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10.1038/ncomms13272 http://scihub22266oqcxt.onion/10.1038/ncomms13272 C5105158!5105158 !27827362     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 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27827362 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Nat+Commun 2016 ; 7 (ä): 13272 Nephropedia Template TP {{tp|p=27827362 |t=2016. Contracting CAG/CTG repeats using the CRISPR-Cas9 nickase |pdf=|usr=}}{{27827362 }} gab.com Text Contracting CAG/CTG repeats using the CRISPR-Cas9 nickase JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=27827362 #FOAvip CAG/CTG repeat expansions cause over 13 neurological diseases that remain without a cure. Because longer tracts cause more severe phenotypes, contracting them may provide a therapeutic avenue. No currently known agent can specifically generate contractions. Using a GFP-based chromosomal reporter that monitors expansions and contractions in the same cell population, here we find that inducing double-strand breaks within the repeat tract causes instability in both directions. In contrast, the CRISPR-Cas9 D10A nickase induces mainly contractions independently of single-strand break repair. Nickase-induced contractions depend on the DNA damage response kinase ATM, whereas ATR inhibition increases both expansions and contractions in a MSH2- and XPA-dependent manner. We propose that DNA gaps lead to contractions and that the type of DNA damage present within the repeat tract dictates the levels and the direction of CAG repeat instability. Our study paves the way towards deliberate induction of CAG/CTG repeat contractions in vivo. Twit Text FOAVip Contracting CAG/CTG repeats using the CRISPR-Cas9 nickase ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=27827362 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27827362 #FOAvip English Wikipedia <ref>{{Cite pmid|27827362 }}</ref> Contracting CAG/CTG repeats using the CRISPR-Cas9 nickase #MMPMID27827362 Cinesi C ; Aeschbach L ; Yang B ; Dion V Nat Commun 2016[Nov]; 7 (ä): 13272 PMID27827362 show ga CAG/CTG repeat expansions cause over 13 neurological diseases that remain without a cure. Because longer tracts cause more severe phenotypes, contracting them may provide a therapeutic avenue. No currently known agent can specifically generate contractions. Using a GFP-based chromosomal reporter that monitors expansions and contractions in the same cell population, here we find that inducing double-strand breaks within the repeat tract causes instability in both directions. In contrast, the CRISPR-Cas9 D10A nickase induces mainly contractions independently of single-strand break repair. Nickase-induced contractions depend on the DNA damage response kinase ATM, whereas ATR inhibition increases both expansions and contractions in a MSH2- and XPA-dependent manner. We propose that DNA gaps lead to contractions and that the type of DNA damage present within the repeat tract dictates the levels and the direction of CAG repeat instability. Our study paves the way towards deliberate induction of CAG/CTG repeat contractions in vivo. |*CRISPR-Cas Systems [MESH] |*DNA Breaks, Single-Stranded [MESH] |*DNA Repair [MESH] |DNA/genetics/metabolism [MESH] |Deoxyribonuclease I/*metabolism [MESH] |Genomic Instability [MESH] |Green Fluorescent Proteins/genetics/metabolism [MESH] |HEK293 Cells [MESH] |Humans [MESH] |MutS Homolog 2 Protein/genetics/metabolism [MESH] |Trinucleotide Repeat Expansion/*genetics [MESH]Contracting CAG/CTG repeats using the CRISPR-Cas9 nickase (epmc).pdf DeepDyve Pubget Overpricing