Research Paper Volume 10, Issue 12 pp 3745—3760
TAp73 regulates ATP7A: possible implications for ageing-related diseases
- 1 MRC Toxicology Unit, University of Cambridge, Leicester LE1 7HB, United Kingdom
- 2 Department of Clinical & Experimental Medicine, University of Foggia, Foggia, Italy
- 3 Department of Systems Medicine, Nephrology and Hypertension Unit, Tor Vergata University Hospital, Rome, Italy
- 4 Department of Experimental Medicine and Surgery, University of Rome Tor Vergata, Rome, Italy
received: October 4, 2018 ; accepted: November 15, 2018 ; published: December 8, 2018 ;https://doi.org/10.18632/aging.101669
How to Cite
Copyright: Lopriore et al. This is an open‐access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
The p53 family member p73 controls a wide range of cellular function. Deletion of p73 in mice results in increased tumorigenesis, infertility, neurological defects and altered immune system. Despite the extensive effort directed to define the molecular underlying mechanism of p73 function a clear definition of its transcriptional signature and the extent of overlap with the other p53 family members is still missing. Here we describe a novel TAp73 target, ATP7A a member of a large family of P-type ATPases implicated in human neurogenerative conditions and cancer chemoresistance. Modulation of TAp73 expression influences basal expression level of ATP7A in different cellular models and chromatin immunoprecipitation confirmed a physical direct binding of TAp73 on ATP7A genomic regions. Bioinformatic analysis of expression profile datasets of human lung cancer patients suggests a possible implication of TAp73/ATP7A axis in human cancer. These data provide a novel TAp73-dependent target which might have implications in ageing-related diseases such as cancer and neurodegeneration.