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<article article-type="research-article" dtd-version="1.3" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xml:lang="ru"><front><journal-meta><journal-id journal-id-type="publisher-id">medgen</journal-id><journal-title-group><journal-title xml:lang="ru">Медицинская генетика</journal-title><trans-title-group xml:lang="en"><trans-title>Medical Genetics</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2073-7998</issn><publisher><publisher-name>Publishing House «Genius Media» LLC</publisher-name></publisher></journal-meta><article-meta><article-id custom-type="elpub" pub-id-type="custom">medgen-1820</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>КРАТКИЕ СООБЩЕНИЯ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>BRIEF REPORT</subject></subj-group></article-categories><title-group><article-title>Количественный полиморфизм тандемных повторов как способ эпигенетической регуляции ответа клеток человека на окислительный стресс</article-title><trans-title-group xml:lang="en"><trans-title>Quantitative polymorphism of tandem repeats as a method of epigenetic regulation of the of human cells response to oxidative stress</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Вейко</surname><given-names>Н. Н.</given-names></name><name name-style="western" xml:lang="en"><surname>Veiko</surname><given-names>N. N.</given-names></name></name-alternatives><email xlink:type="simple">satelit32006@yandex.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Ершова</surname><given-names>Е. С.</given-names></name><name name-style="western" xml:lang="en"><surname>Ershova</surname><given-names>E. S.</given-names></name></name-alternatives><email xlink:type="simple">noemail@neicon.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Конькова</surname><given-names>М. С.</given-names></name><name name-style="western" xml:lang="en"><surname>Konkova</surname><given-names>M. C.</given-names></name></name-alternatives><email xlink:type="simple">noemail@neicon.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Малиновская</surname><given-names>Е. М.</given-names></name><name name-style="western" xml:lang="en"><surname>Malinovskaya</surname><given-names>E. M.</given-names></name></name-alternatives><email xlink:type="simple">noemail@neicon.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Костюк</surname><given-names>С. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Kostyuk</surname><given-names>S. V.</given-names></name></name-alternatives><email xlink:type="simple">noemail@neicon.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Медико-генетический научный центр им. академика Н.П. Бочкова</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Research Centre for Medical Genetics</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2020</year></pub-date><pub-date pub-type="epub"><day>02</day><month>02</month><year>2021</year></pub-date><volume>19</volume><issue>12</issue><fpage>68</fpage><lpage>70</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Вейко Н.Н., Ершова Е.С., Конькова М.С., Малиновская Е.М., Костюк С.В., 2021</copyright-statement><copyright-year>2021</copyright-year><copyright-holder xml:lang="ru">Вейко Н.Н., Ершова Е.С., Конькова М.С., Малиновская Е.М., Костюк С.В.</copyright-holder><copyright-holder xml:lang="en">Veiko N.N., Ershova E.S., Konkova M.C., Malinovskaya E.M., Kostyuk S.V.</copyright-holder><license xml:lang="ru" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>Данная работа распространяется под лицензией Creative Commons Attribution 4.0.</license-p></license><license xml:lang="en" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>This work is licensed under a Creative Commons Attribution 4.0 License.</license-p></license></permissions><self-uri xlink:href="https://www.medgen-journal.ru/jour/article/view/1820">https://www.medgen-journal.ru/jour/article/view/1820</self-uri><abstract><p>Пространственная организация хроматина важна для нормального функционирования клетки. На архитектуру ядра влияют размеры отдельных фрагментов генома, которые коррелируют с числом копий этих фрагментов. Перемещение локусов 1q12 от поверхности ядра в центральные области является ключевой стадией адаптивного ответа клетки на стресс. Мы предположили, что размер локусов 1q12, который коррелирует с содержанием повтора f-SatIII, может влиять на перемещение этих участков хроматина в ядре. Методом FISH на выделенных лимфоцитах показали, что в контроле локусы 1q12 расположены вблизи поверхности ядра, в ядрах лимфоцитов больных шизофренией (БШ) и облученных контрольных клеток локусы 1q12 расположены в центральных районах ядра. Длительное культивирование облученных лимфоцитов сопровождалось гибелью клеток, и снижением содержания f-SatIII в ДНК. Очевидно, что погибали клетки с большим размером 1q12 (много f-SatIII), обогащая популяцию клетками с низким содержанием f-SatIII. В клетках БШ и в облученных клетках мы обнаружили повышение уровня РНК SATIII. Размеры гетерохроматина 1q12 в клетках человека могут влиять на процессы пролиферации и ответа клетки на стресс. Количественный полиморфизм тандемных повторов генома - один из эпигенетических механизмов регуляции ответа клеток на окислительный стресс.</p></abstract><trans-abstract xml:lang="en"><p>The spatial organization of chromatin is important for the normal functioning of the cell. Genome repeat cluster sizes can affect the chromatin spatial configuration and function. The 1q12 heterochromatin loci movement from the periphery to the center of the nucleus is the cells’ universal response to various types of stress. We hypothesized that a large 1q12 domain could affect chromatin movement, thereby inhibiting adaptive response (AR). Using the FISH method, we shown that in the control, 1q12 loci are located near the surface of the nucleus; in the lymphocyte nuclei of schizophrenic patients and irradiated control cells, 1q12 loci are located in the central regions of the nucleus. During prolonged cultivation, the irradiated cells with a large Large f-SatIII amount die and the population is enriched with the cells with low f-SatIII content. In intact SZ patients’ lymphocytes and in irradiated cells we found an increase in SATIII RNA levels. The size of heterochromatin 1q12 loci in human cells can affect to the proliferation and cells’ adaptive response to stress. Quantitative polymorphism of tandem genome repeats is one of the epigenetic mechanisms of genome expression’s regulation.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>CNVs</kwd><kwd>сателлит III</kwd><kwd>рибосомная ДНК</kwd><kwd>шизофрения</kwd><kwd>1q12</kwd><kwd>окислительный стресс</kwd></kwd-group><kwd-group xml:lang="en"><kwd>CNVs</kwd><kwd>satellite III</kwd><kwd>rDNA</kwd><kwd>schizophrenia</kwd><kwd>1q12cell-free dna</kwd><kwd>oxidative stress</kwd></kwd-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Paredes S., Maggert, K. A. Ribosomal DNA contributes to global chromatin regulation. Proc. Natl. Acad. Sci. U.S.A. 2009; 106 (42): 17829-17834.</mixed-citation><mixed-citation xml:lang="en">Paredes S., Maggert, K. A. Ribosomal DNA contributes to global chromatin regulation. Proc. Natl. Acad. Sci. 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