p53 family · Metabolism · Comparative oncology
Mapping the p53 family across cancer and physiology
We investigate p53, p63 and p73 as an interconnected tumor-suppression network spanning transcription, RNA regulation, metabolism, inflammation and comparative oncology.
Our research
One family. Many biological systems.
The p53 family regulates far more than a single stress response. Our laboratory studies how p53, p63 and p73 share and divide their functions; how RNA-binding proteins and feedback loops tune their expression; and how these pathways influence metabolism, development, cancer progression and therapeutic response. Comparative models connect fundamental mechanisms with naturally occurring disease and translational opportunities.
Read about our research programmes →Research programmes
What we study
The p53 family network
We define the overlapping and isoform-specific functions of p53, p63 and p73 in tumor suppression, development and stress responses.
Learn more →02RNA-binding proteins and feedback control
We study how RBM38 and related RNA regulators shape translation and feedback within the p53-family pathway.
Learn more →03FDXR, ferredoxins and metabolic homeostasis
We investigate how the FDXR–FDX1/2 electron-transfer system connects p53-family signaling to lipid metabolism, development and spontaneous tumor suppression.
Learn more →04Ninjurins and translational oncology
We study p53–NINJ1/2 feedback loops, inflammation and cell adhesion, then test pathway-derived peptides as potential therapeutic tools.
Learn more →Principal investigator
Xinbin Chen, PhD
Professor of Surgical and Radiological Sciences
Xinbin Chen is Professor in the Department of Surgical and Radiological Sciences at the UC Davis Weill School of Veterinary Medicine and leads the Comparative Oncology Laboratory. His research has defined common and distinct functions of the p53 family, uncovered regulatory feedback loops involving RNA-binding proteins, and established roles for the FDXR–ferredoxin pathway and Ninjurin proteins in tumor suppression, metabolism and disease.
Meet the lab →Join the lab