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10.1016/j.celrep.2018.03.056 http://scihub22266oqcxt.onion/10.1016/j.celrep.2018.03.056 C5929158!5929158!29641996     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       Cell+Rep 2018 ; 23 (2): 349-60 Nephropedia Template TP {{tp|p=29641996|t=2018. Transcriptional Dysregulation of MYC Reveals Common Enhancer-Docking Mechanism |pdf=|usr=}}{{29641996}} gab.com Text Transcriptional Dysregulation of MYC Reveals Common Enhancer-Docking Mechanism JO: Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=29641996 #FOAvip Transcriptional dysregulation of the MYC oncogene is among the most frequent events in aggressive tumor cells, and this is generally accomplished by acquisition of a super-enhancer somewhere within the 2.8 Mb TAD where MYC resides. We find that these diverse cancer-specific super-enhancers, differing in size and location, interact with the MYC gene through a common and conserved CTCF binding site located 2 kb upstream of the MYC promoter. Genetic perturbation of this enhancer-docking site in tumor cells reduces CTCF binding, super-enhancer interaction, MYC gene expression, and cell proliferation. CTCF binding is highly sensitive to DNA methylation, and this enhancer-docking site, which is hypomethylated in diverse cancers, can be inactivated through epigenetic editing with dCas9-DNMT. Similar enhancer-docking sites occur at other genes, including genes with prominent roles in multiple cancers, suggesting a mechanism by which tumor cell oncogenes can generally hijack enhancers. These results provide insights into mechanisms that allow a single target gene to be regulated by diverse enhancer elements in different cell types. Twit Text FOAVip Transcriptional Dysregulation of MYC Reveals Common Enhancer-Docking Mechanism ????Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=29641996 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29641996 #FOAvip English Wikipedia <ref>{{Cite pmid|29641996}}</ref> Transcriptional Dysregulation of MYC Reveals Common Enhancer-Docking Mechanism #MMPMID29641996 Schuijers J; Manteiga JC; Weintraub AS; Day DS; Zamudio AV; Hnisz D; Lee TI; Young RA Cell Rep 2018[Apr]; 23 (2): 349-60 PMID29641996show ga Transcriptional dysregulation of the MYC oncogene is among the most frequent events in aggressive tumor cells, and this is generally accomplished by acquisition of a super-enhancer somewhere within the 2.8 Mb TAD where MYC resides. We find that these diverse cancer-specific super-enhancers, differing in size and location, interact with the MYC gene through a common and conserved CTCF binding site located 2 kb upstream of the MYC promoter. Genetic perturbation of this enhancer-docking site in tumor cells reduces CTCF binding, super-enhancer interaction, MYC gene expression, and cell proliferation. CTCF binding is highly sensitive to DNA methylation, and this enhancer-docking site, which is hypomethylated in diverse cancers, can be inactivated through epigenetic editing with dCas9-DNMT. Similar enhancer-docking sites occur at other genes, including genes with prominent roles in multiple cancers, suggesting a mechanism by which tumor cell oncogenes can generally hijack enhancers. These results provide insights into mechanisms that allow a single target gene to be regulated by diverse enhancer elements in different cell types. äTranscriptional Dysregulation of MYC Reveals Common Enhancer-Docking M(epmc).pdf DeepDyve Pubget Overpricing