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Microtubule-associated proteins MAP7 and MAP7D1 promote DNA double-strand break repair in the G1 cell cycle phase
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SYSNO ASEP 0582795 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title Microtubule-associated proteins MAP7 and MAP7D1 promote DNA double-strand break repair in the G1 cell cycle phase Author(s) Dullovi, A. (GB)
Ozgencil, M. (GB)
Rajvee, V. (GB)
Tse, W. Y. (GB)
Cutillas, P. R. (GB)
Martin, S. A. (GB)
Hořejší, Zuzana (UOCHB-X)Article number 106107 Source Title iScience. - : Cell Press
Roč. 26, č. 3 (2023)Number of pages 21 s. Language eng - English Country US - United States Keywords DNA damage ; microtubules ; microtubule-associated proteins OECD category Biochemistry and molecular biology Method of publishing Open access Institutional support UOCHB-X - RVO:61388963 UT WOS 000993587500001 EID SCOPUS 85148005797 DOI 10.1016/j.isci.2023.106107 Annotation The DNA-damage response is a complex signaling network that guards genomic integrity. The microtubule cytoskeleton is involved in the repair of DNA doublestrand breaks, however, little is known about which cytoskeleton-related pro-teins are involved in DNA repair and how. Using quantitative proteomics, we discovered that microtubule associated proteins MAP7 and MAP7D1 interact with several DNA repair proteins including DNA double-strand break repair pro-teins RAD50, BRCA1 and 53BP1. We observed that downregulation of MAP7 and MAP7D1 leads to increased phosphorylation of p53 after girradiation. More-over, we determined that the downregulation of MAP7D1 leads to a strong G1 arrest and that the downregulation of MAP7 and MAP7D1 in G1 arrested cells negatively affects DNA repair, recruitment of RAD50 to chromatin and localiza-tion of 53BP1 to the sites of damage. These findings describe for the first time a novel function of MAP7 and MAP7D1 in cell cycle regulation and repair of DNA double-strand breaks. Workplace Institute of Organic Chemistry and Biochemistry Contact asep@uochb.cas.cz ; Kateřina Šperková, Tel.: 232 002 584 ; Jana Procházková, Tel.: 220 183 418 Year of Publishing 2024 Electronic address https://doi.org/10.1016/j.isci.2023.106107
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