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Article: Inactivation of Chk2 and Mus81 leads to impaired lymphocytes development, reduced genomic instability, and suppression of cancer

TitleInactivation of Chk2 and Mus81 leads to impaired lymphocytes development, reduced genomic instability, and suppression of cancer
Authors
Issue Date2011
Citation
PLoS Genetics, 2011, v. 7, n. 5, article no. e1001385 How to Cite?
AbstractChk2 is an effector kinase important for the activation of cell cycle checkpoints, p53, and apoptosis in response to DNA damage. Mus81 is required for the restart of stalled replication forks and for genomic integrity. Mus81Δex3-4/Δex3-4 mice have increased cancer susceptibility that is exacerbated by p53 inactivation. In this study, we demonstrate that Chk2 inactivation impairs the development of Mus81Δex3-4/Δex3-4 lymphoid cells in a cell-autonomous manner. Importantly, in contrast to its predicted tumor suppressor function, loss of Chk2 promotes mitotic catastrophe and cell death, and it results in suppressed oncogenic transformation and tumor development in Mus81Δex3-4/Δex3-4 background. Thus, our data indicate that an important role for Chk2 is maintaining lymphocyte development and that dual inactivation of Chk2 and Mus81 remarkably inhibits cancer.
Persistent Identifierhttp://hdl.handle.net/10722/292636
ISSN
2014 Impact Factor: 7.528
2023 SCImago Journal Rankings: 2.219
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorEl Ghamrasni, Samah-
dc.contributor.authorPamidi, Ashwin-
dc.contributor.authorHalaby, Marie Jo-
dc.contributor.authorBohgaki, Miyuki-
dc.contributor.authorCardoso, Renato-
dc.contributor.authorLi, Li-
dc.contributor.authorVenkatesan, Shriram-
dc.contributor.authorSethu, Swaminathan-
dc.contributor.authorHirao, Atsushi-
dc.contributor.authorMak, Tak W.-
dc.contributor.authorHande, Manoor Prakash-
dc.contributor.authorHakem, Anne-
dc.contributor.authorHakem, Razqallah-
dc.date.accessioned2020-11-17T14:56:54Z-
dc.date.available2020-11-17T14:56:54Z-
dc.date.issued2011-
dc.identifier.citationPLoS Genetics, 2011, v. 7, n. 5, article no. e1001385-
dc.identifier.issn1553-7390-
dc.identifier.urihttp://hdl.handle.net/10722/292636-
dc.description.abstractChk2 is an effector kinase important for the activation of cell cycle checkpoints, p53, and apoptosis in response to DNA damage. Mus81 is required for the restart of stalled replication forks and for genomic integrity. Mus81Δex3-4/Δex3-4 mice have increased cancer susceptibility that is exacerbated by p53 inactivation. In this study, we demonstrate that Chk2 inactivation impairs the development of Mus81Δex3-4/Δex3-4 lymphoid cells in a cell-autonomous manner. Importantly, in contrast to its predicted tumor suppressor function, loss of Chk2 promotes mitotic catastrophe and cell death, and it results in suppressed oncogenic transformation and tumor development in Mus81Δex3-4/Δex3-4 background. Thus, our data indicate that an important role for Chk2 is maintaining lymphocyte development and that dual inactivation of Chk2 and Mus81 remarkably inhibits cancer.-
dc.languageeng-
dc.relation.ispartofPLoS Genetics-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.titleInactivation of Chk2 and Mus81 leads to impaired lymphocytes development, reduced genomic instability, and suppression of cancer-
dc.typeArticle-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1371/journal.pgen.1001385-
dc.identifier.pmid21625617-
dc.identifier.pmcidPMC3098187-
dc.identifier.scopuseid_2-s2.0-79957973567-
dc.identifier.volume7-
dc.identifier.issue5-
dc.identifier.spagearticle no. e1001385-
dc.identifier.epagearticle no. e1001385-
dc.identifier.eissn1553-7404-
dc.identifier.isiWOS:000291014600002-
dc.identifier.issnl1553-7390-

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