DNA damage · p53 structure · Evolution
Reading p53 across structure, stress and evolution
We investigate how protein–protein and protein–RNA interactions control DNA-damage signaling, mutant p53 activity and the evolution of cancer protection.
Our research
One system.
Multiple molecular scales.
The Karakostis Lab studies p53 as a molecular system that operates simultaneously through protein structure, mRNA architecture, stress signaling and evolutionary adaptation. The group combines mechanistic cancer biology with comparative models—from marine invertebrates to elephants—and translational experience in genomics and molecular diagnostics. Its central aim is to explain how p53 is regulated, how cancer-associated variants create new functions, and how these insights can support precision oncology.
Read about our research programmes →Research programmes
What we study
DNA-damage sensing and signaling
We investigate structural interactions connecting ATM, the MRN complex, H2AX and p53 during the detection and repair of DNA double-strand breaks.
Learn more →02p53 mRNA as a regulatory molecule
We study secondary structures in TP53 mRNA that control translation, co-translational events and the production of functionally distinct p53 proteins.
Learn more →03Mutant p53 gain of function
We use p53 as a model to determine how cancer-associated mutations acquire new activities through altered structural and signaling interactions.
Learn more →04Evolutionary cancer protection
We compare p53 systems across invertebrates, mammals and elephants to understand how development, stress adaptation and tumor suppression co-evolved.
Learn more →Principal investigator
Konstantinos Karakostis, PhD
Ramón y Cajal Principal Investigator
Konstantinos Karakostis leads a research group in the Department of Biochemistry and Molecular Biology at the University of Valencia. Trained across chemistry, developmental biology, cancer signaling, molecular diagnostics and functional genomics, he investigates structural interfaces in the DNA-damage response, p53 gain-of-function mutations, p53 mRNA regulation and the evolutionary conservation of tumor suppression.
Meet the lab →Join the lab