Replication Fork Reversal and Protection

During genome replication, replication forks often encounter obstacles that impede their progression. Arrested forks are unstable structures that can give rise to collapse and rearrange if they are not properly processed and restarted. Replication fork reversal is a critical protective mechanism in...
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Autor*in:	Shan Qiu [verfasserIn] Guixing Jiang [verfasserIn] Liping Cao [verfasserIn] Jun Huang [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2021

Schlagwörter:	replication stress replication fork stalling genome instability replication fork reversal DNA translocase

Übergeordnetes Werk:	In: Frontiers in Cell and Developmental Biology - Frontiers Media S.A., 2014, 9(2021)
Übergeordnetes Werk:	volume:9 ; year:2021

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3389/fcell.2021.670392

Katalog-ID:	DOAJ057450250

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520			\|a During genome replication, replication forks often encounter obstacles that impede their progression. Arrested forks are unstable structures that can give rise to collapse and rearrange if they are not properly processed and restarted. Replication fork reversal is a critical protective mechanism in higher eukaryotic cells in response to replication stress, in which forks reverse their direction to form a Holliday junction-like structure. The reversed replication forks are protected from nuclease degradation by DNA damage repair proteins, such as BRCA1, BRCA2, and RAD51. Some of these molecules work cooperatively, while others have unique functions. Once the stress is resolved, the replication forks can restart with the help of enzymes, including human RECQ1 helicase, but restart will not be considered here. Here, we review research on the key factors and mechanisms required for the remodeling and protection of stalled replication forks in mammalian cells.
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allfieldsGer	10.3389/fcell.2021.670392 doi (DE-627)DOAJ057450250 (DE-599)DOAJc2870b6b5d3a4011a16eb78e5105b007 DE-627 ger DE-627 rakwb eng QH301-705.5 Shan Qiu verfasserin aut Replication Fork Reversal and Protection 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier During genome replication, replication forks often encounter obstacles that impede their progression. Arrested forks are unstable structures that can give rise to collapse and rearrange if they are not properly processed and restarted. Replication fork reversal is a critical protective mechanism in higher eukaryotic cells in response to replication stress, in which forks reverse their direction to form a Holliday junction-like structure. The reversed replication forks are protected from nuclease degradation by DNA damage repair proteins, such as BRCA1, BRCA2, and RAD51. Some of these molecules work cooperatively, while others have unique functions. Once the stress is resolved, the replication forks can restart with the help of enzymes, including human RECQ1 helicase, but restart will not be considered here. Here, we review research on the key factors and mechanisms required for the remodeling and protection of stalled replication forks in mammalian cells. replication stress replication fork stalling genome instability replication fork reversal DNA translocase Biology (General) Shan Qiu verfasserin aut Shan Qiu verfasserin aut Guixing Jiang verfasserin aut Liping Cao verfasserin aut Jun Huang verfasserin aut Jun Huang verfasserin aut In Frontiers in Cell and Developmental Biology Frontiers Media S.A., 2014 9(2021) (DE-627)770398138 (DE-600)2737824-X 2296634X nnns volume:9 year:2021 https://doi.org/10.3389/fcell.2021.670392 kostenfrei https://doaj.org/article/c2870b6b5d3a4011a16eb78e5105b007 kostenfrei https://www.frontiersin.org/articles/10.3389/fcell.2021.670392/full kostenfrei https://doaj.org/toc/2296-634X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2021
allfieldsSound	10.3389/fcell.2021.670392 doi (DE-627)DOAJ057450250 (DE-599)DOAJc2870b6b5d3a4011a16eb78e5105b007 DE-627 ger DE-627 rakwb eng QH301-705.5 Shan Qiu verfasserin aut Replication Fork Reversal and Protection 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier During genome replication, replication forks often encounter obstacles that impede their progression. Arrested forks are unstable structures that can give rise to collapse and rearrange if they are not properly processed and restarted. Replication fork reversal is a critical protective mechanism in higher eukaryotic cells in response to replication stress, in which forks reverse their direction to form a Holliday junction-like structure. The reversed replication forks are protected from nuclease degradation by DNA damage repair proteins, such as BRCA1, BRCA2, and RAD51. Some of these molecules work cooperatively, while others have unique functions. Once the stress is resolved, the replication forks can restart with the help of enzymes, including human RECQ1 helicase, but restart will not be considered here. Here, we review research on the key factors and mechanisms required for the remodeling and protection of stalled replication forks in mammalian cells. replication stress replication fork stalling genome instability replication fork reversal DNA translocase Biology (General) Shan Qiu verfasserin aut Shan Qiu verfasserin aut Guixing Jiang verfasserin aut Liping Cao verfasserin aut Jun Huang verfasserin aut Jun Huang verfasserin aut In Frontiers in Cell and Developmental Biology Frontiers Media S.A., 2014 9(2021) (DE-627)770398138 (DE-600)2737824-X 2296634X nnns volume:9 year:2021 https://doi.org/10.3389/fcell.2021.670392 kostenfrei https://doaj.org/article/c2870b6b5d3a4011a16eb78e5105b007 kostenfrei https://www.frontiersin.org/articles/10.3389/fcell.2021.670392/full kostenfrei https://doaj.org/toc/2296-634X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2021
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topic_title	QH301-705.5 Replication Fork Reversal and Protection replication stress replication fork stalling genome instability replication fork reversal DNA translocase
topic	misc QH301-705.5 misc replication stress misc replication fork stalling misc genome instability misc replication fork reversal misc DNA translocase misc Biology (General)
topic_unstemmed	misc QH301-705.5 misc replication stress misc replication fork stalling misc genome instability misc replication fork reversal misc DNA translocase misc Biology (General)
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title	Replication Fork Reversal and Protection
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title_auth	Replication Fork Reversal and Protection
abstract	During genome replication, replication forks often encounter obstacles that impede their progression. Arrested forks are unstable structures that can give rise to collapse and rearrange if they are not properly processed and restarted. Replication fork reversal is a critical protective mechanism in higher eukaryotic cells in response to replication stress, in which forks reverse their direction to form a Holliday junction-like structure. The reversed replication forks are protected from nuclease degradation by DNA damage repair proteins, such as BRCA1, BRCA2, and RAD51. Some of these molecules work cooperatively, while others have unique functions. Once the stress is resolved, the replication forks can restart with the help of enzymes, including human RECQ1 helicase, but restart will not be considered here. Here, we review research on the key factors and mechanisms required for the remodeling and protection of stalled replication forks in mammalian cells.
abstractGer	During genome replication, replication forks often encounter obstacles that impede their progression. Arrested forks are unstable structures that can give rise to collapse and rearrange if they are not properly processed and restarted. Replication fork reversal is a critical protective mechanism in higher eukaryotic cells in response to replication stress, in which forks reverse their direction to form a Holliday junction-like structure. The reversed replication forks are protected from nuclease degradation by DNA damage repair proteins, such as BRCA1, BRCA2, and RAD51. Some of these molecules work cooperatively, while others have unique functions. Once the stress is resolved, the replication forks can restart with the help of enzymes, including human RECQ1 helicase, but restart will not be considered here. Here, we review research on the key factors and mechanisms required for the remodeling and protection of stalled replication forks in mammalian cells.
abstract_unstemmed	During genome replication, replication forks often encounter obstacles that impede their progression. Arrested forks are unstable structures that can give rise to collapse and rearrange if they are not properly processed and restarted. Replication fork reversal is a critical protective mechanism in higher eukaryotic cells in response to replication stress, in which forks reverse their direction to form a Holliday junction-like structure. The reversed replication forks are protected from nuclease degradation by DNA damage repair proteins, such as BRCA1, BRCA2, and RAD51. Some of these molecules work cooperatively, while others have unique functions. Once the stress is resolved, the replication forks can restart with the help of enzymes, including human RECQ1 helicase, but restart will not be considered here. Here, we review research on the key factors and mechanisms required for the remodeling and protection of stalled replication forks in mammalian cells.
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title_short	Replication Fork Reversal and Protection
url	https://doi.org/10.3389/fcell.2021.670392 https://doaj.org/article/c2870b6b5d3a4011a16eb78e5105b007 https://www.frontiersin.org/articles/10.3389/fcell.2021.670392/full https://doaj.org/toc/2296-634X
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