
Furthermore, stimulation of hPTH1R with PTH analogues, [Trp1]PTHrp-(1-36) and [d-Trp12,Tyr34]PTH-(7-34), selectively activated G(s)/PKA-mediated ERK1/2 activation or G protein-independent/beta-arrestin-dependent ERK1/2 activation, respectively. (duke.edu)
The binding of beta-arrestin, a cytoplasmic protein, to an activated receptor deactivates the GPCR signaling and initiates the translocation of the receptor into the cell where the ligand is removed, and the receptor is recycled back to the cell membrane. (aatbio.com)
By attaching a fluorescent label, such as GFP, to beta-arrestin, the location of the receptor arrestin complex can be monitored. (aatbio.com)
Since desensitization only occurs with an activated receptor, monitoring beta-arrestin translocation and subsequent receptor recycling provides a reliable method to detect the activation of a GPCR target. (aatbio.com)
Cell Meter™ Beta-Arrestin translocation GPCR Signaling Kit provides a powerful functional assay to screen activities of target compounds against known or orphan GPCR targets via fluorescence imaging. (aatbio.com)
Add 10 µL of ddH 2 O to the vial of beta-arrestin-GFP DNA (Component A), mix well to have the final concentration of 1 µg/µL. (aatbio.com)
Mix 3 µg of DNA [for example, 1.5 µg of Beta-arrestin-GFP DNA stock solution and 1.5 µg DNA of the GPCR that you are interested] with 200 µL of serum-free medium. (aatbio.com)
Monitor the beta-arrestin translocation induced by the receptor activation under a fluorescence microscope with the FITC filter (Ex/Em = 488/530 nm). (aatbio.com)
The movie shows the movement of GFP-beta-arrestin after TRH addition. (rochester.edu)
the phospho-receptor binds to beta-arrestin. (rochester.edu)

It really is interesting in this respect that a accurate' mammalian arrestin, -arrestin 2, has been proven to do something as an adaptor for the WW-domain-containing Electronic3 ubiquitin ligase NEDD4 to market agonist-stimulated ubiquitination of the 2-adrenergic receptor (Shenoy em et al /em , 2008). (bioskinrevive.com)
arrestins possess an amphipathic helix (helix 1) that's sequestered in to the inactive conformation of the N-terminal domain and is normally presumably released on activation by receptor engagement, whereas -arrestins usually do not. (bioskinrevive.com)
GPCR kinases (GRKs) and β-arrestins are activated by agonist-bound GPCRs and interact with the receptor cavity. (drgpcr.com)
Notably, GRKs phosphorylate active GPCRs, enabling high-affinity arrestin binding, which is crucial for receptor internalization. (drgpcr.com)
With different collaborators we solved crystal structures of all four vertebrate arrestins, the arrestin-rhodopsin complex, and pre-activated arrestin-3 in the absence of receptor. (hstalks.com)
We identified key residues responsible for receptor preference of arrestins. (hstalks.com)

The formation of functional complexes involving GPCRs and β-arrestins hinges on their specific conformational states, influenced by their intricate three-dimensional structures. (drgpcr.com)
read more constructed enhanced arrestins that bind active unphosphorylated GPCRs. (hstalks.com)
We proved that monomeric GPCRs are necessary and sufficient for GRK phosphorylation and arrestin binding. (hstalks.com)

Mouse cone photoreceptors express two distinct visual arrestins: Arr1 and Arr4. (nih.gov)
The arrestin clan now comprises ARTs, -arrestins, visual-arrestins and the Vps26 families in eukaryotes, and the Spo0M family in archaea and bacteria (Alvarez, 2008). (bioskinrevive.com)

While it is well established that normal inactivation of photoexcited rhodopsin, the GPCR of rod phototransduction, requires arrestin (Arr1), it has been controversial whether the same requirement holds for cone opsin inactivation. (nih.gov)
We showed that enhanced mutants of visual arrestin-1 compensate for defects in rhodopsin phosphorylation in vivo. (hstalks.com)
Arrestin quenches G-protein activation by binding to phosphorylated photolyzed rhodopsin. (bvsalud.org)

The hypothesis arises that GPCR and β-arrestin-centered effector complexes vary based on subcellular localization, potentially scaffolding distinct signaling platforms. (drgpcr.com)

However, it is now well recognized that both β -arrestins can also act as direct modulators of numerous cellular processes via either GPCR-dependent or -independent mechanisms. (aspetjournals.org)

The useful homology of Cvs7 to mammalian arrestins was set up by verifying that the mutation of conserved residues within the arrestin motif ablated Cvs7 function. (bioskinrevive.com)

This review also highlights potential therapeutic implications of these studies and discusses strategies that could prove useful for targeting specific β -arrestin-regulated signaling pathways for therapeutic purposes. (aspetjournals.org)

β-Arrestins facilitate this process by interacting with adapter protein 2 (AP-2) and clathrin. (drgpcr.com)
The thioredoxin-interacting protein (TXNIP) is a multi-functional protein of the alpha-arrestin family implicated in redox regulation, glucose uptake, cell proliferation, and activation of NLRP3. (cdc.gov)

arrestin 2 will not include any legitimate PY motifs, but was nevertheless proven to bind to NEDD4. (bioskinrevive.com)

By means of recordings from cones of mice with one or both arrestins knocked out, this investigation establishes that a visual arrestin is required for normal cone inactivation. (nih.gov)
Studies with β -arrestin mutant mice have identified numerous physiologic and pathophysiological processes regulated by β -arrestin-1 and/or -2. (aspetjournals.org)
The outcome of studies with β-arrestin mutant mice and cultured cells, complemented by novel insights into β-arrestin structure and function, should pave the way for the development of novel classes of therapeutically useful drugs capable of regulating specific β-arrestin functions. (aspetjournals.org)

We identified arrestin elements involved in scaffolding ASK1-MKK4/4-JNK1/2/3 cascades and constructed novel tools for manipulation of JNK signaling, including short peptides that facilitate JNK3 activation in cells. (hstalks.com)

Dual arrestin expression in cones could be a holdover from ancient genome duplication events that led to multiple isoforms of arrestin, allowing evolutionary specialization of one form while the other maintains the basic function. (nih.gov)
Research focus: structure and function of arrestins. (hstalks.com)

Furthermore to ARTs, Vps26a component of the five-subunit retromer complex involved in retrograde transport from endosomes to the em trans /em -Golgi networkhas been STMY shown to present the same overall fold as the arrestins (Shi em et al /em , 2006). (bioskinrevive.com)

Hence, the mammalian arrestins have got expanded from 4 preliminary memberstwo visible and two -arrestinsto 14 members with the addition of 6 -arrestins (ARTs) and 4 VPS26 members (which buy Clofarabine talk about higher sequence similarity with -arrestins). (bioskinrevive.com)

Following a short summary of recent structural studies, this review primarily focuses on β -arrestin-regulated physiologic functions, with particular focus on the central nervous system and the roles of β -arrestins in carcinogenesis and key metabolic processes including the maintenance of glucose and energy homeostasis. (aspetjournals.org)

GPCR function is modulated by a pair of proteins known as beta-arrestin-1 and -2 ( barr1 and barr2, respectively), which can terminate GPCR signaling and/or mediate GPCR-independent signaling. (nih.gov)
The high expression of recoverin and arrestin-1 in kidney tumors suggests the use of these proteins in future as a marker for the diagnosis or even as a potential target for immunotherapy. (eco-vector.com)
Arrestins (abbreviated Arr) are a family of proteins which are important in the regulation of signal transduction G-protein coupled receptors, which at first was discovered, as part of a conserved two step mechanism for regulating the activity of G protein-coupled receptors (GPCR) in rhodopsin visual system by Ursula Kuhn found Scott court, and β-called Global Martin J. Lohse system and kidney and colleagues. (arrestins.com)
Receptor phosphorylation may attenuate signaling per se and/or may facilitate recruitment of arrestin proteins ( Krupnick and Benovic, 1998 ). (jneurosci.org)
Structural studies including determination of 3D structures of ligands, receptors, receptors with associated G-proteins, beta-arrestin etc. (nih.gov)

1. Differential nucleocytoplasmic shuttling of beta-arrestins. (nih.gov)
2. Subcellular localization of beta-arrestins is determined by their intact N domain and the nuclear export signal at the C terminus. (nih.gov)
7. Termination of protease-activated receptor-1 signaling by beta-arrestins is independent of receptor phosphorylation. (nih.gov)
19. beta -Arrestins regulate protease-activated receptor-1 desensitization but not internalization or Down-regulation. (nih.gov)

Activated ß-arrestin-1 (yellow) binds a G-protein coupled receptor (green) that crosses the cell membrane (gray). (nih.gov)
It has been reported recently that T cells lacking β-arrestin-2, a G protein-coupled receptor regulatory protein, demonstrate impaired migration in vitro. (jci.org)
6. The stability of the G protein-coupled receptor-beta-arrestin interaction determines the mechanism and functional consequence of ERK activation. (nih.gov)

GRK1-dependent phosphorylation of S and M opsins and their binding to cone arrestin during cone phototransduction in the mouse retina. (nih.gov)

Here we show that allergen-sensitized mice having a targeted deletion of the β-arrestin-2 gene do not accumulate T lymphocytes in their airways, nor do they demonstrate other physiological and inflammatory features characteristic of asthma. (jci.org)
Using permanent and primary human bronchial epithelial (HBE) cells at air-liquid interface, we show that DEPs activate the human MMP-1 gene via RAS and subsequent activation of RAF-MEK-ERK1/2 mitogen-activated protein kinase signaling, which can be scaffolded by β-arrestins. (nih.gov)
The gene, arrestin domain containing 5 ( ARRDC5 ) is present in several mammalian species and controls the last step in sperm maturation. (nih.gov)
A previous study found that overactivity and inactivation of another gene in the arrestin domain containing family, ARRDC4 , found in the male reproductive tract, resulted in sperm with less ability to move and less ability to fertilize an egg. (nih.gov)

In contrast, the airway inflammatory response to LPS, an event not coordinated by Th2 cells, is fully functional in mice lacking β-arrestin-2. (jci.org)

Aim: To evaluate the possibility of using arrestin-1 (Arr-1), recoverin (Rec) and autoantibodies against arrestin-1 (AAA1) and recoverin (AAR) as a kidney tumor biomarker. (eco-vector.com)

Compared to previously determined inactive state structures, activated β-arrestin-1 has pronounced structural changes. (nih.gov)
These scientists found similar changes between the active and inactive states of arrestin p44. (nih.gov)
13. Visual and both non-visual arrestins in their "inactive" conformation bind JNK3 and Mdm2 and relocalize them from the nucleus to the cytoplasm. (nih.gov)

The researchers were studying the interactions between β-arrestin-1 and a human GPCR called the V2 vasopressin receptor. (nih.gov)

8. Beta-arrestin 2: a receptor-regulated MAPK scaffold for the activation of JNK3. (nih.gov)

Here we report the use of extracellular vesicles, known as arrestin domain containing protein 1 [ARRDC1]-mediated microvesicles (ARMMs), for packaging and intracellular delivery of a myriad of macromolecules, including the tumor suppressor p53 protein, RNAs, and the genome-editing CRISPR-Cas9/guide RNA complex. (nih.gov)

This ELISA test kit for detection of Human beta-arrestin,ARRB should be stored refrigerated at temperatures between 2 and 8 degrees Celsius. (arrestins.com)

This report provides the first evidence that β-arrestin-2 is required for the manifestation of allergic asthma. (jci.org)

Anatomy4

Organisms3

Chemicals and Drugs23

Analytical, Diagnostic and Therapeutic Techniques and Equipment4

Psychiatry and Psychology1

Phenomena and Processes13

Information Science2

Arrestin function in G protein-coupled receptor endocytosis requires phosphoinositide binding. (1/1016)

Targeted construction of phosphorylation-independent beta-arrestin mutants with constitutive activity in cells. (2/1016)

Real-time visualization of the cellular redistribution of G protein-coupled receptor kinase 2 and beta-arrestin 2 during homologous desensitization of the substance P receptor. (3/1016)

Internalization of the TXA2 receptor alpha and beta isoforms. Role of the differentially spliced cooh terminus in agonist-promoted receptor internalization. (4/1016)

The absence of a direct correlation between the loss of [D-Ala2, MePhe4,Gly5-ol]Enkephalin inhibition of adenylyl cyclase activity and agonist-induced mu-opioid receptor phosphorylation. (5/1016)

Decreased expression and activity of G-protein-coupled receptor kinases in peripheral blood mononuclear cells of patients with rheumatoid arthritis. (6/1016)

The beta2-adrenergic receptor/betaarrestin complex recruits the clathrin adaptor AP-2 during endocytosis. (7/1016)

Identification of NSF as a beta-arrestin1-binding protein. Implications for beta2-adrenergic receptor regulation. (8/1016)

Arrestins

Arrestin

Mitogen-Activated Protein Kinase 10

G-Protein-Coupled Receptor Kinases

Rhodopsin

Receptors, Adrenergic, beta-2

G-Protein-Coupled Receptor Kinase 3

Receptors, G-Protein-Coupled

G-Protein-Coupled Receptor Kinase 2

Dynamins

Endocytosis

Killifishes

G-Protein-Coupled Receptor Kinase 1

Clathrin

Receptors, Formyl Peptide

G-Protein-Coupled Receptor Kinase 5

Eye Proteins

COS Cells

Protein Transport

Protein Binding

Signal Transduction

Receptors, Muscarinic

Cattle

Amino Acid Sequence

Molecular Sequence Data

Vision, Ocular

Transfection

Cell Line

Phosphorylation

GTP-Binding Proteins

Antigens

Photoreceptor Cells, Vertebrate

Cercopithecus aethiops

Sequence Homology, Amino Acid

Fluorescent Antibody Technique, Indirect

Microscopy, Fluorescence

Photoreceptor Cells

Phosphoproteins

Recombinant Fusion Proteins

Proto-Oncogene Proteins c-mdm2

Protein Structure, Tertiary

Protein Conformation

Green Fluorescent Proteins

Amino Acid Motifs

Mutagenesis, Site-Directed

Binding Sites

Receptors, Cell Surface

Arrestin function in G protein-coupled receptor endocytosis requires phosphoinositide binding. (1/1016)

Targeted construction of phosphorylation-independent beta-arrestin mutants with constitutive activity in cells. (2/1016)

Real-time visualization of the cellular redistribution of G protein-coupled receptor kinase 2 and beta-arrestin 2 during homologous desensitization of the substance P receptor. (3/1016)

Internalization of the TXA2 receptor alpha and beta isoforms. Role of the differentially spliced cooh terminus in agonist-promoted receptor internalization. (4/1016)

The absence of a direct correlation between the loss of [D-Ala2, MePhe4,Gly5-ol]Enkephalin inhibition of adenylyl cyclase activity and agonist-induced mu-opioid receptor phosphorylation. (5/1016)

Decreased expression and activity of G-protein-coupled receptor kinases in peripheral blood mononuclear cells of patients with rheumatoid arthritis. (6/1016)

The beta2-adrenergic receptor/betaarrestin complex recruits the clathrin adaptor AP-2 during endocytosis. (7/1016)

Identification of NSF as a beta-arrestin1-binding protein. Implications for beta2-adrenergic receptor regulation. (8/1016)

Arrestin

Alpha Arrestin

Arrestin beta 2

Arrestin beta 1

CLTC

Thyrotropin-releasing hormone receptor

SAG (gene)

GRK4

G protein-coupled receptor kinase 2

GRK5

G protein-coupled receptor kinase 3

G protein-coupled receptor kinase

GRK6

Raymond C. Stevens

Κ-opioid receptor

VPS26A

Denis Baylor

Herkinorin

Retinal degeneration (rhodopsin mutation)

Trevena Inc

Jonathan Stamler

Alpha-2C adrenergic receptor

GPR64

5-HT7 receptor

Raul Gainetdinov