What HaveWe Learned fromGWAS?
Author:
Publisher
Springer International Publishing
Link
http://link.springer.com/content/pdf/10.1007/978-3-030-61646-5_7
Reference99 articles.
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2. Anderson CA, Soranzo N, Zeggini E, Barrett JC (2011) Synthetic associations are unlikely to account for many common disease genome-wide association signals. PLoS Biol 9:e1000580
3. Bauer DE, Kamran SC, Lessard S, Xu J, Fujiwara Y, Lin C, Shao Z, Canver MC, Smith EC, Pinello L, Sabo PJ, Vierstra J, Voit RA, Yuan GC, Porteus MH, Stamatoyannopoulos JA, Lettre G, Orkin SH (2013) An erythroid enhancer of BCL11A subject to genetic variation determines fetal hemoglobin level. Science 342:253–257
4. Beer NL, Tribble ND, McCulloch LJ, Roos C, Johnson PR, Orho-Melander M, Gloyn AL (2009) The P446L variant in GCKR associated with fasting plasma glucose and triglyceride levels exerts its effect through increased glucokinase activity in liver. Hum Mol Genet 18:4081–4088
5. Bodmer W, Bonilla C (2008) Common and rare variants in multifactorial susceptibility to common diseases. Nat Genet 40:695–701
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