Acquisition of aneuploidy drives mutant p53-associated gain-of-function phenotypes

Previous studies report that mutant p53 proteins have gain-of-function activities and cause oncogenic phenotypes. Herein, the authors engineered two isogenic epithelial cell lines to express wild-type or missense mutant p53 or be deficient for p53 protein and show that aneuploidy drives several of t...

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Autores principales: Lindsay N. Redman-Rivera, Timothy M. Shaver, Hailing Jin, Clayton B. Marshall, Johanna M. Schafer, Quanhu Sheng, Rachel A. Hongo, Kathryn E. Beckermann, Ferrin C. Wheeler, Brian D. Lehmann, Jennifer A. Pietenpol
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Publicado: Nature Portfolio 2021
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Acceso en línea:https://doaj.org/article/10bdca26a8b945f9a336e6d86641208a
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spelling oai:doaj.org-article:10bdca26a8b945f9a336e6d86641208a2021-12-02T19:04:19ZAcquisition of aneuploidy drives mutant p53-associated gain-of-function phenotypes10.1038/s41467-021-25359-z2041-1723https://doaj.org/article/10bdca26a8b945f9a336e6d86641208a2021-08-01T00:00:00Zhttps://doi.org/10.1038/s41467-021-25359-zhttps://doaj.org/toc/2041-1723Previous studies report that mutant p53 proteins have gain-of-function activities and cause oncogenic phenotypes. Herein, the authors engineered two isogenic epithelial cell lines to express wild-type or missense mutant p53 or be deficient for p53 protein and show that aneuploidy drives several of the GOF phenotypes previously ascribed to mutant p53.Lindsay N. Redman-RiveraTimothy M. ShaverHailing JinClayton B. MarshallJohanna M. SchaferQuanhu ShengRachel A. HongoKathryn E. BeckermannFerrin C. WheelerBrian D. LehmannJennifer A. PietenpolNature PortfolioarticleScienceQENNature Communications, Vol 12, Iss 1, Pp 1-15 (2021)
institution DOAJ
collection DOAJ
language EN
topic Science
Q
spellingShingle Science
Q
Lindsay N. Redman-Rivera
Timothy M. Shaver
Hailing Jin
Clayton B. Marshall
Johanna M. Schafer
Quanhu Sheng
Rachel A. Hongo
Kathryn E. Beckermann
Ferrin C. Wheeler
Brian D. Lehmann
Jennifer A. Pietenpol
Acquisition of aneuploidy drives mutant p53-associated gain-of-function phenotypes
description Previous studies report that mutant p53 proteins have gain-of-function activities and cause oncogenic phenotypes. Herein, the authors engineered two isogenic epithelial cell lines to express wild-type or missense mutant p53 or be deficient for p53 protein and show that aneuploidy drives several of the GOF phenotypes previously ascribed to mutant p53.
format article
author Lindsay N. Redman-Rivera
Timothy M. Shaver
Hailing Jin
Clayton B. Marshall
Johanna M. Schafer
Quanhu Sheng
Rachel A. Hongo
Kathryn E. Beckermann
Ferrin C. Wheeler
Brian D. Lehmann
Jennifer A. Pietenpol
author_facet Lindsay N. Redman-Rivera
Timothy M. Shaver
Hailing Jin
Clayton B. Marshall
Johanna M. Schafer
Quanhu Sheng
Rachel A. Hongo
Kathryn E. Beckermann
Ferrin C. Wheeler
Brian D. Lehmann
Jennifer A. Pietenpol
author_sort Lindsay N. Redman-Rivera
title Acquisition of aneuploidy drives mutant p53-associated gain-of-function phenotypes
title_short Acquisition of aneuploidy drives mutant p53-associated gain-of-function phenotypes
title_full Acquisition of aneuploidy drives mutant p53-associated gain-of-function phenotypes
title_fullStr Acquisition of aneuploidy drives mutant p53-associated gain-of-function phenotypes
title_full_unstemmed Acquisition of aneuploidy drives mutant p53-associated gain-of-function phenotypes
title_sort acquisition of aneuploidy drives mutant p53-associated gain-of-function phenotypes
publisher Nature Portfolio
publishDate 2021
url https://doaj.org/article/10bdca26a8b945f9a336e6d86641208a
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