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  1. Article ; Online: Nontraditional Roles of DNA Polymerase Eta Support Genome Duplication and Stability.

    Eckert, Kristin A

    Genes

    2023  Volume 14, Issue 1

    Abstract: DNA polymerase eta (Pol η) is a Y-family polymerase and the product of ... ...

    Abstract DNA polymerase eta (Pol η) is a Y-family polymerase and the product of the
    MeSH term(s) Humans ; Gene Duplication ; DNA-Directed DNA Polymerase/genetics ; DNA-Directed DNA Polymerase/metabolism ; DNA/metabolism ; Genomic Instability
    Chemical Substances Rad30 protein (EC 2.7.7.7) ; DNA-Directed DNA Polymerase (EC 2.7.7.7) ; DNA (9007-49-2)
    Language English
    Publishing date 2023-01-09
    Publishing country Switzerland
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2527218-4
    ISSN 2073-4425 ; 2073-4425
    ISSN (online) 2073-4425
    ISSN 2073-4425
    DOI 10.3390/genes14010175
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Nontraditional Roles of DNA Polymerase Eta Support Genome Duplication and Stability

    Eckert, Kristin A.

    Genes (Basel). 2023 Jan. 09, v. 14, no. 1

    2023  

    Abstract: DNA polymerase eta (Pol η) is a Y-family polymerase and the product of the POLH gene. Autosomal recessive inheritance of POLH mutations is the cause of the xeroderma pigmentosum variant, a cancer predisposition syndrome. This review summarizes mounting ... ...

    Abstract DNA polymerase eta (Pol η) is a Y-family polymerase and the product of the POLH gene. Autosomal recessive inheritance of POLH mutations is the cause of the xeroderma pigmentosum variant, a cancer predisposition syndrome. This review summarizes mounting evidence for expanded Pol η cellular functions in addition to DNA lesion bypass that are critical for maintaining genome stability. In vitro, Pol η displays efficient DNA synthesis through difficult-to-replicate sequences, catalyzes D-loop extensions, and utilizes RNA–DNA hybrid templates. Human Pol η is constitutively present at the replication fork. In response to replication stress, Pol η is upregulated at the transcriptional and protein levels, and post-translational modifications regulate its localization to chromatin. Numerous studies show that Pol η is required for efficient common fragile site replication and stability. Additionally, Pol η can be recruited to stalled replication forks through protein–protein interactions, suggesting a broader role in replication fork recovery. During somatic hypermutations, Pol η is recruited by mismatch repair proteins and is essential for VH gene A:T basepair mutagenesis. Within the global context of repeat-dense genomes, the recruitment of Pol η to perform specialized functions during replication could promote genome stability by interrupting pure repeat arrays with base substitutions. Alternatively, not engaging Pol η in genome duplication is costly, as the absence of Pol η leads to incomplete replication and increased chromosomal instability.
    Keywords DNA damage ; DNA replication ; DNA-directed DNA polymerase ; chromatin ; chromosomal instability ; genes ; humans ; hybrids ; mutagenesis ; photosensitivity disorders ; transcription (genetics)
    Language English
    Dates of publication 2023-0109
    Publishing place Multidisciplinary Digital Publishing Institute
    Document type Article ; Online
    ZDB-ID 2527218-4
    ISSN 2073-4425
    ISSN 2073-4425
    DOI 10.3390/genes14010175
    Database NAL-Catalogue (AGRICOLA)

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  3. Article ; Online: Replication of [AT/TA]

    Pytko, Kara G / Dannenberg, Rachel L / Eckert, Kristin A / Hedglin, Mark

    Biochemistry

    2024  Volume 63, Issue 8, Page(s) 969–983

    Abstract: Fragile sites are unstable genomic regions that are prone to breakage during stressed DNA replication. Several common fragile sites (CFS) contain A+T-rich regions including perfect [AT/TA] microsatellite repeats that may collapse into hairpins when in ... ...

    Abstract Fragile sites are unstable genomic regions that are prone to breakage during stressed DNA replication. Several common fragile sites (CFS) contain A+T-rich regions including perfect [AT/TA] microsatellite repeats that may collapse into hairpins when in single-stranded DNA (ssDNA) form and coincide with chromosomal hotspots for breakage and rearrangements. While many factors contribute to CFS instability, evidence exists for replication stalling within [AT/TA] microsatellite repeats. Currently, it is unknown how stress causes replication stalling within [AT/TA] microsatellite repeats. To investigate this, we utilized FRET to characterize the structures of [AT/TA]
    MeSH term(s) Humans ; DNA Polymerase III/genetics ; DNA Polymerase III/metabolism ; DNA Replication ; DNA, Single-Stranded/genetics ; Holoenzymes/genetics ; Microsatellite Repeats ; Nucleotides
    Chemical Substances DNA Polymerase III (EC 2.7.7.7) ; DNA, Single-Stranded ; Holoenzymes ; Nucleotides ; RPA1 protein, human
    Language English
    Publishing date 2024-03-26
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1108-3
    ISSN 1520-4995 ; 0006-2960
    ISSN (online) 1520-4995
    ISSN 0006-2960
    DOI 10.1021/acs.biochem.4c00006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 217: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article ; Online: Special Issue "DNA Replication/Repair, and the DNA Damage Response in Human Disease".

    Zhang, Dong / Eckert, Kristin A / Lee, Marietta Y W T

    Genes

    2023  Volume 14, Issue 4

    Abstract: Mutations of numerous genes involved in DNA replication, DNA repair, and DNA damage response (DDR) pathways lead to a variety of human diseases, including aging and cancer [ ... ]. ...

    Abstract Mutations of numerous genes involved in DNA replication, DNA repair, and DNA damage response (DDR) pathways lead to a variety of human diseases, including aging and cancer [...].
    MeSH term(s) Humans ; DNA Damage/genetics ; DNA Repair/genetics ; Mutation ; Neoplasms/genetics ; DNA Replication/genetics
    Language English
    Publishing date 2023-04-11
    Publishing country Switzerland
    Document type Editorial ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2527218-4
    ISSN 2073-4425 ; 2073-4425
    ISSN (online) 2073-4425
    ISSN 2073-4425
    DOI 10.3390/genes14040893
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Replication of [AT/TA]

    Pytko, Kara G / Dannenberg, Rachel L / Eckert, Kristin A / Hedglin, Mark

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Difficult-to-Replicate Sequences (DiToRS) are natural impediments in the human genome that inhibit DNA replication under endogenous replication. Some of the most widely-studied DiToRS are A+T-rich, high "flexibility regions," including long stretches of ... ...

    Abstract Difficult-to-Replicate Sequences (DiToRS) are natural impediments in the human genome that inhibit DNA replication under endogenous replication. Some of the most widely-studied DiToRS are A+T-rich, high "flexibility regions," including long stretches of perfect [AT/TA] microsatellite repeats that have the potential to collapse into hairpin structures when in single-stranded DNA (ssDNA) form and are sites of recurrent structural variation and double-stranded DNA (dsDNA) breaks. Currently, it is unclear how these flexibility regions impact DNA replication, greatly limiting our fundamental understanding of human genome stability. To investigate replication through flexibility regions, we utilized FRET to characterize the effects of the major ssDNA-binding complex, RPA, on the structure of perfect [AT/TA]
    Language English
    Publishing date 2023-11-08
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.11.07.566133
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Impact of G-Quadruplexes and Chronic Inflammation on Genome Instability: Additive Effects during Carcinogenesis.

    Stein, MaryElizabeth / Eckert, Kristin A

    Genes

    2021  Volume 12, Issue 11

    Abstract: Genome instability is an enabling characteristic of cancer, essential for cancer cell evolution. Hotspots of genome instability, from small-scale point mutations to large-scale structural variants, are associated with sequences that potentially form non- ... ...

    Abstract Genome instability is an enabling characteristic of cancer, essential for cancer cell evolution. Hotspots of genome instability, from small-scale point mutations to large-scale structural variants, are associated with sequences that potentially form non-B DNA structures. G-quadruplex (G4) forming motifs are enriched at structural variant endpoints in cancer genomes. Chronic inflammation is a physiological state underlying cancer development, and oxidative DNA damage is commonly invoked to explain how inflammation promotes genome instability. We summarize where G4s and oxidative stress overlap, with a focus on DNA replication. Guanine has low ionization potential, making G4s vulnerable to oxidative damage. Impacts to G4 structure are dependent upon lesion type, location, and G4 conformation. Occasionally, G4s pose a challenge to replicative DNA polymerases, requiring specialized DNA polymerases to maintain genome stability. Therefore, chronic inflammation creates a dual challenge for DNA polymerases to maintain genome stability: faithful G4 synthesis and bypassing unrepaired oxidative lesions. Inflammation is also accompanied by global transcriptome changes that may impact mutagenesis. Several studies suggest a regulatory role for G4s within cancer- and inflammatory-related gene promoters. We discuss the extent to which inflammation could influence gene regulation by G4s, thereby impacting genome instability, and highlight key areas for new investigation.
    MeSH term(s) Carcinogenesis/genetics ; DNA, Neoplasm/chemistry ; G-Quadruplexes ; Genomic Instability ; Humans ; Inflammation/complications ; Inflammation/genetics ; Oxidative Stress ; Promoter Regions, Genetic
    Chemical Substances DNA, Neoplasm
    Language English
    Publishing date 2021-11-09
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2527218-4
    ISSN 2073-4425 ; 2073-4425
    ISSN (online) 2073-4425
    ISSN 2073-4425
    DOI 10.3390/genes12111779
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: DNA polymerases as chemotherapy targets: promise and challenges.

    Eckert, Kristin A / Barnes, Ryan P

    Oncotarget

    2019  Volume 10, Issue 6, Page(s) 620–621

    Language English
    Publishing date 2019-01-18
    Publishing country United States
    Document type Editorial
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.26572
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Special Issue “DNA Replication/Repair, and the DNA Damage Response in Human Disease”

    Zhang, Dong / Eckert, Kristin A. / Lee, Marietta Y. W. T.

    Genes (Basel). 2023 Apr. 11, v. 14, no. 4

    2023  

    Abstract: Mutations of numerous genes involved in DNA replication, DNA repair, and DNA damage response (DDR) pathways lead to a variety of human diseases, including aging and cancer [ ... ] ...

    Abstract Mutations of numerous genes involved in DNA replication, DNA repair, and DNA damage response (DDR) pathways lead to a variety of human diseases, including aging and cancer [...]
    Keywords DNA damage ; DNA repair ; DNA replication ; human diseases ; humans
    Language English
    Dates of publication 2023-0411
    Publishing place Multidisciplinary Digital Publishing Institute
    Document type Article ; Online
    ZDB-ID 2527218-4
    ISSN 2073-4425
    ISSN 2073-4425
    DOI 10.3390/genes14040893
    Database NAL-Catalogue (AGRICOLA)

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  9. Article ; Online: Detours to Replication: Functions of Specialized DNA Polymerases during Oncogene-induced Replication Stress.

    Tsao, Wei-Chung / Eckert, Kristin A

    International journal of molecular sciences

    2018  Volume 19, Issue 10

    Abstract: Incomplete and low-fidelity genome duplication contribute to genomic instability and cancer development. Difficult-to-Replicate Sequences, or DiToRS, are natural impediments in the genome that require specialized DNA polymerases and repair pathways to ... ...

    Abstract Incomplete and low-fidelity genome duplication contribute to genomic instability and cancer development. Difficult-to-Replicate Sequences, or DiToRS, are natural impediments in the genome that require specialized DNA polymerases and repair pathways to complete and maintain faithful DNA synthesis. DiToRS include non B-DNA secondary structures formed by repetitive sequences, for example within chromosomal fragile sites and telomeres, which inhibit DNA replication under endogenous stress conditions. Oncogene activation alters DNA replication dynamics and creates oncogenic replication stress, resulting in persistent activation of the DNA damage and replication stress responses, cell cycle arrest, and cell death. The response to oncogenic replication stress is highly complex and must be tightly regulated to prevent mutations and tumorigenesis. In this review, we summarize types of known DiToRS and the experimental evidence supporting replication inhibition, with a focus on the specialized DNA polymerases utilized to cope with these obstacles. In addition, we discuss different causes of oncogenic replication stress and its impact on DiToRS stability. We highlight recent findings regarding the regulation of DNA polymerases during oncogenic replication stress and the implications for cancer development.
    MeSH term(s) Animals ; DNA Damage ; DNA Replication ; DNA-Directed DNA Polymerase/genetics ; DNA-Directed DNA Polymerase/metabolism ; Humans ; Neoplasms/genetics ; Oncogene Proteins/genetics ; Oncogene Proteins/metabolism
    Chemical Substances Oncogene Proteins ; DNA-Directed DNA Polymerase (EC 2.7.7.7)
    Language English
    Publishing date 2018-10-20
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms19103255
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article: Impact of G-Quadruplexes and Chronic Inflammation on Genome Instability: Additive Effects during Carcinogenesis

    Stein, MaryElizabeth / Eckert, Kristin A.

    Genes. 2021 Nov. 09, v. 12, no. 11

    2021  

    Abstract: Genome instability is an enabling characteristic of cancer, essential for cancer cell evolution. Hotspots of genome instability, from small-scale point mutations to large-scale structural variants, are associated with sequences that potentially form non- ... ...

    Abstract Genome instability is an enabling characteristic of cancer, essential for cancer cell evolution. Hotspots of genome instability, from small-scale point mutations to large-scale structural variants, are associated with sequences that potentially form non-B DNA structures. G-quadruplex (G4) forming motifs are enriched at structural variant endpoints in cancer genomes. Chronic inflammation is a physiological state underlying cancer development, and oxidative DNA damage is commonly invoked to explain how inflammation promotes genome instability. We summarize where G4s and oxidative stress overlap, with a focus on DNA replication. Guanine has low ionization potential, making G4s vulnerable to oxidative damage. Impacts to G4 structure are dependent upon lesion type, location, and G4 conformation. Occasionally, G4s pose a challenge to replicative DNA polymerases, requiring specialized DNA polymerases to maintain genome stability. Therefore, chronic inflammation creates a dual challenge for DNA polymerases to maintain genome stability: faithful G4 synthesis and bypassing unrepaired oxidative lesions. Inflammation is also accompanied by global transcriptome changes that may impact mutagenesis. Several studies suggest a regulatory role for G4s within cancer- and inflammatory-related gene promoters. We discuss the extent to which inflammation could influence gene regulation by G4s, thereby impacting genome instability, and highlight key areas for new investigation.
    Keywords DNA ; DNA damage ; DNA replication ; carcinogenesis ; evolution ; genes ; genetic instability ; guanine ; inflammation ; ionization ; mutagenesis ; neoplasm cells ; oxidative stress ; physiological state ; transcriptome
    Language English
    Dates of publication 2021-1109
    Publishing place Multidisciplinary Digital Publishing Institute
    Document type Article
    ZDB-ID 2527218-4
    ISSN 2073-4425
    ISSN 2073-4425
    DOI 10.3390/genes12111779
    Database NAL-Catalogue (AGRICOLA)

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