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RAD52: Viral Friend or Foe?
Mammalian Radiation Sensitive 52 (RAD52) is a gene whose scientific reputation has recently seen a strong resurgence. In the past decade, RAD52, which was thought to be dispensable for most DNA repair and recombination reactions in mammals, has been shown to be important for a bevy of DNA metabolic...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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MDPI
2020
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7072633/ https://www.ncbi.nlm.nih.gov/pubmed/32046320 http://dx.doi.org/10.3390/cancers12020399 |
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author | Hendrickson, Eric A. |
author_facet | Hendrickson, Eric A. |
author_sort | Hendrickson, Eric A. |
collection | PubMed |
description | Mammalian Radiation Sensitive 52 (RAD52) is a gene whose scientific reputation has recently seen a strong resurgence. In the past decade, RAD52, which was thought to be dispensable for most DNA repair and recombination reactions in mammals, has been shown to be important for a bevy of DNA metabolic pathways. One of these processes is termed break-induced replication (BIR), a mechanism that can be used to re-start broken replication forks and to elongate the ends of chromosomes in telomerase-negative cells. Viruses have historically evolved a myriad of mechanisms in which they either conscript cellular factors or, more frequently, inactivate them as a means to enable their own replication and survival. Recent data suggests that Adeno-Associated Virus (AAV) may replicate its DNA in a BIR-like fashion and/or utilize RAD52 to facilitate viral transduction and, as such, likely conscripts/requires the host RAD52 protein to promote its perpetuation. |
format | Online Article Text |
id | pubmed-7072633 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-70726332020-03-19 RAD52: Viral Friend or Foe? Hendrickson, Eric A. Cancers (Basel) Review Mammalian Radiation Sensitive 52 (RAD52) is a gene whose scientific reputation has recently seen a strong resurgence. In the past decade, RAD52, which was thought to be dispensable for most DNA repair and recombination reactions in mammals, has been shown to be important for a bevy of DNA metabolic pathways. One of these processes is termed break-induced replication (BIR), a mechanism that can be used to re-start broken replication forks and to elongate the ends of chromosomes in telomerase-negative cells. Viruses have historically evolved a myriad of mechanisms in which they either conscript cellular factors or, more frequently, inactivate them as a means to enable their own replication and survival. Recent data suggests that Adeno-Associated Virus (AAV) may replicate its DNA in a BIR-like fashion and/or utilize RAD52 to facilitate viral transduction and, as such, likely conscripts/requires the host RAD52 protein to promote its perpetuation. MDPI 2020-02-08 /pmc/articles/PMC7072633/ /pubmed/32046320 http://dx.doi.org/10.3390/cancers12020399 Text en © 2020 by the author. 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 Hendrickson, Eric A. RAD52: Viral Friend or Foe? |
title | RAD52: Viral Friend or Foe? |
title_full | RAD52: Viral Friend or Foe? |
title_fullStr | RAD52: Viral Friend or Foe? |
title_full_unstemmed | RAD52: Viral Friend or Foe? |
title_short | RAD52: Viral Friend or Foe? |
title_sort | rad52: viral friend or foe? |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7072633/ https://www.ncbi.nlm.nih.gov/pubmed/32046320 http://dx.doi.org/10.3390/cancers12020399 |
work_keys_str_mv | AT hendricksonerica rad52viralfriendorfoe |