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10.1016/j.cell.2016.05.052 http://scihub22266oqcxt.onion/10.1016/j.cell.2016.05.052 C5004630!5004630!27374332     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       Cell 2016 ; 166 (2): 328-42 Nephropedia Template TP {{tp|p=27374332|t=2016. Nfib promotes Metastasis through a Widespread Increase in Chromatin Accessibility |pdf=|usr=}}{{27374332}} gab.com Text Nfib promotes Metastasis through a Widespread Increase in Chromatin Accessibility JO: Cell http://www.kidney.de/pget.php?&tw=1&pmid=27374332 #FOAvip Metastases are the main cause of cancer deaths, but the mechanisms underlying metastatic progression remain poorly understood. We isolated pure populations of cancer cells from primary tumors and metastases from a genetically engineered mouse model of human small cell lung cancer (SCLC) to investigate the mechanisms that drive the metastatic spread of this lethal cancer. Genome-wide characterization of chromatin accessibility revealed the opening of large numbers of distal regulatory elements across the genome during metastatic progression. These changes correlate with copy number amplification of the Nfib locus, and differentially accessible sites were highly enriched for Nfib transcription factor binding sites. Nfib is necessary and sufficient to increase chromatin accessibility at a large subset of the intergenic regions. Nfib promotes pro-metastatic neuronal gene expression programs and drives the metastatic ability of SCLC cells. The identification of widespread chromatin changes during SCLC progression reveals an unexpected global reprogramming during metastatic progression. Twit Text FOAVip Nfib promotes Metastasis through a Widespread Increase in Chromatin Accessibility ????Cell http://www.kidney.de/pget.php?&tw=1&pmid=27374332 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27374332 #FOAvip English Wikipedia <ref>{{Cite pmid|27374332}}</ref> Nfib promotes Metastasis through a Widespread Increase in Chromatin Accessibility #MMPMID27374332 Denny SK; Yang D; Chuang CH; Brady JJ; Lim JS; Grüner BM; Chiou SH; Schep AN; Baral J; Hamard C; Antoine M; Wislez M; Kong CS; Connolly AJ; Park KS; Sage J; Greenleaf WJ; Winslow MM Cell 2016[Jul]; 166 (2): 328-42 PMID27374332show ga Metastases are the main cause of cancer deaths, but the mechanisms underlying metastatic progression remain poorly understood. We isolated pure populations of cancer cells from primary tumors and metastases from a genetically engineered mouse model of human small cell lung cancer (SCLC) to investigate the mechanisms that drive the metastatic spread of this lethal cancer. Genome-wide characterization of chromatin accessibility revealed the opening of large numbers of distal regulatory elements across the genome during metastatic progression. These changes correlate with copy number amplification of the Nfib locus, and differentially accessible sites were highly enriched for Nfib transcription factor binding sites. Nfib is necessary and sufficient to increase chromatin accessibility at a large subset of the intergenic regions. Nfib promotes pro-metastatic neuronal gene expression programs and drives the metastatic ability of SCLC cells. The identification of widespread chromatin changes during SCLC progression reveals an unexpected global reprogramming during metastatic progression. äNfib promotes Metastasis through a Widespread Increase in Chromatin Ac(epmc).pdf DeepDyve Pubget Overpricing