@article{TEXTUAL,
      recid = {10377},
      author = {Patel, Sanjay R. and Goodloe, Robert and De, Gourab and  Kowgier, Matthew and Weng, Jia and Buxbaum, Sarah G. and  Cade, Brian and Fulop, Tibor and Gharib, Sina A. and  Gottlieb, Daniel J. and Hillman, David and Larkin, Emma K.  and Lauderdale, Diane S. and Li, Li and Mukherjee, Sutapa  and Palmer, Lyle and Zee, Phyllis and Zhu, Xiaofeng},
      title = {Association of Genetic Loci with Sleep Apnea in European  Americans and African-Americans: The Candidate Gene  Association Resource (CARe)},
      journal = {PLOS ONE},
      address = {2012-11-14},
      number = {TEXTUAL},
      abstract = {<p>Although obstructive sleep apnea (OSA) is known to have  a strong familial basis, no genetic polymorphisms  influencing apnea risk have been identified in cross-cohort  analyses. We utilized the National Heart, Lung, and Blood  Institute (NHLBI) Candidate Gene Association Resource  (CARe) to identify sleep apnea susceptibility loci. Using a  panel of 46,449 polymorphisms from roughly 2,100 candidate  genes on a customized Illumina iSelect chip, we tested for  association with the apnea hypopnea index (AHI) as well as  moderate to severe OSA (AHI≥15) in 3,551 participants of  the Cleveland Family Study and two cohorts participating in  the Sleep Heart Health Study.</p><p>Among 647  African-Americans, rs11126184 in the pleckstrin (PLEK) gene  was associated with OSA while rs7030789 in the  lysophosphatidic acid receptor 1 (LPAR1) gene was  associated with AHI using a chip-wide significance  threshold of p-value<2×10<sup>−6</sup>. Among 2,904  individuals of European ancestry, rs1409986 in the  prostaglandin E2 receptor (PTGER3) gene was significantly  associated with OSA. Consistency of effects between  rs7030789 and rs1409986 in LPAR1 and PTGER3 and apnea  phenotypes were observed in independent clinic-based  cohorts.</p><p>Novel genetic loci for apnea phenotypes were  identified through the use of customized gene chips and  meta-analyses of cohort data with replication in  clinic-based samples. The identified SNPs all lie in genes  associated with inflammation suggesting inflammation may  play a role in OSA pathogenesis.</p>},
      url = {http://knowledge.uchicago.edu/record/10377},
}