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10.1038/cr.2015.109 http://scihub22266oqcxt.onion/10.1038/cr.2015.109 C4650626!4650626!26358189     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Res 2015 ; 25 (10): 1093-107 Nephropedia Template TP {{tp|p=26358189|t=2015. G protein-coupled receptor 183 facilitates endothelial-to-hematopoietic transition via Notch1 inhibition |pdf=|usr=}}{{26358189}} gab.com Text G protein-coupled receptor 183 facilitates endothelial-to-hematopoietic transition via Notch1 inhibition JO: Cell Res http://www.kidney.de/pget.php?&tw=1&pmid=26358189 #FOAvip In vertebrates, embryonic hematopoietic stem and progenitor cells (HSPCs) are derived from a subset of endothelial cells, the hemogenic endothelium (HE), through the endothelial-to-hematopoietic transition (EHT). Notch signaling is essential for HSPC development during embryogenesis across vertebrates. However, whether and how it regulates EHT remains unclear. Here, we show that G protein-coupled receptor 183 (Gpr183) signaling serves as an indispensable switch for HSPC emergence by repressing Notch signaling before the onset of EHT. Inhibition of Gpr183 significantly upregulates Notch signaling and abolishes HSPC emergence. Upon activation by its ligand 7?-25-OHC, Gpr183 recruits ?-arrestin1 and the E3 ligase Nedd4 to degrade Notch1 in specified HE cells and then facilitates the subsequent EHT. Importantly, 7?-25-OHC stimulation promotes HSPC emergence in vivo and in vitro, providing an attractive strategy for enhancing the in vitro generation of functional HSPCs. Twit Text FOAVip G protein-coupled receptor 183 facilitates endothelial-to-hematopoietic transition via Notch1 inhibition ????Cell Res http://www.kidney.de/pget.php?&tw=1&pmid=26358189 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26358189 #FOAvip English Wikipedia <ref>{{Cite pmid|26358189}}</ref> G protein-coupled receptor 183 facilitates endothelial-to-hematopoietic transition via Notch1 inhibition #MMPMID26358189 Zhang P; He Q; Chen D; Liu W; Wang L; Zhang C; Ma D; Li W; Liu B; Liu F Cell Res 2015[Oct]; 25 (10): 1093-107 PMID26358189show ga In vertebrates, embryonic hematopoietic stem and progenitor cells (HSPCs) are derived from a subset of endothelial cells, the hemogenic endothelium (HE), through the endothelial-to-hematopoietic transition (EHT). Notch signaling is essential for HSPC development during embryogenesis across vertebrates. However, whether and how it regulates EHT remains unclear. Here, we show that G protein-coupled receptor 183 (Gpr183) signaling serves as an indispensable switch for HSPC emergence by repressing Notch signaling before the onset of EHT. Inhibition of Gpr183 significantly upregulates Notch signaling and abolishes HSPC emergence. Upon activation by its ligand 7?-25-OHC, Gpr183 recruits ?-arrestin1 and the E3 ligase Nedd4 to degrade Notch1 in specified HE cells and then facilitates the subsequent EHT. Importantly, 7?-25-OHC stimulation promotes HSPC emergence in vivo and in vitro, providing an attractive strategy for enhancing the in vitro generation of functional HSPCs. äG protein-coupled receptor 183 facilitates endothelial-to-hematopoieti(epmc).pdf DeepDyve Pubget Overpricing