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10.1007/s40142-013-0012-8 http://scihub22266oqcxt.onion/10.1007/s40142-013-0012-8 C3665418!3665418!23730541     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=23730541&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 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\23730541.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Curr+Genet+Med+Rep 2013 ; 1 (2): 81-90 Nephropedia Template TP {{tp|p=23730541|t=2013. Mechanisms for Structural Variation in the Human Genome |pdf=|usr=}}{{23730541}} gab.com Text Mechanisms for Structural Variation in the Human Genome JO: Curr Genet Med Rep http://www.kidney.de/pget.php?&tw=1&pmid=23730541 #FOAvip It has been known for several decades that genetic variation involving changes to chromosomal structure (i.e., structural variants) can contribute to disease; however this relationship has been brought into acute focus in recent years largely based on innovative new genomics approaches and technology. Structural variants (SVs) arise from improperly repaired DNA double-strand breaks (DSB). DSBs are a frequent occurrence in all cells and two major pathways are involved in their repair: homologous recombination and non-homologous end joining. Errors during these repair mechanisms can result in SVs that involve losses, gains and rearrangements ranging from a few nucleotides to entire chromosomal arms. Factors such as rearrangements, hotspots and induced DSBs are implicated in the formation of SVs. While de novo SVs are often associated with disease, some SVs are conserved within human subpopulations and may have had a meaningful influence on primate evolution. As the ability to sequence the whole human genome rapidly evolves, the diversity of SVs is illuminated, including very complex rearrangements involving multiple DSBs in a process recently designated as ?chromothripsis?. Elucidating mechanisms involved in the etiology of SVs informs disease pathogenesis as well as the dynamic function associated with the biology and evolution of human genomes. Twit Text FOAVip Mechanisms for Structural Variation in the Human Genome ????Curr Genet Med Rep http://www.kidney.de/pget.php?&tw=1&pmid=23730541 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23730541 #FOAvip English Wikipedia <ref>{{Cite pmid|23730541}}</ref> Mechanisms for Structural Variation in the Human Genome #MMPMID23730541 Currall BB; Chiang C; Talkowski ME; Morton CC Curr Genet Med Rep 2013[Jun]; 1 (2): 81-90 PMID23730541show ga It has been known for several decades that genetic variation involving changes to chromosomal structure (i.e., structural variants) can contribute to disease; however this relationship has been brought into acute focus in recent years largely based on innovative new genomics approaches and technology. Structural variants (SVs) arise from improperly repaired DNA double-strand breaks (DSB). DSBs are a frequent occurrence in all cells and two major pathways are involved in their repair: homologous recombination and non-homologous end joining. Errors during these repair mechanisms can result in SVs that involve losses, gains and rearrangements ranging from a few nucleotides to entire chromosomal arms. Factors such as rearrangements, hotspots and induced DSBs are implicated in the formation of SVs. While de novo SVs are often associated with disease, some SVs are conserved within human subpopulations and may have had a meaningful influence on primate evolution. As the ability to sequence the whole human genome rapidly evolves, the diversity of SVs is illuminated, including very complex rearrangements involving multiple DSBs in a process recently designated as ?chromothripsis?. Elucidating mechanisms involved in the etiology of SVs informs disease pathogenesis as well as the dynamic function associated with the biology and evolution of human genomes. äMechanisms for Structural Variation in the Human Genome (epmc).pdf DeepDyve Pubget Overpricing