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10.1016/j.gde.2013.10.009

http://scihub22266oqcxt.onion/10.1016/j.gde.2013.10.009
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C4073234!4073234!24287333
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suck abstract from ncbi


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pmid24287333      Curr+Opin+Genet+Dev 2013 ; 23 (6): 635-41
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  • Using chromatin marks to interpret and localize genetic associations to complex human traits and diseases #MMPMID24287333
  • Trynka G; Raychaudhuri S
  • Curr Opin Genet Dev 2013[Dec]; 23 (6): 635-41 PMID24287333show ga
  • While studies to associate genomic variants to complex traits have gradually become increasingly productive, the molecular mechanisms that underlie these associations are rarely understood. Because only a small fraction of trait-associated variants can be linked to coding sequences, investigators have speculated that many of the underlying causal alleles influence non-coding gene regulatory sites. Recent studies have successfully identified examples of mechanisms for non-coding alleles at individual loci. Now, genome-wide chromatin assays have resulted in maps of dozens of genomic annotations of the non-coding genome across multiple different tissues, cell types and cell lines. This gives a tremendous opportunity to integrate these annotations with complex trait signals to globally interpret associated variants, and prioritize likely causal alleles. Here, we review the examples of mechanisms by which non-coding, common alleles result in phenotypes. We discuss the efforts to integrate common trait-associated variants with genomic annotations. Finally, we highlight some caveats of these approaches and outline future directions for improvement.
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