The ATM gene (mutated in the disease ataxia telangiectasia) activates the p53 tumor suppressor protein in response to DNA damage, explaining the higher incidence of cancer in AT patients.

However, imaging the p53 structure is not easy. “It's a really hard protein to work on because most of it is flexible. There's a lot of disorder,” Kelly explained. “It’s amazing that an individual ...

One such mechanism involves a protein called p53 ... developed small molecules that can bind to mutant p53 and stabilize its faulty structure, restoring its ability to bind DNA and regulate ...

the chaperones—provide protection not only to the properly functioning p53 but also to its cancerous version. Chaperones stabilize the cancerous proteins' unstable structure and prevent them ...