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10.3389/fgene.2017.00067 http://scihub22266oqcxt.onion/10.3389/fgene.2017.00067 C5440461!5440461!28588610     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Front+Genet 2017 ; 8 (ä): ä Nephropedia Template TP {{tp|p=28588610|t=2017. Ubiquitination and SUMOylation in Telomere Maintenance and Dysfunction |pdf=|usr=}}{{28588610}} gab.com Text Ubiquitination and SUMOylation in Telomere Maintenance and Dysfunction JO: Front Genet http://www.kidney.de/pget.php?&tw=1&pmid=28588610 #FOAvip Telomeres are essential nucleoprotein structures at linear chromosomes that maintain genome integrity by protecting chromosome ends from being recognized and processed as damaged DNA. In addition, they limit the cell?s proliferative capacity, as progressive loss of telomeric DNA during successive rounds of cell division eventually causes a state of telomere dysfunction that prevents further cell division. When telomeres become critically short, the cell elicits a DNA damage response resulting in senescence, apoptosis or genomic instability, thereby impacting on aging and tumorigenesis. Over the past years substantial progress has been made in understanding the role of post-translational modifications in telomere-related processes, including telomere maintenance, replication and dysfunction. This review will focus on recent findings that establish an essential role for ubiquitination and SUMOylation at telomeres. Twit Text FOAVip Ubiquitination and SUMOylation in Telomere Maintenance and Dysfunction ????Front Genet http://www.kidney.de/pget.php?&tw=1&pmid=28588610 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28588610 #FOAvip English Wikipedia <ref>{{Cite pmid|28588610}}</ref> Ubiquitination and SUMOylation in Telomere Maintenance and Dysfunction #MMPMID28588610 Yalçin Z; Selenz C; Jacobs JJL Front Genet 2017[]; 8 (ä): ä PMID28588610show ga Telomeres are essential nucleoprotein structures at linear chromosomes that maintain genome integrity by protecting chromosome ends from being recognized and processed as damaged DNA. In addition, they limit the cell?s proliferative capacity, as progressive loss of telomeric DNA during successive rounds of cell division eventually causes a state of telomere dysfunction that prevents further cell division. When telomeres become critically short, the cell elicits a DNA damage response resulting in senescence, apoptosis or genomic instability, thereby impacting on aging and tumorigenesis. Over the past years substantial progress has been made in understanding the role of post-translational modifications in telomere-related processes, including telomere maintenance, replication and dysfunction. This review will focus on recent findings that establish an essential role for ubiquitination and SUMOylation at telomeres. äUbiquitination and SUMOylation in Telomere Maintenance and Dysfunction(epmc).pdf DeepDyve Pubget Overpricing