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10.1038/ncomms15021 http://scihub22266oqcxt.onion/10.1038/ncomms15021 C5414047!5414047!28443643     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 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       Nat+Commun 2017 ; 8 (ä): ä Nephropedia Template TP {{tp|p=28443643|t=2017. FAF1 phosphorylation by AKT accumulates TGF-? type II receptor and drives breast cancer metastasis |pdf=|usr=}}{{28443643}} gab.com Text FAF1 phosphorylation by AKT accumulates TGF- type II receptor and drives breast cancer metastasis JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=28443643 #FOAvip TGF-? is pro-metastatic for the late-stage breast cancer cells. Despite recent progress, the regulation of TGF-? type II receptor remains uncertain. Here we report that FAF1 destabilizes T?RII on the cell surface by recruiting the VCP/E3 ligase complex, thereby limiting excessive TGF-? response. Importantly, activated AKT directly phosphorylates FAF1 at Ser 582, which disrupts the FAF1?VCP complex and reduces FAF1 at the plasma membrane. The latter results in an increase in T?RII at the cell surface that promotes both TGF-?-induced SMAD and non-SMAD signalling. We uncover a metastasis suppressing role for FAF1 through analyses of FAF1-knockout animals, various in vitro and in vivo models of epithelial-to-mesenchymal transition and metastasis, an MMTV-PyMT transgenic mouse model of mammary tumour progression and clinical breast cancer samples. These findings describe a previously uncharacterized mechanism by which T?RII is tightly controlled. Together, we reveal how SMAD and AKT pathways interact to confer pro-oncogenic responses to TGF-?. Twit Text FOAVip FAF1 phosphorylation by AKT accumulates TGF- type II receptor and drives breast cancer metastasis ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=28443643 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28443643 #FOAvip English Wikipedia <ref>{{Cite pmid|28443643}}</ref> FAF1 phosphorylation by AKT accumulates TGF-? type II receptor and drives breast cancer metastasis #MMPMID28443643 Xie F; Jin K; Shao L; Fan Y; Tu Y; Li Y; Yang B; van Dam H; ten Dijke P; Weng H; Dooley S; Wang S; Jia J; Jin J; Zhou F; Zhang L Nat Commun 2017[]; 8 (ä): ä PMID28443643show ga TGF-? is pro-metastatic for the late-stage breast cancer cells. Despite recent progress, the regulation of TGF-? type II receptor remains uncertain. Here we report that FAF1 destabilizes T?RII on the cell surface by recruiting the VCP/E3 ligase complex, thereby limiting excessive TGF-? response. Importantly, activated AKT directly phosphorylates FAF1 at Ser 582, which disrupts the FAF1?VCP complex and reduces FAF1 at the plasma membrane. The latter results in an increase in T?RII at the cell surface that promotes both TGF-?-induced SMAD and non-SMAD signalling. We uncover a metastasis suppressing role for FAF1 through analyses of FAF1-knockout animals, various in vitro and in vivo models of epithelial-to-mesenchymal transition and metastasis, an MMTV-PyMT transgenic mouse model of mammary tumour progression and clinical breast cancer samples. These findings describe a previously uncharacterized mechanism by which T?RII is tightly controlled. Together, we reveal how SMAD and AKT pathways interact to confer pro-oncogenic responses to TGF-?. äFAF1 phosphorylation by AKT accumulates TGF-? type II receptor and dri(epmc).pdf DeepDyve Pubget Overpricing