Kristiaan Lenos

TL;DR: The results show that c-Abl not only targets Hdm2, but also Hdmx, which together contribute to p53 activation in response to DNA damage.

TL;DR: A novel role is proposed for alternative splicing of HDMX, whereby it serves as a mechanism by which HDMX protein levels are reduced in cancer cells that have already inhibited p53 activity, and could serve as a more effective biomarker for p53 pathway attenuation in cancers than p53 gene mutation.

TL;DR: It is demonstrated that HDMX-L cooperates with HDM2 to promote the ubiquitination of p53 and that p53-induced HDMX transcription from the P2 promoter can play a key role in the attenuation phase of the p53 response, to effectively diminish p53 abundance as cells recover from stress.

TL;DR: The various mechanisms by whichMDMX protein levels are downregulated upon various types of stress are discussed, including posttranslational modifications of the MDMX protein and the regulation of mdmx mRNA expression, including alternative splicing.

TL;DR: Both p53-knockdown and hMDMX overexpression accelerated proliferation and prevented growth suppression induced by introduction of oncogenic Ras, which was required for anchorage-independent growth and the ability to form tumors in vivo.