Giulia Fontemaggi

TL;DR: It is found that YAP requires the promyelocytic leukemia gene (PML) and nuclear body localization to coactivate p73 and contributes to the DNA damage-induced accumulation of p 73 and potentiates the p300-mediated acetylation of p73.

TL;DR: The results suggest that DNA damage-induced acetylation potentiates the apoptotic function of p 73 by enhancing the ability of p73 to selectively activate the transcription of proapoptotic target genes.

TL;DR: This review will focus mainly on the transcriptional activity of mutant p53 proteins as one of the potential molecular mechanisms of inactivation of tumor-suppressor genes.

TL;DR: The identification of hTERT as a target of estrogens represents a novel finding which advances the understanding of telomerase regulation in hormone-dependent cells and has implications for a potential role of hormones in their senescence and malignant conversion.

TL;DR: It is reported that human tumor-derived p53 mutants can associate in vitro and in vivo with p63 through their respective core domains and it is shown that the interaction with mutant p53 impairs in vitroand in vivo sequence-specific DNA binding of p63 and consequently affects its transcriptional activity.