RAD52: Viral Friend or Foe?

Mammalian Radiation Sensitive 52 (<i>RAD52</i>) 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 bev...

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Main Author: Eric A. Hendrickson
Format: Article
Language:English
Published: MDPI AG 2020-02-01
Series:Cancers
Subjects:
Online Access:https://www.mdpi.com/2072-6694/12/2/399
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author Eric A. Hendrickson
author_facet Eric A. Hendrickson
author_sort Eric A. Hendrickson
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description Mammalian Radiation Sensitive 52 (<i>RAD52</i>) 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.
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spelling doaj.art-1910d070cf3443c6ba68742f69a011362023-09-03T01:39:31ZengMDPI AGCancers2072-66942020-02-0112239910.3390/cancers12020399cancers12020399RAD52: Viral Friend or Foe?Eric A. Hendrickson0Department of Biochemistry, Molecular Biology and Biophysics, University of Minnesota Medical School, 6-155 Jackson Hall, 321 Church St., SE., Minneapolis, MN 55455, USAMammalian Radiation Sensitive 52 (<i>RAD52</i>) 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.https://www.mdpi.com/2072-6694/12/2/399rad52break-induced replicationbirsingle-strand annealingssaalternative non-homologous end joininga-nhejadeno-associated virusaavhuman immunodeficiency virushivherpes simplex virushsv
spellingShingle Eric A. Hendrickson
RAD52: Viral Friend or Foe?
Cancers
rad52
break-induced replication
bir
single-strand annealing
ssa
alternative non-homologous end joining
a-nhej
adeno-associated virus
aav
human immunodeficiency virus
hiv
herpes simplex virus
hsv
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 rad52
break-induced replication
bir
single-strand annealing
ssa
alternative non-homologous end joining
a-nhej
adeno-associated virus
aav
human immunodeficiency virus
hiv
herpes simplex virus
hsv
url https://www.mdpi.com/2072-6694/12/2/399
work_keys_str_mv AT ericahendrickson rad52viralfriendorfoe