Arrestin
Mostrando 1-12 de 80 artigos, teses e dissertações.
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1. Effect of high energy intake on carcass composition and hypothalamic gene expression in Bos indicus heifers
ABSTRACT The objective of this study was to evaluate the effect of high or low energy intake on carcass composition and expression of hypothalamic genes related to the onset of puberty. Twenty-four prepubertal Nellore heifers, 18-20- months-old, with 275.3±18.0 kg body weight (BW), and 4.9±0.2 (1-9 scale) body condition score (BCS) were randomly assigned t
R. Bras. Zootec.. Publicado em: 2017-08
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2. Effect of penehyclidine hydrochloride on β-arrestin-1 expression in lipopolysaccharide-induced human pulmonary microvascular endothelial cells
β-arrestins are expressed proteins that were first described, and are well-known, as negative regulators of G protein-coupled receptor signaling. Penehyclidine hydrochloride (PHC) is a new anti-cholinergic drug that can inhibit biomembrane lipid peroxidation, and decrease cytokines and oxyradicals. However, to date, no reports on the effects of PHC on β-ar
Braz J Med Biol Res. Publicado em: 02/12/2013
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3. Evidências sorológicas e experimentais da resposta autoimune humoral contra a retina em uveites causada por Toxoplasma gondii / Experimental and serological evidence of humoral autoimmune response against retina in Toxoplasma gondii uveitis
Ocular toxoplasmosis is attributed to the parasite, but autoimmunity could have a role in this process. Human sera, positive of anti-T. gondii IgG, show high levels of anti-retina IgG, measured by several antigens, as compared to T. gondii seronegative samples. Sera from patients with uveitis from other origins also had higher anti-retina abs levels. Challen
Publicado em: 2008
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4. Insulin Induces Heterologous Desensitization of G Protein-Coupled Receptor and Insulin-Like Growth Factor I Signaling by Downregulating β-Arrestin-1
β-Arrestin-1 mediates agonist-dependent desensitization and internalization of G protein-coupled receptors (GPCRs) and is also essential for GPCR mitogenic signaling. In addition, insulin-like growth factor I receptor (IGF-IR) endocytosis is facilitated by β-arrestin-1, and internalization is necessary for IGF-I-stimulated mitogen-activated protein (MAP) k
American Society for Microbiology.
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5. β-Arrestin-1 Competitively Inhibits Insulin-Induced Ubiquitination and Degradation of Insulin Receptor Substrate 1
β-Arrestin-1 is an adaptor protein that mediates agonist-dependent internalization and desensitization of G-protein-coupled receptors (GPCRs) and also participates in the process of heterologous desensitization between receptor tyrosine kinases and GPCR signaling. In the present study, we determined whether β-arrestin-1 is involved in insulin-induced insul
American Society for Microbiology.
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6. Structure of an Arrestin2-Clathrin Complex Reveals a Novel Clathrin Binding Domain That Modulates Receptor Trafficking*
Non-visual arrestins play a pivotal role as adaptor proteins in regulating the signaling and trafficking of multiple classes of receptors. Although arrestin interaction with clathrin, AP-2, and phosphoinositides contributes to receptor trafficking, little is known about the configuration and dynamics of these interactions. Here, we identify a novel interface
American Society for Biochemistry and Molecular Biology.
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7. β-Arrestin2 Regulates RANKL and Ephrins Gene Expression in Response to Bone Remodeling in Mice
PTH-stimulated intracellular signaling is regulated by the cytoplasmic adaptor molecule β-arrestin. We reported that the response of cancellous bone to intermittent PTH is reduced in β-arrestin2−/− mice and suggested that β-arrestins could influence the bone mineral balance by controlling RANKL and osteoprotegerin (OPG) gene expression. Here, we study
Amer Soc Bone & Mineral Res..
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8. Different G protein-coupled receptor kinases govern G protein and β-arrestin-mediated signaling of V2 vasopressin receptor
Signaling through β-arrestins is a recently appreciated mechanism used by seven-transmembrane receptors. Because G protein-coupled receptor kinase (GRK) phosphorylation of such receptors is generally a prerequisite for β-arrestin binding, we studied the roles of different GRKs in promoting β-arrestin-mediated extracellular signal-regulated kinase (ERK) ac
National Academy of Sciences.
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9. Activation and targeting of extracellular signal-regulated kinases by β-arrestin scaffolds
Using both confocal immunofluorescence microscopy and biochemical approaches, we have examined the role of β-arrestins in the activation and targeting of extracellular signal-regulated kinase 2 (ERK2) following stimulation of angiotensin II type 1a receptors (AT1aR). In HEK-293 cells expressing hemagglutinin-tagged AT1aR, angiotensin stimulation trigge
The National Academy of Sciences.
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10. β-Arrestin2, interacting with phosphodiesterase 4, regulates synaptic release probability and presynaptic inhibition by opioids
Most μ-opioid receptor agonists recruit β-arrestin2, with some exceptions such as morphine. Surprisingly, however, the acute analgesic effect of morphine is enhanced in the absence of β-arrestin2. To resolve this paradox, we examined the effects of morphine and fentanyl in acute brain slices of the locus coeruleus and the periaqueductal gray from β-arres
National Academy of Sciences.
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11. β-Arrestin inhibits NF-κB activity by means of its interaction with the NF-κB inhibitor IκBα
In addition to their roles in desensitization and signaling of seven-membrane-spanning receptors, β-arrestins have been more recently implicated in regulating non-seven-membrane-spanning receptor pathways. By using a yeast two-hybrid screen, we identified the inhibitor of NF-κB, IκBα, as a binding partner of β-arrestin 1. Both β-arrestin 1 and 2 intera
National Academy of Sciences.
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12. Beta-arrestin and arrestin are recognized by autoantibodies in sera from multiple sclerosis patients.
Multiple sclerosis (MS), one of the most common chronic neurologic diseases, is characterized by the presence of multiple plaques of demyelination throughout the central nervous system. Although the etiology of the disease has not been established, it is believed to involve autoimmune mechanisms. We have examined sera from patients with MS for the presence o