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10.1038/ncomms15021 http://scihub22266oqcxt.onion/10.1038/ncomms15021 C5414047!5414047 !28443643     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28443643 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Nat+Commun 2017 ; 8 (ä): 15021 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[Apr]; 8 (ä): 15021 PMID28443643 show 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-?. |A549 Cells [MESH] |Adaptor Proteins, Signal Transducing/genetics/*metabolism [MESH] |Animals [MESH] |Apoptosis Regulatory Proteins [MESH] |Breast Neoplasms/genetics/*metabolism/pathology [MESH] |Cell Line, Tumor [MESH] |Cell Movement [MESH] |Female [MESH] |HEK293 Cells [MESH] |HeLa Cells [MESH] |Humans [MESH] |MCF-7 Cells [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Mice, Nude [MESH] |Neoplasm Metastasis [MESH] |Phosphorylation [MESH] |Protein Serine-Threonine Kinases/*metabolism [MESH] |Proto-Oncogene Proteins c-akt/*metabolism [MESH] |Receptor, Transforming Growth Factor-beta Type II [MESH] |Receptors, Transforming Growth Factor beta/*metabolism [MESH]FAF1 phosphorylation by AKT accumulates TGF-? type II receptor and dri(epmc).pdf DeepDyve Pubget Overpricing