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Mitotic and DNA Damage Response Proteins: Maintaining the Genome Stability and Working for the Common Good

Cellular function is highly dependent on genomic stability, which is mainly ensured by two cellular mechanisms: the DNA damage response (DDR) and the Spindle Assembly Checkpoint (SAC). The former provides the repair of damaged DNA, and the latter ensures correct chromosome segregation. This review f...

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Detalles Bibliográficos
Autores principales: Luna-Maldonado, Fernando, Andonegui-Elguera, Marco A., Díaz-Chávez, José, Herrera, Luis A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8710681/
https://www.ncbi.nlm.nih.gov/pubmed/34966733
http://dx.doi.org/10.3389/fcell.2021.700162
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author Luna-Maldonado, Fernando
Andonegui-Elguera, Marco A.
Díaz-Chávez, José
Herrera, Luis A.
author_facet Luna-Maldonado, Fernando
Andonegui-Elguera, Marco A.
Díaz-Chávez, José
Herrera, Luis A.
author_sort Luna-Maldonado, Fernando
collection PubMed
description Cellular function is highly dependent on genomic stability, which is mainly ensured by two cellular mechanisms: the DNA damage response (DDR) and the Spindle Assembly Checkpoint (SAC). The former provides the repair of damaged DNA, and the latter ensures correct chromosome segregation. This review focuses on recently emerging data indicating that the SAC and the DDR proteins function together throughout the cell cycle, suggesting crosstalk between both checkpoints to maintain genome stability.
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spelling pubmed-87106812021-12-28 Mitotic and DNA Damage Response Proteins: Maintaining the Genome Stability and Working for the Common Good Luna-Maldonado, Fernando Andonegui-Elguera, Marco A. Díaz-Chávez, José Herrera, Luis A. Front Cell Dev Biol Cell and Developmental Biology Cellular function is highly dependent on genomic stability, which is mainly ensured by two cellular mechanisms: the DNA damage response (DDR) and the Spindle Assembly Checkpoint (SAC). The former provides the repair of damaged DNA, and the latter ensures correct chromosome segregation. This review focuses on recently emerging data indicating that the SAC and the DDR proteins function together throughout the cell cycle, suggesting crosstalk between both checkpoints to maintain genome stability. Frontiers Media S.A. 2021-12-13 /pmc/articles/PMC8710681/ /pubmed/34966733 http://dx.doi.org/10.3389/fcell.2021.700162 Text en Copyright © 2021 Luna-Maldonado, Andonegui-Elguera, Díaz-Chávez and Herrera. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Cell and Developmental Biology
Luna-Maldonado, Fernando
Andonegui-Elguera, Marco A.
Díaz-Chávez, José
Herrera, Luis A.
Mitotic and DNA Damage Response Proteins: Maintaining the Genome Stability and Working for the Common Good
title Mitotic and DNA Damage Response Proteins: Maintaining the Genome Stability and Working for the Common Good
title_full Mitotic and DNA Damage Response Proteins: Maintaining the Genome Stability and Working for the Common Good
title_fullStr Mitotic and DNA Damage Response Proteins: Maintaining the Genome Stability and Working for the Common Good
title_full_unstemmed Mitotic and DNA Damage Response Proteins: Maintaining the Genome Stability and Working for the Common Good
title_short Mitotic and DNA Damage Response Proteins: Maintaining the Genome Stability and Working for the Common Good
title_sort mitotic and dna damage response proteins: maintaining the genome stability and working for the common good
topic Cell and Developmental Biology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8710681/
https://www.ncbi.nlm.nih.gov/pubmed/34966733
http://dx.doi.org/10.3389/fcell.2021.700162
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