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Emerging Roles of RAD52 in Genome Maintenance

The maintenance of genome integrity is critical for cell survival. Homologous recombination (HR) is considered the major error-free repair pathway in combatting endogenously generated double-stranded lesions in DNA. Nevertheless, a number of alternative repair pathways have been described as protect...

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Autores principales: Jalan, Manisha, Olsen, Kyrie S., Powell, Simon N.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6679097/
https://www.ncbi.nlm.nih.gov/pubmed/31340507
http://dx.doi.org/10.3390/cancers11071038
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author Jalan, Manisha
Olsen, Kyrie S.
Powell, Simon N.
author_facet Jalan, Manisha
Olsen, Kyrie S.
Powell, Simon N.
author_sort Jalan, Manisha
collection PubMed
description The maintenance of genome integrity is critical for cell survival. Homologous recombination (HR) is considered the major error-free repair pathway in combatting endogenously generated double-stranded lesions in DNA. Nevertheless, a number of alternative repair pathways have been described as protectors of genome stability, especially in HR-deficient cells. One of the factors that appears to have a role in many of these pathways is human RAD52, a DNA repair protein that was previously considered to be dispensable due to a lack of an observable phenotype in knock-out mice. In later studies, RAD52 deficiency has been shown to be synthetically lethal with defects in BRCA genes, making RAD52 an attractive therapeutic target, particularly in the context of BRCA-deficient tumors.
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spelling pubmed-66790972019-08-19 Emerging Roles of RAD52 in Genome Maintenance Jalan, Manisha Olsen, Kyrie S. Powell, Simon N. Cancers (Basel) Review The maintenance of genome integrity is critical for cell survival. Homologous recombination (HR) is considered the major error-free repair pathway in combatting endogenously generated double-stranded lesions in DNA. Nevertheless, a number of alternative repair pathways have been described as protectors of genome stability, especially in HR-deficient cells. One of the factors that appears to have a role in many of these pathways is human RAD52, a DNA repair protein that was previously considered to be dispensable due to a lack of an observable phenotype in knock-out mice. In later studies, RAD52 deficiency has been shown to be synthetically lethal with defects in BRCA genes, making RAD52 an attractive therapeutic target, particularly in the context of BRCA-deficient tumors. MDPI 2019-07-23 /pmc/articles/PMC6679097/ /pubmed/31340507 http://dx.doi.org/10.3390/cancers11071038 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Jalan, Manisha
Olsen, Kyrie S.
Powell, Simon N.
Emerging Roles of RAD52 in Genome Maintenance
title Emerging Roles of RAD52 in Genome Maintenance
title_full Emerging Roles of RAD52 in Genome Maintenance
title_fullStr Emerging Roles of RAD52 in Genome Maintenance
title_full_unstemmed Emerging Roles of RAD52 in Genome Maintenance
title_short Emerging Roles of RAD52 in Genome Maintenance
title_sort emerging roles of rad52 in genome maintenance
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6679097/
https://www.ncbi.nlm.nih.gov/pubmed/31340507
http://dx.doi.org/10.3390/cancers11071038
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