The Evolution of TP53 Mutations: From Loss-of-Function to Separation-of-Function Mutants

Miller, M., Shirole, N., Tian, R., Pal, D., Sordella, R. (December 2016) The Evolution of TP53 Mutations: From Loss-of-Function to Separation-of-Function Mutants. J Cancer Biol Res, 4 (4). ISSN 2373-9436

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Abstract

As the most mutated gene in cancer, it is no surprise that TP53 has 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.

Item Type:	Paper
Uncontrolled Keywords:	Alternative splicing Gain-of-function Hot-spot mutations Loss-of-function Separation-of-function Silent mutations Truncating mutations p53 p53 isoforms p53-psi
Subjects:	bioinformatics > genomics and proteomics > genetics & nucleic acid processing > DNA, RNA structure, function, modification > Alternative Splicing bioinformatics > genomics and proteomics > genetics & nucleic acid processing > DNA, RNA structure, function, modification > genes, structure and function > loss of function bioinformatics > genomics and proteomics > genetics & nucleic acid processing > DNA, RNA structure, function, modification > genes, structure and function > genes: types > p53
CSHL Authors:	Sordella, Raffaella Pal, Debjani Shirole, Nitin Miller, Madison
Communities:	CSHL Cancer Center Program > Signal Transduction CSHL Cancer Center Program > Cellular Communication in Cancer Program CSHL labs > Sordella lab
Depositing User:	Matt Covey
Date:	December 2016
Date Deposited:	16 Feb 2017 21:30
Last Modified:	11 Sep 2024 16:06
PMCID:	PMC5298884
URI:	https://repository.cshl.edu/id/eprint/34125

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