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10.1038/cddis.2017.483 http://scihub22266oqcxt.onion/10.1038/cddis.2017.483 C5682651!5682651!28981102     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Death+Dis 2017 ; 8 (10): e3084- Nephropedia Template TP {{tp|p=28981102|t=2017. Regulation of RIP3 by the transcription factor Sp1 and the epigenetic regulator UHRF1 modulates cancer cell necroptosis |pdf=|usr=}}{{28981102}} gab.com Text Regulation of RIP3 by the transcription factor Sp1 and the epigenetic regulator UHRF1 modulates cancer cell necroptosis JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=28981102 #FOAvip Receptor-interacting kinase-3 (RIP3) is a key regulator of necroptosis. It has been shown that the expression of RIP3 is silenced in most cancer cells and tissues due to genomic methylation. However, the regulatory mechanisms controlling RIP3 expression in cancer cells have not been fully elucidated. Here, we report that Sp1, a well-characterized zinc-finger transcription factor, directly regulates RIP3 expression in cancer cells. Knockdown of endogenous Sp1 significantly decreases the transcription of Rip3, thereby further inhibiting necroptosis. The re-expression of Sp1 restores the necroptotic response. In addition, knockdown of epigenetic regulator UHRF1 (ubiquitin-like, containing PHD and RING finger domains 1) in RIP3-null cancer cells reduces the methylation level of the Rip3 promoter. This effect is sufficient to trigger the expression of RIP3 in RIP3-null cancer cells. The induced expression of RIP3 by UHRF1 RNAi depends on the presence of Sp1. Remarkably, the ectopic expression of RIP3 in RIP3-null cancer cells results in a decrease in tumor growth in mice. Therefore, our findings offer insights into RIP3 expression control in cancer cells and suggest an inhibitory effect of RIP3 on tumorigenesis. Twit Text FOAVip Regulation of RIP3 by the transcription factor Sp1 and the epigenetic regulator UHRF1 modulates cancer cell necroptosis ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=28981102 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28981102 #FOAvip English Wikipedia <ref>{{Cite pmid|28981102}}</ref> Regulation of RIP3 by the transcription factor Sp1 and the epigenetic regulator UHRF1 modulates cancer cell necroptosis #MMPMID28981102 Yang C; Li J; Yu L; Zhang Z; Xu F; Jiang L; Zhou X; He S Cell Death Dis 2017[Oct]; 8 (10): e3084- PMID28981102show ga Receptor-interacting kinase-3 (RIP3) is a key regulator of necroptosis. It has been shown that the expression of RIP3 is silenced in most cancer cells and tissues due to genomic methylation. However, the regulatory mechanisms controlling RIP3 expression in cancer cells have not been fully elucidated. Here, we report that Sp1, a well-characterized zinc-finger transcription factor, directly regulates RIP3 expression in cancer cells. Knockdown of endogenous Sp1 significantly decreases the transcription of Rip3, thereby further inhibiting necroptosis. The re-expression of Sp1 restores the necroptotic response. In addition, knockdown of epigenetic regulator UHRF1 (ubiquitin-like, containing PHD and RING finger domains 1) in RIP3-null cancer cells reduces the methylation level of the Rip3 promoter. This effect is sufficient to trigger the expression of RIP3 in RIP3-null cancer cells. The induced expression of RIP3 by UHRF1 RNAi depends on the presence of Sp1. Remarkably, the ectopic expression of RIP3 in RIP3-null cancer cells results in a decrease in tumor growth in mice. Therefore, our findings offer insights into RIP3 expression control in cancer cells and suggest an inhibitory effect of RIP3 on tumorigenesis. äRegulation of RIP3 by the transcription factor Sp1 and the epigenetic (epmc).pdf DeepDyve Pubget Overpricing