Oocyte DNA damage quality control requires consecutive interplay of CHK2 and CK1 to activate p63 View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2018-03

AUTHORS

Marcel Tuppi, Sebastian Kehrloesser, Daniel W. Coutandin, Valerio Rossi, Laura M. Luh, Alexander Strubel, Katharina Hötte, Meike Hoffmeister, Birgit Schäfer, Tiago De Oliveira, Florian Greten, Ernst H. K. Stelzer, Stefan Knapp, Massimo De Felici, Christian Behrends, Francesca Gioia Klinger, Volker Dötsch

ABSTRACT

The survival rate of cancer patients is steadily increasing, owing to more efficient therapies. Understanding the molecular mechanisms of chemotherapy-induced premature ovarian insufficiency (POI) could identify targets for prevention of POI. Loss of the primordial follicle reserve is the most important cause of POI, with the p53 family member p63 being responsible for DNA-damage-induced apoptosis of resting oocytes. Here, we provide the first detailed mechanistic insight into the activation of p63, a process that requires phosphorylation by both the priming kinase CHK2 and the executioner kinase CK1 in mouse primordial follicles. We further describe the structural changes induced by phosphorylation that enable p63 to adopt its active tetrameric conformation and demonstrate that previously discussed phosphorylation by c-Abl is not involved in this process. Inhibition of CK1 rescues primary oocytes from doxorubicin and cisplatin-induced apoptosis, thus uncovering a new target for the development of fertoprotective therapies. More... »

PAGES

261-269

References to SciGraph publications

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41594-018-0035-7

    DOI

    http://dx.doi.org/10.1038/s41594-018-0035-7

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1101211499

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/29483652


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