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10.1038/s41598-018-28795-y http://scihub22266oqcxt.onion/10.1038/s41598-018-28795-y C6045645!6045645!30006568     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=30006568&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Sci+Rep 2018 ; 8 (ä): ä Nephropedia Template TP {{tp|p=30006568|t=2018. VHL inactivation without hypoxia is sufficient to achieve genome hypermethylation |pdf=|usr=}}{{30006568}} gab.com Text VHL inactivation without hypoxia is sufficient to achieve genome hypermethylation JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=30006568 #FOAvip VHL inactivation is a key oncogenic event for renal carcinomas. In normoxia, VHL suppresses HIF1a-mediated transcriptional response, which is characteristic to hypoxia. It has previously been shown that hypoxic conditions inhibit TET-dependent hydroxymethylation of cytosines and cause DNA hypermethylation at gene promoters. In this work, we performed VHL inactivation by CRISPR/Cas9 and studied its effects on gene expression and DNA methylation. We showed that even without hypoxia, VHL inactivation leads to hypermethylation of the genome. Hypermethylated cytosines were evenly distributed throughout the genome with a slight preference for AP-1 (JUN and FOS) binding sites. Hypermethylated cytosines tended to be enriched within the binding sites of transcription factors that showed increased gene expression after VHL inactivation. We also observed promoter hypermethylation associated with decreased gene expression for several regulators of transcription and DNA methylation including SALL3. Twit Text FOAVip VHL inactivation without hypoxia is sufficient to achieve genome hypermethylation ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=30006568 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30006568 #FOAvip English Wikipedia <ref>{{Cite pmid|30006568}}</ref> VHL inactivation without hypoxia is sufficient to achieve genome hypermethylation #MMPMID30006568 Artemov AV; Zhigalova N; Zhenilo S; Mazur AM; Prokhortchouk EB Sci Rep 2018[]; 8 (ä): ä PMID30006568show ga VHL inactivation is a key oncogenic event for renal carcinomas. In normoxia, VHL suppresses HIF1a-mediated transcriptional response, which is characteristic to hypoxia. It has previously been shown that hypoxic conditions inhibit TET-dependent hydroxymethylation of cytosines and cause DNA hypermethylation at gene promoters. In this work, we performed VHL inactivation by CRISPR/Cas9 and studied its effects on gene expression and DNA methylation. We showed that even without hypoxia, VHL inactivation leads to hypermethylation of the genome. Hypermethylated cytosines were evenly distributed throughout the genome with a slight preference for AP-1 (JUN and FOS) binding sites. Hypermethylated cytosines tended to be enriched within the binding sites of transcription factors that showed increased gene expression after VHL inactivation. We also observed promoter hypermethylation associated with decreased gene expression for several regulators of transcription and DNA methylation including SALL3. äVHL inactivation without hypoxia is sufficient to achieve genome hyper(epmc).pdf DeepDyve Pubget Overpricing