2026-06-14T05:06:19Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/262092025-12-18T12:55:43Zcom_20.500.12105_2327com_20.500.12105_2290col_20.500.12105_16991
Repisalud
author
Cerqueira, Antonio
author
Santamaría, David
author
Martínez-Pastor, Bárbara
author
Cuadrado, Miriam
author
Fernandez-Capetillo, Oscar
author
Barbacid, Mariano
author
Barbacid, Mariano
funder
MINISTERIO DE CIENCIA E INNOVACION (ESPAÑA)
funder
Comunidad de Madrid
funder
European Union (EU)
funder
European Research Council (ERC)
funder
Instituto de Salud Carlos III
2025-01-30T09:35:34Z
2025-01-30T09:35:34Z
2009-12-14
J Cell Biol . 2009 Dec 14;187(6):773-80.
J Cell Biol
19995934
https://hdl.handle.net/20.500.12105/26209
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.
eng
DOUBLE-STRAND BREAKS
CYCLIN-DEPENDENT KINASES
END RESECTION
HOMOLOGOUS RECOMBINATION
CHECKPOINT RESPONSE
INVIVO
S-PHASE
ATM
PHOSPHORYLATION
REPAIR
Overall Cdk activity modulates the DNA damage response in mammalian cells.
research article
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URL
https://repisalud.isciii.es/bitstreams/a2f019ff-83cf-46fe-af9b-d61c0a7be8ef/download
File
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application/pdf
overallcdkactivity-2009.pdf
URL
https://repisalud.isciii.es/bitstreams/4c2a00d9-b862-45af-aeba-f223d9d1b9f6/download
File
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