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Title: Уровень метилирования гистона H3 в клеточных линиях с нокаутом ADAMTS1, THBS1 и RBFOX2
Other Titles: H3 gistone methylation level in the ADAMTS1, THBS1 and RBFOX2 knockout cell lines
Authors: Савченко, Р. Р.
Васильев, С. А.
Фишман, В. С.
metadata.dc.contributor.advisor: Лебедев, И. Н.
Keywords: метилирование; гистоны; разрыв; ДНК; ионизирующие излучения; лимфоциты
Issue Date: 2018
Publisher: Издательский Дом Томского государственного университета
Citation: Савченко Р. Р. Уровень метилирования гистона H3 в клеточных линиях с нокаутом ADAMTS1, THBS1 и RBFOX2 / Р. Р. Савченко, С. А. Васильев, В. С. Фишман ; науч. рук. И. Н. Лебедев // Перспективы развития фундаментальных наук : сборник научных трудов XV Международной конференции студентов, аспирантов и молодых ученых, г. Томск, 24-27 апреля 2018 г. : в 7 т. — Томск : Издательский Дом Томского государственного университета, 2018. — Т. 4 : Биология и фундаментальная медицина. — [С. 137-139].
Abstract: At present, there is an increasing interest in indirect participants of the DNA double-strand breaks repair processes. In this study we aimed to appreciate the effects of ADAMTS1, THBS1, and RBFOX2 genes on the transcriptional regulation through a change in H3K9, H3K27, H3K4 and H3K36 methylation levels in the knockout cell lines. It was shown that the THBS1 and RBFOX2 knockout cell lines were characterized by an elevated the histone H3K9me3 level (1.8- and 1.6-fold, respectively (p < 0.01)), while no significant differences were found in other knockout cell lines. Moreover, THBS1 knockout cell line was characterized by an 1.2-fold increase in histone H3K27me3 level (p = 0.05). The H3K4 and H3K36 methylation levels were significantly decreased only in RBFOX2 knockout cell line (1.6 and 1.7-fold, respectively (p < 0.05)) in comparison with the intact HeLa. Given the effects of knockout of analyzed genes on the DNA repair effectiveness, changes in the pattern of H3 histone methylation can lead to a change in the gene expression level and, as a consequence, affect the regulation of the radiation-induced cell response to DNA damage.
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