RAD52: Paradigm of Synthetic Lethality and New Developments

DNA double-strand breaks and inter-strand cross-links are the most harmful types of DNA damage that cause genomic instability that lead to cancer development. The highest fidelity pathway for repairing damaged double-stranded DNA is termed Homologous recombination (HR). Rad52 is one of the key HR pr...

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Autores principales:	Matthew J. Rossi, Sarah F. DiDomenico, Mikir Patel, Alexander V. Mazin
Formato:	article
Lenguaje:	EN
Publicado:	Frontiers Media S.A. 2021
Materias:	Rad52 homologous recombination single strand annealing break induced replication synthetic lethality Genetics QH426-470
Acceso en línea:	https://doaj.org/article/22dfb44279204a3e8ebf84451e384a14
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spelling	oai:doaj.org-article:22dfb44279204a3e8ebf84451e384a142021-11-30T13:06:06ZRAD52: Paradigm of Synthetic Lethality and New Developments1664-802110.3389/fgene.2021.780293https://doaj.org/article/22dfb44279204a3e8ebf84451e384a142021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fgene.2021.780293/fullhttps://doaj.org/toc/1664-8021DNA double-strand breaks and inter-strand cross-links are the most harmful types of DNA damage that cause genomic instability that lead to cancer development. The highest fidelity pathway for repairing damaged double-stranded DNA is termed Homologous recombination (HR). Rad52 is one of the key HR proteins in eukaryotes. Although it is critical for most DNA repair and recombination events in yeast, knockouts of mammalian RAD52 lack any discernable phenotypes. As a consequence, mammalian RAD52 has been long overlooked. That is changing now, as recent work has shown RAD52 to be critical for backup DNA repair pathways in HR-deficient cancer cells. Novel findings have shed light on RAD52’s biochemical activities. RAD52 promotes DNA pairing (D-loop formation), single-strand DNA and DNA:RNA annealing, and inverse strand exchange. These activities contribute to its multiple roles in DNA damage repair including HR, single-strand annealing, break-induced replication, and RNA-mediated repair of DNA. The contributions of RAD52 that are essential to the viability of HR-deficient cancer cells are currently under investigation. These new findings make RAD52 an attractive target for the development of anti-cancer therapies against BRCA-deficient cancers.Matthew J. RossiSarah F. DiDomenicoMikir PatelAlexander V. MazinFrontiers Media S.A.articleRad52homologous recombinationsingle strand annealingbreak induced replicationsynthetic lethalityGeneticsQH426-470ENFrontiers in Genetics, Vol 12 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Rad52 homologous recombination single strand annealing break induced replication synthetic lethality Genetics QH426-470
spellingShingle	Rad52 homologous recombination single strand annealing break induced replication synthetic lethality Genetics QH426-470 Matthew J. Rossi Sarah F. DiDomenico Mikir Patel Alexander V. Mazin RAD52: Paradigm of Synthetic Lethality and New Developments
description	DNA double-strand breaks and inter-strand cross-links are the most harmful types of DNA damage that cause genomic instability that lead to cancer development. The highest fidelity pathway for repairing damaged double-stranded DNA is termed Homologous recombination (HR). Rad52 is one of the key HR proteins in eukaryotes. Although it is critical for most DNA repair and recombination events in yeast, knockouts of mammalian RAD52 lack any discernable phenotypes. As a consequence, mammalian RAD52 has been long overlooked. That is changing now, as recent work has shown RAD52 to be critical for backup DNA repair pathways in HR-deficient cancer cells. Novel findings have shed light on RAD52’s biochemical activities. RAD52 promotes DNA pairing (D-loop formation), single-strand DNA and DNA:RNA annealing, and inverse strand exchange. These activities contribute to its multiple roles in DNA damage repair including HR, single-strand annealing, break-induced replication, and RNA-mediated repair of DNA. The contributions of RAD52 that are essential to the viability of HR-deficient cancer cells are currently under investigation. These new findings make RAD52 an attractive target for the development of anti-cancer therapies against BRCA-deficient cancers.
format	article
author	Matthew J. Rossi Sarah F. DiDomenico Mikir Patel Alexander V. Mazin
author_facet	Matthew J. Rossi Sarah F. DiDomenico Mikir Patel Alexander V. Mazin
author_sort	Matthew J. Rossi
title	RAD52: Paradigm of Synthetic Lethality and New Developments
title_short	RAD52: Paradigm of Synthetic Lethality and New Developments
title_full	RAD52: Paradigm of Synthetic Lethality and New Developments
title_fullStr	RAD52: Paradigm of Synthetic Lethality and New Developments
title_full_unstemmed	RAD52: Paradigm of Synthetic Lethality and New Developments
title_sort	rad52: paradigm of synthetic lethality and new developments
publisher	Frontiers Media S.A.
publishDate	2021
url	https://doaj.org/article/22dfb44279204a3e8ebf84451e384a14
work_keys_str_mv	AT matthewjrossi rad52paradigmofsyntheticlethalityandnewdevelopments AT sarahfdidomenico rad52paradigmofsyntheticlethalityandnewdevelopments AT mikirpatel rad52paradigmofsyntheticlethalityandnewdevelopments AT alexandervmazin rad52paradigmofsyntheticlethalityandnewdevelopments
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RAD52: Paradigm of Synthetic Lethality and New Developments

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