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10.1080/15384101.2016.1198864 http://scihub22266oqcxt.onion/10.1080/15384101.2016.1198864 C5026799!5026799!27315462     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       Cell+Cycle 2016 ; 15 (18): 2398-404 Nephropedia Template TP {{tp|p=27315462|t=2016. Twist1 and Slug mediate H2AX-regulated epithelial-mesenchymal transition in breast cells |pdf=|usr=}}{{27315462}} gab.com Text Twist1 and Slug mediate H2AX-regulated epithelial-mesenchymal transition in breast cells JO: Cell Cycle http://www.kidney.de/pget.php?&tw=1&pmid=27315462 #FOAvip The epithelial-mesenchymal transition (EMT) is thought to be essential for cancer metastasis. While chromatin remodeling is involved in EMT, which processes contribute to this remodeling remain poorly investigated. Recently, we showed that silencing or removal of the histone variant H2A.X induced mesenchymal-like characteristics, including activation of the EMT transcription factors, Slug and Zeb1 in human colon cancer cells. Here, we provide the evidence that H2A.X loss in human non-tumorigenic breast cell line MCF10A results in a robust EMT activation, as substantiated by a genome-wide expression analysis. Cells deficient for H2A.X exhibit enhanced migration and invasion, along with an activation of a set of mesenchymal genes and a concomitant repression of epithelial genes. In the breast model, the EMT-related transcription factor Twist1 cooperates with Slug to regulate EMT upon H2A.X Loss. Of interest, H2A.X expression level tightly correlates with Twist1, and to a lesser extent with Slug in the panel of human breast cancer cell lines of the NCI-60 datasets. These new findings indicate that H2A.X is involved in the EMT processes in cells of different origins but pairing with transcription factors for EMT may be tissue specific. Twit Text FOAVip Twist1 and Slug mediate H2AX-regulated epithelial-mesenchymal transition in breast cells ????Cell Cycle http://www.kidney.de/pget.php?&tw=1&pmid=27315462 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27315462 #FOAvip English Wikipedia <ref>{{Cite pmid|27315462}}</ref> Twist1 and Slug mediate H2AX-regulated epithelial-mesenchymal transition in breast cells #MMPMID27315462 Weyemi U; Redon CE; Sethi TK; Burrell AS; Jailwala P; Kasoji M; Abrams N; Merchant A; Bonner WM Cell Cycle 2016[]; 15 (18): 2398-404 PMID27315462show ga The epithelial-mesenchymal transition (EMT) is thought to be essential for cancer metastasis. While chromatin remodeling is involved in EMT, which processes contribute to this remodeling remain poorly investigated. Recently, we showed that silencing or removal of the histone variant H2A.X induced mesenchymal-like characteristics, including activation of the EMT transcription factors, Slug and Zeb1 in human colon cancer cells. Here, we provide the evidence that H2A.X loss in human non-tumorigenic breast cell line MCF10A results in a robust EMT activation, as substantiated by a genome-wide expression analysis. Cells deficient for H2A.X exhibit enhanced migration and invasion, along with an activation of a set of mesenchymal genes and a concomitant repression of epithelial genes. In the breast model, the EMT-related transcription factor Twist1 cooperates with Slug to regulate EMT upon H2A.X Loss. Of interest, H2A.X expression level tightly correlates with Twist1, and to a lesser extent with Slug in the panel of human breast cancer cell lines of the NCI-60 datasets. These new findings indicate that H2A.X is involved in the EMT processes in cells of different origins but pairing with transcription factors for EMT may be tissue specific. δTwist1 and Slug mediate H2AX-regulated epithelial-mesenchymal transiti(epmc).pdf DeepDyve Pubget Overpricing