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Badania nad regulacją resekcji DNA w przypadku dwuniciowych pęknięc DNA (DSB) wywolanych jonami
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ISBN10: 6208984173
ISBN13: 9786208984175
Publisher: Wydawnictwo Nasza Wiedza
Published: Jun 20 2025
Pages: 116
Weight: 0.36
Height: 0.28 Width: 6.00 Depth: 9.00
Language: Polish
ISBN13: 9786208984175
Publisher: Wydawnictwo Nasza Wiedza
Published: Jun 20 2025
Pages: 116
Weight: 0.36
Height: 0.28 Width: 6.00 Depth: 9.00
Language: Polish
Zlożone podwójne pęknięcia nici DNA (DSB) są najpoważniejszym uszkodzeniem DNA, ponieważ stanowią ogromne wyzwanie dla komórki, zarówno pod względem wiernej naprawy, jak i samej możliwości naprawy. Znane są dwie glówne ścieżki naprawy DSB: klasyczne niehomologiczne lączenie końców (c-NHEJ) i rekombinacja homologiczna (HR). c-NHEJ jest dostępne we wszystkich fazach cyklu komórkowego, podczas gdy szlak HR funkcjonuje tylko w fazie S/G2, gdy chromatyd siostrzana jest dostępna jako matryca. Ponadto komórki mają do dyspozycji jeszcze jeden szlak naprawy - alternatywne niehomologiczne lączenie końców (alt-NHEJ), które może dzialac na resekowane końce pęknięc DNA. Resekcja DNA jest ważnym etapem w podejmowaniu przez komórkę decyzji o wyborze szlaku naprawy DSB. Resekcja DNA zachodzi nie tylko w komórkach S/G2, ale także w komórkach G1 po zlożonym uszkodzeniu DNA wywolanym promieniowaniem ciężkimi jonami. Celem tej pracy jest wyjaśnienie mechanizmu regulacji resekcji w komórkach G1 po napromieniowaniu ciężkimi jonami. Skupia się ona w szczególności na roli czynników regulujących resekcję RIF1 i BRCA1. Przydatnym modelem do badania mechanizmu ograniczenia resekcji są komórki w stanie spoczynku, komórki G0.
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