Disorder in circadian rhythm has been revealed as a risk factor for coronary heart disease. Several studies in molecular biology established a gene interaction network using coronary heart susceptibility genes and the circadian rhythm pathway. However, cross talk between genes was mostly discovered in single gene pairs. There might be combination sets of genes intergraded as a unit to regulate the network. To resolve multiple variables in coronary heart susceptibility genes controlling circadian rhythm pathways, a multiple correlation analysis was applied to the transcriptome. Nine genes, including CUGBP, Elav-like family member (CELF); sodium leak channel, nonselective (NALCN); protein phosphatase 2 regulatory subunit B gamma (PPP2R2C); tubulin alpha 1c (TUBA1C); microtubule-associated protein 4 (MAP4); cofilin 1 (CFL1); myosin heavy chain 7 (MYH7);QKI, KH domain containing RNA binding (QKI); and maternal embryonic leucine zipper kinase (MELK), from coronary heart susceptibility were identified to predict the outcome of a linear combination of circadian rhythm pathway genes withRfactor more than 0.7. G protein subunit alpha o1 (GNAO1), protein kinase C gamma (PRKCG),RBX, and G protein subunit beta 1 (GNB1) in the circadian rhythm pathway are characterized as combination variables to coexpress with coronary heart susceptibility genes.
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