Asset Details
Do you wish to reserve the book?
Recovery from a DNA-damage-induced G2 arrest requires Cdk-dependent activation of FoxM1
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Recovery from a DNA-damage-induced G2 arrest requires Cdk-dependent activation of FoxM1
Do you wish to request the book?
Recovery from a DNA-damage-induced G2 arrest requires Cdk-dependent activation of FoxM1
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Recovery from a DNA-damage-induced G2 arrest requires Cdk-dependent activation of FoxM1
2010
Overview
Activation of the DNA‐damage checkpoint culminates in the inhibition of cyclin‐dependent kinase (Cdk) complexes to prevent cell‐cycle progression. We have shown recently that Cdk activity is required for activation of the Forkhead transcription factor FoxM1, an important regulator of gene expression in the G2 phase of the cell cycle. Here, we show that FoxM1 is transcriptionally active during a DNA‐damage‐induced G2 arrest and is essential for checkpoint recovery. Paradoxically, Cdk activity, although reduced after checkpoint activation, is required to maintain FoxM1‐dependent transcription during the arrest and for expression of pro‐mitotic targets such as cyclin A, cyclin B and Plk1. Indeed, we find that cells need to retain sufficient levels of Cdk activity during the DNA‐damage response to maintain cellular competence to recover from a DNA‐damaging insult.
After DNA‐damage checkpoint activation, Cdk activity is reduced in order to arrest the cell cycle. Alvarez‐Fernández and colleagues demonstrate that during arrest, residual Cdk activity maintains FoxM1‐dependent transcription and the expression of mitotic inducers, such as cyclin B1 and Plk1, in order to allow efficient re‐entry into the cell cycle after checkpoint recovery.
Publisher
John Wiley & Sons, Ltd,Nature Publishing Group UK,Springer Nature B.V,Nature Publishing Group
