{"entity": "researcher", "timestamp": "2026-09-25T21:34:05.621Z", "family": "Macurek", "given": "Libor", "initials": "L", "orcid": "0000-0002-0987-1238", "affiliations": ["Laboratory of Cancer Cell Biology, Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, Prague, Czech Republic libor.macurek@img.cas.cz arne.lindqvist@ki.se."], "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/researcher/9909eebb78b846598ab506b1867aded3.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/researcher/9909eebb78b846598ab506b1867aded3"}}, "publications": [{"entity": "publication", "iuid": "6a0daacfb368470cb012e6862d5da631", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/6a0daacfb368470cb012e6862d5da631.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/6a0daacfb368470cb012e6862d5da631"}}, "title": "ATM/Wip1 activities at chromatin control Plk1 re-activation to determine G2 checkpoint duration.", "authors": [{"family": "Jaiswal", "given": "Himjyot", "initials": "H"}, {"family": "Benada", "given": "Jan", "initials": "J"}, {"family": "M\u00fcllers", "given": "Erik", "initials": "E"}, {"family": "Akopyan", "given": "Karen", "initials": "K"}, {"family": "Burdova", "given": "Kamila", "initials": "K"}, {"family": "Koolmeister", "given": "Tobias", "initials": "T"}, {"family": "Helleday", "given": "Thomas", "initials": "T"}, {"family": "Medema", "given": "Ren\u00e9 H", "initials": "RH", "orcid": "0000-0002-6754-0381", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/75280704a0444efcb076fdfaa34b1e49.json"}}, {"family": "Macurek", "given": "Libor", "initials": "L", "orcid": "0000-0002-0987-1238", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/9909eebb78b846598ab506b1867aded3.json"}}, {"family": "Lindqvist", "given": "Arne", "initials": "A", "orcid": "0000-0002-0141-1579", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/4e3ecdaacf3d4e6bb5616f0ad3b818ac.json"}}], "type": "journal article", "published": "2017-07-14", "journal": {"title": "EMBO J.", "issn": "1460-2075", "volume": "36", "issue": "14", "pages": "2161-2176", "issn-l": "0261-4189"}, "abstract": "After DNA damage, the cell cycle is arrested to avoid propagation of mutations. Arrest in G2 phase is initiated by ATM-/ATR-dependent signaling that inhibits mitosis-promoting kinases such as Plk1. At the same time, Plk1 can counteract ATR-dependent signaling and is required for eventual resumption of the cell cycle. However, what determines when Plk1 activity can resume remains unclear. Here, we use FRET-based reporters to show that a global spread of ATM activity on chromatin and phosphorylation of ATM targets including KAP1 control Plk1 re-activation. These phosphorylations are rapidly counteracted by the chromatin-bound phosphatase Wip1, allowing cell cycle restart despite persistent ATM activity present at DNA lesions. Combining experimental data and mathematical modeling, we propose a model for how the minimal duration of cell cycle arrest is controlled. Our model shows how cell cycle restart can occur before completion of DNA repair and suggests a mechanism for checkpoint adaptation in human cells.", "doi": "10.15252/embj.201696082", "pmid": "28607002", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC5510006"}, {"db": "pii", "key": "embj.201696082"}], "notes": [], "created": "2018-12-05T12:10:42.194Z", "modified": "2026-09-23T09:29:07.141Z"}]}