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
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
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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: |
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Communities: |
CSHL Cancer Center Program > Signal Transduction CSHL labs > Sordella lab CSHL Cancer Center Program > Cellular Communication in Cancer Program |
Depositing User: |
Matt Covey
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Date: |
December 2016 |
Date Deposited: |
16 Feb 2017 21:30 |
Last Modified: |
26 Oct 2020 17:03 |
PMCID: |
PMC5298884 |
URI: |
https://repository.cshl.edu/id/eprint/34125 |
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