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10.1016/j.coemr.2020.07.011 http://scihub22266oqcxt.onion/10.1016/j.coemr.2020.07.011 32838054!7431397!32838054     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       Curr+Opin+Endocr+Metab+Res 2021 ; 16 (ä): 37-42 Nephropedia Template TP {{tp|p=32838054|t=2021. Subcellular hot spots of GPCR signaling promote vascular inflammation |pdf=|usr=}}{{32838054}} gab.com Text Subcellular hot spots of GPCR signaling promote vascular inflammation JO: Curr Opin Endocr Metab Res http://www.kidney.de/pget.php?&tw=1&pmid=32838054 #FOAvip G-coupled protein receptors (GPCRs) comprise the largest class of druggable targets. Signaling by GPCRs is initiated from subcellular hot spots including the plasma membrane, signalosomes, and endosomes to contribute to vascular inflammation. GPCR-G protein signaling at the plasma membrane causes endothelial barrier disruption and also cross-talks with growth factor receptors to promote proinflammatory signaling. A second surge of GPCR signaling is initiated by cytoplasmic NFkappaB activation mediated by beta-arrestins and CARMA-BCL10-MALT1 signalosomes. Once internalized, ubiquitinated GPCRs initiate signaling from endosomes via assembly of the transforming growth factor-beta-activated kinase binding protein-1 (TAB1)-TAB2-p38 MAPK complex to promote vascular inflammation. Understanding the complexities of GPCR signaling is critical for development of new strategies to treat vascular inflammation such as that associated with COVID-19. Twit Text FOAVip Subcellular hot spots of GPCR signaling promote vascular inflammation ????Curr Opin Endocr Metab Res http://www.kidney.de/pget.php?&tw=1&pmid=32838054 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32838054 #FOAvip English Wikipedia <ref>{{Cite pmid|32838054}}</ref> Subcellular hot spots of GPCR signaling promote vascular inflammation #MMPMID32838054 Birch CA; Molinar-Inglis O; Trejo J Curr Opin Endocr Metab Res 2021[Feb]; 16 (ä): 37-42 PMID32838054show ga G-coupled protein receptors (GPCRs) comprise the largest class of druggable targets. Signaling by GPCRs is initiated from subcellular hot spots including the plasma membrane, signalosomes, and endosomes to contribute to vascular inflammation. GPCR-G protein signaling at the plasma membrane causes endothelial barrier disruption and also cross-talks with growth factor receptors to promote proinflammatory signaling. A second surge of GPCR signaling is initiated by cytoplasmic NFkappaB activation mediated by beta-arrestins and CARMA-BCL10-MALT1 signalosomes. Once internalized, ubiquitinated GPCRs initiate signaling from endosomes via assembly of the transforming growth factor-beta-activated kinase binding protein-1 (TAB1)-TAB2-p38 MAPK complex to promote vascular inflammation. Understanding the complexities of GPCR signaling is critical for development of new strategies to treat vascular inflammation such as that associated with COVID-19. äSubcellular hot spots of GPCR signaling promote vascular inflammation (epmc).pdf DeepDyve Pubget Overpricing