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10.15252/embr.201541532 http://scihub22266oqcxt.onion/10.15252/embr.201541532 C5341524!5341524!27113758     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       EMBO+Rep 2016 ; 17 (5): 739-52 Nephropedia Template TP {{tp|p=27113758|t=2016. An essential role for Grk2 in Hedgehog signalling downstream of Smoothened |pdf=|usr=}}{{27113758}} gab.com Text An essential role for Grk2 in Hedgehog signalling downstream of Smoothened JO: EMBO Rep http://www.kidney.de/pget.php?&tw=1&pmid=27113758 #FOAvip The G?protein?coupled receptor kinase 2 (adrbk2/GRK2) has been implicated in vertebrate Hedgehog (Hh) signalling based on the effects of its transient knock?down in mammalian cells and zebrafish embryos. Here, we show that the response to Hh signalling is effectively abolished in the absence of Grk2 activity. Zebrafish embryos lacking all Grk2 activity are refractory to both Sonic hedgehog (Shh) and oncogenic Smoothened (Smo) activity, but remain responsive to inhibition of cAMP?dependent protein kinase (PKA) activity. Mutation of the kinase domain abrogates the rescuing activity of grk2 mRNA, suggesting that Grk2 acts in a kinase?dependent manner to regulate the response to Hh. Previous studies have suggested that Grk2 potentiates Smo activity by phosphorylating its C?terminal tail (CTT). In the zebrafish embryo, however, phosphomimetic Smo does not display constitutive activity, whereas phospho?null mutants retain activity, implying phosphorylation is neither sufficient nor necessary for Smo function. Since Grk2 rescuing activity requires the integrity of domains essential for its interaction with GPCRs, we speculate that Grk2 may regulate Hh pathway activity by downregulation of a GPCR. Twit Text FOAVip An essential role for Grk2 in Hedgehog signalling downstream of Smoothened ????EMBO Rep http://www.kidney.de/pget.php?&tw=1&pmid=27113758 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27113758 #FOAvip English Wikipedia <ref>{{Cite pmid|27113758}}</ref> An essential role for Grk2 in Hedgehog signalling downstream of Smoothened #MMPMID27113758 Zhao Z; Lee RTH; Pusapati GV; Iyu A; Rohatgi R; Ingham PW EMBO Rep 2016[May]; 17 (5): 739-52 PMID27113758show ga The G?protein?coupled receptor kinase 2 (adrbk2/GRK2) has been implicated in vertebrate Hedgehog (Hh) signalling based on the effects of its transient knock?down in mammalian cells and zebrafish embryos. Here, we show that the response to Hh signalling is effectively abolished in the absence of Grk2 activity. Zebrafish embryos lacking all Grk2 activity are refractory to both Sonic hedgehog (Shh) and oncogenic Smoothened (Smo) activity, but remain responsive to inhibition of cAMP?dependent protein kinase (PKA) activity. Mutation of the kinase domain abrogates the rescuing activity of grk2 mRNA, suggesting that Grk2 acts in a kinase?dependent manner to regulate the response to Hh. Previous studies have suggested that Grk2 potentiates Smo activity by phosphorylating its C?terminal tail (CTT). In the zebrafish embryo, however, phosphomimetic Smo does not display constitutive activity, whereas phospho?null mutants retain activity, implying phosphorylation is neither sufficient nor necessary for Smo function. Since Grk2 rescuing activity requires the integrity of domains essential for its interaction with GPCRs, we speculate that Grk2 may regulate Hh pathway activity by downregulation of a GPCR. äAn essential role for Grk2 in Hedgehog signalling downstream of Smooth(epmc).pdf DeepDyve Pubget Overpricing