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10.1073/pnas.1702913114 http://scihub22266oqcxt.onion/10.1073/pnas.1702913114 C5402468!5402468!28373572     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       Proc+Natl+Acad+Sci+U+S+A 2017 ; 114 (16): 4159-64 Nephropedia Template TP {{tp|p=28373572|t=2017. Bidirectional KCNQ1:?-catenin interaction drives colorectal cancer cell differentiation |pdf=|usr=}}{{28373572}} gab.com Text Bidirectional KCNQ1: -catenin interaction drives colorectal cancer cell differentiation JO: Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=28373572 #FOAvip The K+ channel KCNQ1 has been proposed as a tumor suppressor in colorectal cancer (CRC), but nothing is known about its regulatory role in early disease stages. KCNQ1 is a target gene of Wnt/?-catenin, which is tonically activated in CRC. We demonstrate a bidirectional interaction between KCNQ1 and ?-catenin as a key regulator of CRC cell differentiation, proliferation, and invasion. KCNQ1 stabilizes ?-catenin at adherent junctions to maintain an epithelial phenotype. The ?-catenin:T-cell factor (TCF)-4 transcriptional pathway directly represses KCNQ1 expression, and the loss of KCNQ1 was associated with an epithelial?mesenchymal transition. The KCNQ1:KCNE3 ion channel complex expression in primary tumors was correlated with good survival outcome for patients with CRC. KCNQ1 is a potential early prognostic biomarker for CRC. Twit Text FOAVip Bidirectional KCNQ1: -catenin interaction drives colorectal cancer cell differentiation ????Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=28373572 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28373572 #FOAvip English Wikipedia <ref>{{Cite pmid|28373572}}</ref> Bidirectional KCNQ1:?-catenin interaction drives colorectal cancer cell differentiation #MMPMID28373572 Rapetti-Mauss R; Bustos V; Thomas W; McBryan J; Harvey H; Lajczak N; Madden SF; Pellissier B; Borgese F; Soriani O; Harvey BJ Proc Natl Acad Sci U S A 2017[Apr]; 114 (16): 4159-64 PMID28373572show ga The K+ channel KCNQ1 has been proposed as a tumor suppressor in colorectal cancer (CRC), but nothing is known about its regulatory role in early disease stages. KCNQ1 is a target gene of Wnt/?-catenin, which is tonically activated in CRC. We demonstrate a bidirectional interaction between KCNQ1 and ?-catenin as a key regulator of CRC cell differentiation, proliferation, and invasion. KCNQ1 stabilizes ?-catenin at adherent junctions to maintain an epithelial phenotype. The ?-catenin:T-cell factor (TCF)-4 transcriptional pathway directly represses KCNQ1 expression, and the loss of KCNQ1 was associated with an epithelial?mesenchymal transition. The KCNQ1:KCNE3 ion channel complex expression in primary tumors was correlated with good survival outcome for patients with CRC. KCNQ1 is a potential early prognostic biomarker for CRC. äBidirectional KCNQ1:?-catenin interaction drives colorectal cancer cel(epmc).pdf DeepDyve Pubget Overpricing