Contribution of classical end-joining to PTEN inactivation in p53-mediated glioblastoma formation and drug-resistant survival

We know that defects in DNA repair genes are associated with cancer development. Here the authors eliminate XRCC4, a non-homologous end-joining protein, and p53 in the developing brain and find that this causes glioblastoma development as a consequence of reduced PTEN function.

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Autores principales:	Youn-Jung Kang, Barbara Balter, Eva Csizmadia, Brian Haas, Himanshu Sharma, Roderick Bronson, Catherine T. Yan
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Science Q
Acceso en línea:	https://doaj.org/article/f33589217b7d48c4b64850b9eada2abb
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spelling	oai:doaj.org-article:f33589217b7d48c4b64850b9eada2abb2021-12-02T15:38:57ZContribution of classical end-joining to PTEN inactivation in p53-mediated glioblastoma formation and drug-resistant survival10.1038/ncomms140132041-1723https://doaj.org/article/f33589217b7d48c4b64850b9eada2abb2017-01-01T00:00:00Zhttps://doi.org/10.1038/ncomms14013https://doaj.org/toc/2041-1723We know that defects in DNA repair genes are associated with cancer development. Here the authors eliminate XRCC4, a non-homologous end-joining protein, and p53 in the developing brain and find that this causes glioblastoma development as a consequence of reduced PTEN function.Youn-Jung KangBarbara BalterEva CsizmadiaBrian HaasHimanshu SharmaRoderick BronsonCatherine T. YanNature PortfolioarticleScienceQENNature Communications, Vol 8, Iss 1, Pp 1-15 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Science Q
spellingShingle	Science Q Youn-Jung Kang Barbara Balter Eva Csizmadia Brian Haas Himanshu Sharma Roderick Bronson Catherine T. Yan Contribution of classical end-joining to PTEN inactivation in p53-mediated glioblastoma formation and drug-resistant survival
description	We know that defects in DNA repair genes are associated with cancer development. Here the authors eliminate XRCC4, a non-homologous end-joining protein, and p53 in the developing brain and find that this causes glioblastoma development as a consequence of reduced PTEN function.
format	article
author	Youn-Jung Kang Barbara Balter Eva Csizmadia Brian Haas Himanshu Sharma Roderick Bronson Catherine T. Yan
author_facet	Youn-Jung Kang Barbara Balter Eva Csizmadia Brian Haas Himanshu Sharma Roderick Bronson Catherine T. Yan
author_sort	Youn-Jung Kang
title	Contribution of classical end-joining to PTEN inactivation in p53-mediated glioblastoma formation and drug-resistant survival
title_short	Contribution of classical end-joining to PTEN inactivation in p53-mediated glioblastoma formation and drug-resistant survival
title_full	Contribution of classical end-joining to PTEN inactivation in p53-mediated glioblastoma formation and drug-resistant survival
title_fullStr	Contribution of classical end-joining to PTEN inactivation in p53-mediated glioblastoma formation and drug-resistant survival
title_full_unstemmed	Contribution of classical end-joining to PTEN inactivation in p53-mediated glioblastoma formation and drug-resistant survival
title_sort	contribution of classical end-joining to pten inactivation in p53-mediated glioblastoma formation and drug-resistant survival
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/f33589217b7d48c4b64850b9eada2abb
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Contribution of classical end-joining to PTEN inactivation in p53-mediated glioblastoma formation and drug-resistant survival

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