Oct 20, 2010 · We investigated the role of single site and multiple site phosphorylation of the p53 transactivation domain in mediating its interaction with CBP and with the ubiquitin ligase HDM2. Phosphorylation at Thr18 functions as an on/off switch to regulate binding to the N-terminal domain of HDM2.

We propose that phosphorylated CREB mediates recruitment of CBP to p53-responsive promoters through direct interaction with p53. These observations provide evidence for a novel pathway that integrates cAMP signaling and p53 transcriptional activity.

CREBZF was identified in a yeast two-hybrid screen using HEY1, recently characterized as an indirect p53 activator, as bait. CREBZF interacts in vitro with both HEY1 and p53, and CREBZF expression stabilizes and activates p53. Moreover, CREBZF cooperates synergistically with HEY1 to enhance p53 transcriptional activity.

May 30, 2023 · Saito et al. demonstrate that OASIS is a critical cell-cycle inhibitor and acts as a functional counterpart to tumor suppressor p53. Recovery of the inhibited OASIS expression in certain types of glioblastomas by their epigenomic engineering treatment suppresses the tumorigenesis, indicating the potential of OASIS as a tumor suppressor.

We propose that phosphorylated CREB mediates recruitment of CBP to p53-responsive promoters through direct interaction with p53. These observations provide evidence for a novel pathway that integrates cAMP signaling and p53 transcriptional activity.

Apr 6, 2017 · In this study, we aimed to investigate the molecular mechanism undergirding hyperpigmentation in the dyschromatosis disorder. Our results revealed that SASH1 binds with MAP2K2 and is induced by p53-POMC-MC1R signal cascade to enhance the phosphorylation level of ERK1/2 and CREB.

In this study, we found that cAMP-responsive element-binding protein (CREB) collaborates with AMP-activated protein kinase alpha (AMPKalpha) to regulate the transcription of p53.

Through physical interaction with p53, p300/CBP can both positively and negatively regulate p53 transactivation, as well as p53 protein turnover depending on cellular context and environmental stimuli, such as DNA damage.

Mar 3, 2016 · The tumor suppressor p53 regulates the cellular response to genomic damage by recruiting the transcriptional coactivator cyclic-AMP response element-binding protein (CREB)-binding protein (CBP) and its paralog p300 to activate stress response genes.

The pleiotropic cellular coactivator CREB binding protein (CBP) plays a critical role in supporting p53-dependent tumor suppressor functions. p53 has been shown to directly interact with a carboxyl-terminal region of CBP for recruitment of the coactivator to p53-responsive genes.