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10.1016/j.gde.2016.03.008 http://scihub22266oqcxt.onion/10.1016/j.gde.2016.03.008 C4880504!4880504 !27111891     free     free     free Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27111891 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Curr+Opin+Genet+Dev 2016 ; 36 (ä): 34-40 Nephropedia Template TP {{tp|p=27111891 |t=2016. TAD disruption as oncogenic driver |pdf=|usr=}}{{27111891 }} gab.com Text TAD disruption as oncogenic driver JO: Curr Opin Genet Dev http://www.kidney.de/pget.php?&tw=1&pmid=27111891 #FOAvip Topologically Associating Domains (TADs) are conserved during evolution and play roles in guiding and constraining long-range regulation of gene expression. Disruption of TAD boundaries results in aberrant gene expression by exposing genes to inappropriate regulatory elements. Recent studies have shown that TAD disruption is often found in cancer cells and contributes to oncogenesis through two mechanisms. One mechanism locally disrupts domains by deleting or mutating a TAD boundary leading to fusion of the two adjacent TADs. The other mechanism involves genomic rearrangements that break up TADs and creates new ones without directly affecting TAD boundaries. Understanding the mechanisms by which TADs form and control long-range chromatin interactions will therefore not only provide insights into the mechanism of gene regulation in general, but will also reveal how genomic rearrangements and mutations in cancer genomes can lead to misregulation of oncogenes and tumor suppressors. Twit Text FOAVip TAD disruption as oncogenic driver ????Curr Opin Genet Dev http://www.kidney.de/pget.php?&tw=1&pmid=27111891 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27111891 #FOAvip English Wikipedia <ref>{{Cite pmid|27111891 }}</ref> TAD disruption as oncogenic driver #MMPMID27111891 Valton AL ; Dekker J Curr Opin Genet Dev 2016[Feb]; 36 (ä): 34-40 PMID27111891 show ga Topologically Associating Domains (TADs) are conserved during evolution and play roles in guiding and constraining long-range regulation of gene expression. Disruption of TAD boundaries results in aberrant gene expression by exposing genes to inappropriate regulatory elements. Recent studies have shown that TAD disruption is often found in cancer cells and contributes to oncogenesis through two mechanisms. One mechanism locally disrupts domains by deleting or mutating a TAD boundary leading to fusion of the two adjacent TADs. The other mechanism involves genomic rearrangements that break up TADs and creates new ones without directly affecting TAD boundaries. Understanding the mechanisms by which TADs form and control long-range chromatin interactions will therefore not only provide insights into the mechanism of gene regulation in general, but will also reveal how genomic rearrangements and mutations in cancer genomes can lead to misregulation of oncogenes and tumor suppressors. |*Genome, Human [MESH] |Carcinogenesis/*genetics [MESH] |Chromatin/genetics [MESH] |Gene Expression Regulation, Neoplastic/*genetics [MESH] |Genomics [MESH] |Humans [MESH] |Oncogene Proteins, Fusion/*genetics [MESH]TAD disruption as oncogenic driver (epmc).pdf DeepDyve Pubget Overpricing