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10.1155/2015/319454 http://scihub22266oqcxt.onion/10.1155/2015/319454 C4442004!4442004!26064897     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       Biomed+Res+Int 2015 ; 2015 (ä): ä Nephropedia Template TP {{tp|p=26064897|t=2015. Prohibitin: A Novel Molecular Player in KDEL Receptor Signalling |pdf=|usr=}}{{26064897}} gab.com Text Prohibitin: A Novel Molecular Player in KDEL Receptor Signalling JO: Biomed Res Int http://www.kidney.de/pget.php?&tw=1&pmid=26064897 #FOAvip The KDEL receptor (KDELR) is a seven-transmembrane-domain protein involved in retrograde transport of protein chaperones from the Golgi complex to the endoplasmic reticulum. Our recent findings have shown that the Golgi-localised KDELR acts as a functional G-protein-coupled receptor by binding to and activating Gs and Gq. These G proteins induce activation of PKA and Src and regulate retrograde and anterograde Golgi trafficking. Here we used an integrated coimmunoprecipitation and mass spectrometry approach to identify prohibitin-1 (PHB) as a KDELR interactor. PHB is a multifunctional protein that is involved in signal transduction, cell-cycle control, and stabilisation of mitochondrial proteins. We provide evidence that depletion of PHB induces intense membrane-trafficking activity at the ER?Golgi interface, as revealed by formation of GM130-positive Golgi tubules, and recruitment of p115, ?-COP, and GBF1 to the Golgi complex. There is also massive recruitment of SEC31 to endoplasmic-reticulum exit sites. Furthermore, absence of PHB decreases the levels of the Golgi-localised KDELR, thus preventing KDELR-dependent activation of Golgi-Src and inhibiting Golgi-to-plasma-membrane transport of VSVG. We propose a model whereby in analogy to previous findings (e.g., the RAS-RAF signalling pathway), PHB can act as a signalling scaffold protein to assist in KDELR-dependent Src activation. Twit Text FOAVip Prohibitin: A Novel Molecular Player in KDEL Receptor Signalling ????Biomed Res Int http://www.kidney.de/pget.php?&tw=1&pmid=26064897 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26064897 #FOAvip English Wikipedia <ref>{{Cite pmid|26064897}}</ref> Prohibitin: A Novel Molecular Player in KDEL Receptor Signalling #MMPMID26064897 Giannotta M; Fragassi G; Tamburro A; Vanessa C; Luini A; Sallese M Biomed Res Int 2015[]; 2015 (ä): ä PMID26064897show ga The KDEL receptor (KDELR) is a seven-transmembrane-domain protein involved in retrograde transport of protein chaperones from the Golgi complex to the endoplasmic reticulum. Our recent findings have shown that the Golgi-localised KDELR acts as a functional G-protein-coupled receptor by binding to and activating Gs and Gq. These G proteins induce activation of PKA and Src and regulate retrograde and anterograde Golgi trafficking. Here we used an integrated coimmunoprecipitation and mass spectrometry approach to identify prohibitin-1 (PHB) as a KDELR interactor. PHB is a multifunctional protein that is involved in signal transduction, cell-cycle control, and stabilisation of mitochondrial proteins. We provide evidence that depletion of PHB induces intense membrane-trafficking activity at the ER?Golgi interface, as revealed by formation of GM130-positive Golgi tubules, and recruitment of p115, ?-COP, and GBF1 to the Golgi complex. There is also massive recruitment of SEC31 to endoplasmic-reticulum exit sites. Furthermore, absence of PHB decreases the levels of the Golgi-localised KDELR, thus preventing KDELR-dependent activation of Golgi-Src and inhibiting Golgi-to-plasma-membrane transport of VSVG. We propose a model whereby in analogy to previous findings (e.g., the RAS-RAF signalling pathway), PHB can act as a signalling scaffold protein to assist in KDELR-dependent Src activation. äProhibitin: A Novel Molecular Player in KDEL Receptor Signalling (epmc).pdf DeepDyve Pubget Overpricing