Related Experiment Video
Updated: Jul 17, 2026

Study of the DNA Damage Checkpoint using Xenopus Egg Extracts
Published on: November 5, 2012
p300/CREB-binding protein interacts with ATR and is required for the DNA replication checkpoint
Daniel Stauffer1, Bill Chang1, Jing Huang1
1Department of Biochemistry, Oregon Health and Sciences University, Portland, Oregon 97201.
Abstract:
The highly related acetyltransferases, p300 and CREB-binding protein (CBP) are coactivators of signal-responsive transcriptional activation. In addition, recent evidence suggests that p300/CBP also interacts directly with complexes that mediate DNA replication and repair. In this report, we show that loss of p300/CBP in mammalian cells results in a defect in the cell cycle arrest induced by stalled DNA replication. We demonstrate that complexes containing p300/CBP and ATR can be detected in mammalian cells, and that the downstream kinase CHK1 fails to be phosphorylated in response to stalled DNA replication in cells that lack p300/CBP. These observations broaden the roles for the p300/CBP acetyltransferases to include the modulation of chromatin structure and function during DNA metabolic events as well as for transcription.
Related Concept Videos
DNA Damage can Stall the Cell Cycle
DNA Damage Can Stall the Cell Cycle
Restarting Stalled Replication Forks
Negative Regulator Molecules
The Spindle Assembly Checkpoint
Many proteins function together to control the spindle assembly checkpoint. Mutations affecting these proteins may allow cells to proceed into anaphase prematurely, resulting in the...
S-Cdk Initiates DNA Replication
Two states at the origin of replication
In eukaryotes, the initiation of replication occurs at many sites on the chromosomes, called the origins of replication.

