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10.1124/pr.116.013367 http://scihub22266oqcxt.onion/10.1124/pr.116.013367 C5482185!5482185!28626043     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Pharmacol+Rev 2017 ; 69 (3): 256-97 Nephropedia Template TP {{tp|p=28626043|t=2017. The Diverse Roles of Arrestin Scaffolds in G Protein?Coupled Receptor Signaling |pdf=|usr=}}{{28626043}} gab.com Text The Diverse Roles of Arrestin Scaffolds in G Protein Coupled Receptor Signaling JO: Pharmacol Rev http://www.kidney.de/pget.php?&tw=1&pmid=28626043 #FOAvip The visual/?-arrestins, a small family of proteins originally described for their role in the desensitization and intracellular trafficking of G protein?coupled receptors (GPCRs), have emerged as key regulators of multiple signaling pathways. Evolutionarily related to a larger group of regulatory scaffolds that share a common arrestin fold, the visual/?-arrestins acquired the capacity to detect and bind activated GPCRs on the plasma membrane, which enables them to control GPCR desensitization, internalization, and intracellular trafficking. By acting as scaffolds that bind key pathway intermediates, visual/?-arrestins both influence the tonic level of pathway activity in cells and, in some cases, serve as ligand-regulated scaffolds for GPCR-mediated signaling. Growing evidence supports the physiologic and pathophysiologic roles of arrestins and underscores their potential as therapeutic targets. Circumventing arrestin-dependent GPCR desensitization may alleviate the problem of tachyphylaxis to drugs that target GPCRs, and find application in the management of chronic pain, asthma, and psychiatric illness. As signaling scaffolds, arrestins are also central regulators of pathways controlling cell growth, migration, and survival, suggesting that manipulating their scaffolding functions may be beneficial in inflammatory diseases, fibrosis, and cancer. In this review we examine the structure?function relationships that enable arrestins to perform their diverse roles, addressing arrestin structure at the molecular level, the relationship between arrestin conformation and function, and sites of interaction between arrestins, GPCRs, and nonreceptor-binding partners. We conclude with a discussion of arrestins as therapeutic targets and the settings in which manipulating arrestin function might be of clinical benefit. Twit Text FOAVip The Diverse Roles of Arrestin Scaffolds in G Protein Coupled Receptor Signaling ????Pharmacol Rev http://www.kidney.de/pget.php?&tw=1&pmid=28626043 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28626043 #FOAvip English Wikipedia <ref>{{Cite pmid|28626043}}</ref> The Diverse Roles of Arrestin Scaffolds in G Protein?Coupled Receptor Signaling #MMPMID28626043 Peterson YK; Luttrell LM Pharmacol Rev 2017[Jul]; 69 (3): 256-97 PMID28626043show ga The visual/?-arrestins, a small family of proteins originally described for their role in the desensitization and intracellular trafficking of G protein?coupled receptors (GPCRs), have emerged as key regulators of multiple signaling pathways. Evolutionarily related to a larger group of regulatory scaffolds that share a common arrestin fold, the visual/?-arrestins acquired the capacity to detect and bind activated GPCRs on the plasma membrane, which enables them to control GPCR desensitization, internalization, and intracellular trafficking. By acting as scaffolds that bind key pathway intermediates, visual/?-arrestins both influence the tonic level of pathway activity in cells and, in some cases, serve as ligand-regulated scaffolds for GPCR-mediated signaling. Growing evidence supports the physiologic and pathophysiologic roles of arrestins and underscores their potential as therapeutic targets. Circumventing arrestin-dependent GPCR desensitization may alleviate the problem of tachyphylaxis to drugs that target GPCRs, and find application in the management of chronic pain, asthma, and psychiatric illness. As signaling scaffolds, arrestins are also central regulators of pathways controlling cell growth, migration, and survival, suggesting that manipulating their scaffolding functions may be beneficial in inflammatory diseases, fibrosis, and cancer. In this review we examine the structure?function relationships that enable arrestins to perform their diverse roles, addressing arrestin structure at the molecular level, the relationship between arrestin conformation and function, and sites of interaction between arrestins, GPCRs, and nonreceptor-binding partners. We conclude with a discussion of arrestins as therapeutic targets and the settings in which manipulating arrestin function might be of clinical benefit. äThe Diverse Roles of Arrestin Scaffolds in G Protein?Coupled Receptor (epmc).pdf DeepDyve Pubget Overpricing