title: The Evolution ofTP53Mutations: From Loss-of-Function to Separation-of-Function Mutants.
abstract: As the most mutated gene in cancer, it is no surprise thatTP53has been the center of cancer biology discourse since its discovery in the late 1970s. Although early demonstrations of p53's role in the modulation of cell proliferation and survival solidified its classification as a tumor suppressor and transcription factor, our conceptualization of p53 is ever-evolving. Here, we present novel evidence of the role of alternative splicing isoforms, truncating/separation-of-function mutations, and hotspot silent mutations in the regulation of p53's activities.
authors.affiliation: Cancer Center, Cold Spring Harbor Laboratory, USA.
authors.forename: Madison
authors.initials: M
authors.lastname: Miller
authors.affiliation: Cancer Center, Cold Spring Harbor Laboratory, USA; Graduate Program in Genetics, Stony Brook University, USA.
authors.forename: Nitin
authors.initials: N
authors.lastname: Shirole
authors.affiliation: Cancer Center, Cold Spring Harbor Laboratory, USA.
authors.forename: Ruxiao
authors.initials: R
authors.lastname: Tian
authors.affiliation: Cancer Center, Cold Spring Harbor Laboratory, USA; Graduate Program in Molecular and Cellular Biology, Stony Brook University, USA.
authors.forename: Debjani
authors.initials: D
authors.lastname: Pal
authors.affiliation: Cancer Center, Cold Spring Harbor Laboratory, USA; Graduate Program in Genetics, Stony Brook University, USA.
authors.forename: Raffaella
authors.initials: R
authors.lastname: Sordella
keywords: Alternative splicing; Gain-of-function; Hot-spot mutations; Loss-of-function; Separation-of-function; Silent mutations; Truncating mutations; p53; p53 isoforms; p53-psi