Candidate SNP markers of atherosclerosis reliably altering the affinity of TATA-binding protein for human gene promoters point to stabilizing natural selection as sum of neutral drift spuring atherogenesis and directional natural selection preventing it

Poster (download) Dmitry Rasskazov1, Irina Chadaeva2, Mikhail Ponomarenko3, Ekaterina Sharypova4, Irina Drachkova5, Maria Nazarenko61Systems Biology Department, Institute of Cytology and Genetics (ICG SB RAS), Novosibirsk, Russia, rassk@bionen.nsc.ru2Systems Biology Department, Institute of Cytology and Genetics (ICG SB RAS), Novosibirsk, Russia, ichadaeva@bionet.nsc.ru3Systems Biology Department, Institute of Cytology and Genetics (ICG SB RAS), Novosibirsk, Russia, pon@bionen.nsc.ru4Molecular Genetics Department, Institute of Cytology and Genetics (ICG SB RAS), Novosibirsk, Russia, sharypova@bionet.nsc.ru5Molecular Genetics Department, Institute of Cytology and Genetics (ICG SB RAS), Novosibirsk, Russia, drachkova@bionet.nsc.ru6Population Genetics Laboratory, Institute of Medical Genetics (IMG TNRMC RAS), Tomsk, Russia, maria.nazarenko@medgenetics.ru In this work we carried out a computer-based whole-genome search for all variants of single-nucleotide polymorphism (SNP) within 70 bp regions upstream the all experimentally proven transcription start sites of the human genes associated with atherogenesis according to the current release #151 of the dbSNP database and GRCh38/hg38 assembly of the human reference genome, both of which are publicly available due to the UCSC Genome Browser. In the end, we first found atherosclerosis-related candidate SNP markers signoficantly changing the affinity of TATA-binding protein for promoters of these human gene, frequencies of which differes from the commonly accepted genome-wide norm as if they were under pressure of stabilizing natural selection, which summing up neutral drift accelerating atherogenesis and directional natural selection slowing it down

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