Cerqueira, AntonioSantamaría, DavidMartínez-Pastor, BárbaraCuadrado, MiriamFernandez-Capetillo, OscarBarbacid, MarianoBarbacid, Mariano2025-01-302025-01-302009-12-14J Cell Biol . 2009 Dec 14;187(6):773-80.https://hdl.handle.net/20.500.12105/26209This work was supported by grants from the Ministry of Science and Innovation (MICINN; SAF2006-11773 to M. Barbacid and RYC-2003-002731, CSD2007-00017, and BFU2005-09429 to O. Fernandez-Capetillo), the OncoCycle Programme from the Comunidad Autonoma de Madrid (S2006/BIO-0232 to M. Barbacid), the Consolider Program (CSD2007-00017 to M. Barbacid), the EU Framework Programme (Chemores LSHG-CT-2007-037665 to M. Barbacid and Epigenome Network of Excellence to O. Fernandez-Capetillo), the European Research Council (StG210520 to O. Fernandez-Capetillo), and Fondo de Investigacion Sanitaria (PI061631 to D. Santamaria). A. Cerqueira and B. Martinez-Pastor were supported by Formacion del Personal Investigador (MICINN) and Fundacion Mario Losantos del Campo fellowships, respectively.In response to DNA damage, cells activate a phosphorylation-based signaling cascade known as the DNA damage response (DDR). One of the main outcomes of DDR activation is inhibition of cyclin-dependent kinase (Cdk) activity to restrain cell cycle progression until lesions are healed. Recent studies have revealed a reverse connection by which Cdk activity modulates processing of DNA break ends and DDR activation. However, the specific contribution of individual Cdks to this process remains poorly understood. To address this issue, we have examined the DDR in murine cells carrying a defined set of Cdks. Our results reveal that genome maintenance programs of postreplicative cells, including DDR, are regulated by the overall level of Cdk activity and not by specific Cdks.engVoRhttp://creativecommons.org/licenses/by-nc-nd/4.0/DOUBLE-STRAND BREAKSCYCLIN-DEPENDENT KINASESEND RESECTIONHOMOLOGOUS RECOMBINATIONCHECKPOINT RESPONSEINVIVOS-PHASEATMPHOSPHORYLATIONREPAIROverall Cdk activity modulates the DNA damage response in mammalian cells.Attribution-NonCommercial-NoDerivatives 4.0 International199959341876773-780J Cell Biolopen access