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  1. Book ; Online: DNA Replication Controls

    Eishi Noguchi (Ed.)

    2017  

    Keywords Biology, life sciences ; DNA helicase ; DNA replication ; replication stress ; replication checkpoint ; DNA polymerase ; telomere replication ; cancer ; genomic instability ; DNA repair ; replisome ; translesion synthesis
    Language English
    Size 1 electronic resource (X, 346 pages)
    Publisher MDPI - Multidisciplinary Digital Publishing Institute
    Document type Book ; Online
    Note English
    HBZ-ID HT030648092
    ISBN 9783038425724 ; 3038425729
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  2. Book: Cell cycle control

    Noguchi, Eishi / Gadaleta, Mariana C.

    Methods and protocols

    (Methods in molecular biology ; 1170 ; Springer protocols)

    2014  

    Author's details ed. by Eishi Noguchi and Mariana C. Gadaleta
    Series title Methods in molecular biology ; 1170
    Springer protocols
    Collection
    Language English
    Size XIV, 623 S. : Ill., graph. Darst.
    Edition 2. ed.
    Publisher Humana Press
    Publishing place New York u.a.
    Publishing country United States
    Document type Book
    HBZ-ID HT018318749
    ISBN 978-1-4939-0887-5 ; 9781493908882 ; 1-4939-0887-1 ; 149390888X
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    2014 A 2712 available for loan (reading room) Lesesaal EG

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  3. Article ; Online: Fanconi anemia: current insights regarding epidemiology, cancer, and DNA repair.

    Peake, Jasmine D / Noguchi, Eishi

    Human genetics

    2022  Volume 141, Issue 12, Page(s) 1811–1836

    Abstract: Fanconi anemia is a genetic disorder that is characterized by bone marrow failure, as well as a predisposition to malignancies including leukemia and squamous cell carcinoma (SCC). At least 22 genes are associated with Fanconi anemia, constituting the ... ...

    Abstract Fanconi anemia is a genetic disorder that is characterized by bone marrow failure, as well as a predisposition to malignancies including leukemia and squamous cell carcinoma (SCC). At least 22 genes are associated with Fanconi anemia, constituting the Fanconi anemia DNA repair pathway. This pathway coordinates multiple processes and proteins to facilitate the repair of DNA adducts including interstrand crosslinks (ICLs) that are generated by environmental carcinogens, chemotherapeutic crosslinkers, and metabolic products of alcohol. ICLs can interfere with DNA transactions, including replication and transcription. If not properly removed and repaired, ICLs cause DNA breaks and lead to genomic instability, a hallmark of cancer. In this review, we will discuss the genetic and phenotypic characteristics of Fanconi anemia, the epidemiology of the disease, and associated cancer risk. The sources of ICLs and the role of ICL-inducing chemotherapeutic agents will also be discussed. Finally, we will review the detailed mechanisms of ICL repair via the Fanconi anemia DNA repair pathway, highlighting critical regulatory processes. Together, the information in this review will underscore important contributions to Fanconi anemia research in the past two decades.
    MeSH term(s) Humans ; Fanconi Anemia/epidemiology ; Fanconi Anemia/genetics ; Fanconi Anemia/metabolism ; Fanconi Anemia Complementation Group Proteins/genetics ; DNA Replication ; DNA Repair/genetics ; DNA Damage ; Neoplasms/epidemiology ; Neoplasms/genetics
    Chemical Substances Fanconi Anemia Complementation Group Proteins
    Language English
    Publishing date 2022-05-21
    Publishing country Germany
    Document type Journal Article ; Review
    ZDB-ID 223009-4
    ISSN 1432-1203 ; 0340-6717
    ISSN (online) 1432-1203
    ISSN 0340-6717
    DOI 10.1007/s00439-022-02462-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Fanconi anemia: current insights regarding epidemiology, cancer, and DNA repair

    Peake, Jasmine D. / Noguchi, Eishi

    Hum Genet. 2022 Dec., v. 141, no. 12, p. 1811-1836

    2022  , Page(s) 1811–1836

    Abstract: Fanconi anemia is a genetic disorder that is characterized by bone marrow failure, as well as a predisposition to malignancies including leukemia and squamous cell carcinoma (SCC). At least 22 genes are associated with Fanconi anemia, constituting the ... ...

    Abstract Fanconi anemia is a genetic disorder that is characterized by bone marrow failure, as well as a predisposition to malignancies including leukemia and squamous cell carcinoma (SCC). At least 22 genes are associated with Fanconi anemia, constituting the Fanconi anemia DNA repair pathway. This pathway coordinates multiple processes and proteins to facilitate the repair of DNA adducts including interstrand crosslinks (ICLs) that are generated by environmental carcinogens, chemotherapeutic crosslinkers, and metabolic products of alcohol. ICLs can interfere with DNA transactions, including replication and transcription. If not properly removed and repaired, ICLs cause DNA breaks and lead to genomic instability, a hallmark of cancer. In this review, we will discuss the genetic and phenotypic characteristics of Fanconi anemia, the epidemiology of the disease, and associated cancer risk. The sources of ICLs and the role of ICL-inducing chemotherapeutic agents will also be discussed. Finally, we will review the detailed mechanisms of ICL repair via the Fanconi anemia DNA repair pathway, highlighting critical regulatory processes. Together, the information in this review will underscore important contributions to Fanconi anemia research in the past two decades.
    Keywords DNA adducts ; DNA repair ; Fanconi anemia ; alcohols ; bone marrow ; crosslinking ; drug therapy ; epidemiology ; genetic instability ; leukemia ; phenotype ; risk ; squamous cell carcinoma
    Language English
    Dates of publication 2022-12
    Size p. 1811-1836
    Publishing place Springer Berlin Heidelberg
    Document type Article ; Online
    Note Review
    ZDB-ID 223009-4
    ISSN 1432-1203 ; 0340-6717
    ISSN (online) 1432-1203
    ISSN 0340-6717
    DOI 10.1007/s00439-022-02462-9
    Database NAL-Catalogue (AGRICOLA)

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    In stock of ZB MED Bonn / Germany

    Z 66/109: Show issues
    Z 5.6: Show issues

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  5. Article ; Online: The p53 DNA damage response and Fanconi anemia DNA repair pathway protect against acetaldehyde-induced replication stress in esophageal keratinocytes.

    Peake, Jasmine D / Horne, Kalisse I / Noguchi, Chiaki / Gilligan, John P / Noguchi, Eishi

    Cell cycle (Georgetown, Tex.)

    2023  Volume 22, Issue 18, Page(s) 2088–2096

    Abstract: Alcohol contributes to cellular accumulation of acetaldehyde, a primary metabolite of alcohol and a major human carcinogen. Acetaldehyde can form DNA adducts and induce interstrand crosslinks (ICLs) that are repaired by the Fanconi anemia DNA repair ... ...

    Abstract Alcohol contributes to cellular accumulation of acetaldehyde, a primary metabolite of alcohol and a major human carcinogen. Acetaldehyde can form DNA adducts and induce interstrand crosslinks (ICLs) that are repaired by the Fanconi anemia DNA repair pathway (FA pathway). Individuals with deficiency in acetaldehyde detoxification or in the FA pathway have an increased risk of squamous-cell carcinomas (SCCs) including those of the esophagus. In a recent report, we described the molecular basis of acetaldehyde-induced DNA damage in esophageal keratinocytes [1]. We demonstrated that, at physiologically relevant concentrations, acetaldehyde induces DNA damage at the DNA replication fork. This resulted in replication stress, leading to activation of the ATR-Chk1-dependent cell cycle checkpoints. We also reported that the p53 DNA damage response is elevated in response to acetaldehyde and that the FA pathway limits acetaldehyde-induced genomic instability. Here, we highlight these findings and present additional results to discuss the role of the FA pathway and p53 DNA damage response in the protection against genomic instability and esophageal carcinogenesis.
    MeSH term(s) Humans ; Acetaldehyde/toxicity ; Acetaldehyde/metabolism ; Tumor Suppressor Protein p53/metabolism ; Fanconi Anemia/genetics ; Fanconi Anemia/metabolism ; DNA Damage ; Ethanol ; Genomic Instability ; DNA Repair ; Esophagus/metabolism ; Keratinocytes/metabolism ; DNA Replication
    Chemical Substances Acetaldehyde (GO1N1ZPR3B) ; Tumor Suppressor Protein p53 ; Ethanol (3K9958V90M)
    Language English
    Publishing date 2023-11-23
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2146183-1
    ISSN 1551-4005 ; 1538-4101 ; 1554-8627
    ISSN (online) 1551-4005
    ISSN 1538-4101 ; 1554-8627
    DOI 10.1080/15384101.2023.2261740
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5881: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  6. Article ; Online: PP2A(Cdc55/B55), a possible therapeutic target in cyclin D1-dependent cancers.

    Noguchi, Eishi

    Cell cycle (Georgetown, Tex.)

    2013  Volume 12, Issue 10, Page(s) 1484

    MeSH term(s) Cell Cycle/physiology ; Cell Cycle Proteins/metabolism ; Cyclin G1/metabolism ; Cyclins/metabolism ; Protein Phosphatase 2/metabolism ; Saccharomyces cerevisiae/physiology ; Saccharomyces cerevisiae Proteins/metabolism
    Chemical Substances Cell Cycle Proteins ; Cyclin G1 ; Cyclins ; Saccharomyces cerevisiae Proteins ; Protein Phosphatase 2 (EC 3.1.3.16)
    Language English
    Publishing date 2013-04-29
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 2146183-1
    ISSN 1551-4005 ; 1538-4101 ; 1554-8627
    ISSN (online) 1551-4005
    ISSN 1538-4101 ; 1554-8627
    DOI 10.4161/cc.24854
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Division of labor of the replication fork protection complex subunits in sister chromatid cohesion and Chk1 activation.

    Noguchi, Eishi

    Cell cycle (Georgetown, Tex.)

    2011  Volume 10, Issue 13, Page(s) 2055–2056

    MeSH term(s) Carrier Proteins/metabolism ; Cell Cycle Proteins/metabolism ; Chromatids/metabolism ; Chromosomal Proteins, Non-Histone/metabolism ; Fibroblasts/metabolism ; Humans ; Intracellular Signaling Peptides and Proteins/metabolism ; Nuclear Proteins/metabolism
    Chemical Substances Carrier Proteins ; Cell Cycle Proteins ; Chromosomal Proteins, Non-Histone ; Intracellular Signaling Peptides and Proteins ; Nuclear Proteins
    Language English
    Publishing date 2011-07-01
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 2146183-1
    ISSN 1551-4005 ; 1538-4101 ; 1554-8627
    ISSN (online) 1551-4005
    ISSN 1538-4101 ; 1554-8627
    DOI 10.4161/cc.10.13.15805
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  8. Article ; Online: Maf1 limits RNA polymerase III-directed transcription to preserve genomic integrity and extend lifespan.

    Noguchi, Chiaki / Wang, Lucy / Shetty, Mihir / Mell, Joshua Chang / Sell, Christian / Noguchi, Eishi

    Cell cycle (Georgetown, Tex.)

    2021  Volume 20, Issue 3, Page(s) 247–255

    Abstract: A key to longevity assurance is the nutrient-sensing mTOR pathway. Inhibition of mTOR extends lifespan in a variety of organisms. However, the downstream effectors of the mTOR pathway for lifespan regulation are elusive. In a recent report, we described ... ...

    Abstract A key to longevity assurance is the nutrient-sensing mTOR pathway. Inhibition of mTOR extends lifespan in a variety of organisms. However, the downstream effectors of the mTOR pathway for lifespan regulation are elusive. In a recent report, we described the role of Maf1 as a critical lifespan regulator downstream of the mTOR pathway in fission yeast. Maf1 is the master negative regulator of RNA polymerase III-directed transcription (e.g. tRNAs and 5S rRNAs) and is regulated by mTOR-mediated phosphorylation. We demonstrated that Maf1 is required for lifespan extension under calorie restriction or when mTOR is inhibited. We also showed that Maf1 prevents DNA damage at tRNA genes, which appears to contribute to lifespan maintenance by Maf1. Here we highlight these observations and present additional results to discuss the role of the mTOR-Maf1-Pol III axis in promoting genomic integrity in the face of DNA replication-transcription conflicts in order to maintain normal lifespan.
    MeSH term(s) Caloric Restriction/methods ; DNA Damage/physiology ; Longevity/physiology ; RNA Polymerase III/genetics ; RNA Polymerase III/metabolism ; Repressor Proteins/genetics ; Repressor Proteins/metabolism ; Schizosaccharomyces ; Schizosaccharomyces pombe Proteins/genetics ; Schizosaccharomyces pombe Proteins/metabolism ; TOR Serine-Threonine Kinases/antagonists & inhibitors ; TOR Serine-Threonine Kinases/genetics ; TOR Serine-Threonine Kinases/metabolism ; Transcription, Genetic/physiology
    Chemical Substances Maf1 protein, S pombe ; Repressor Proteins ; Schizosaccharomyces pombe Proteins ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; RNA Polymerase III (EC 2.7.7.6)
    Language English
    Publishing date 2021-01-21
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2146183-1
    ISSN 1551-4005 ; 1538-4101 ; 1554-8627
    ISSN (online) 1551-4005
    ISSN 1538-4101 ; 1554-8627
    DOI 10.1080/15384101.2021.1874697
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  9. Article: Regulation of DNA Replication through Natural  Impediments in the Eukaryotic Genome.

    Gadaleta, Mariana C / Noguchi, Eishi

    Genes

    2017  Volume 8, Issue 3

    Abstract: All living organisms need to duplicate their genetic information while protecting it from unwanted mutations, which can lead to genetic disorders and cancer development. Inaccuracies during DNA replication are the major cause of genomic instability, as ... ...

    Abstract All living organisms need to duplicate their genetic information while protecting it from unwanted mutations, which can lead to genetic disorders and cancer development. Inaccuracies during DNA replication are the major cause of genomic instability, as replication forks are prone to stalling and collapse, resulting in DNA damage. The presence of exogenous DNA damaging agents as well as endogenous difficult-to-replicate DNA regions containing DNA-protein complexes, repetitive DNA, secondary DNA structures, or transcribing RNA polymerases, increases the risk of genomic instability and thus threatens cell survival. Therefore, understanding the cellular mechanisms required to preserve the genetic information during S phase is of paramount importance. In this review, we will discuss our current understanding of how cells cope with these natural impediments in order to prevent DNA damage and genomic instability during DNA replication.
    Language English
    Publishing date 2017-03-07
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2527218-4
    ISSN 2073-4425
    ISSN 2073-4425
    DOI 10.3390/genes8030098
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Genetic investigation of formaldehyde-induced DNA damage response in Schizosaccharomyces pombe.

    Anandarajan, Vinesh / Noguchi, Chiaki / Oleksak, Julia / Grothusen, Grant / Terlecky, Daniel / Noguchi, Eishi

    Current genetics

    2020  Volume 66, Issue 3, Page(s) 593–605

    Abstract: Formaldehyde is a common environmental pollutant and is associated with adverse health effects. Formaldehyde is also considered to be a carcinogen because it can form DNA adducts, leading to genomic instability. How these adducts are prevented and ... ...

    Abstract Formaldehyde is a common environmental pollutant and is associated with adverse health effects. Formaldehyde is also considered to be a carcinogen because it can form DNA adducts, leading to genomic instability. How these adducts are prevented and removed is not fully understood. In this study, we used the fission yeast Schizosaccharomyces pombe as a model organism to investigate cellular tolerance pathways against formaldehyde exposure. We show that Fmd1 is a major formaldehyde dehydrogenase that functions to detoxify formaldehyde and that Fmd1 is critical to minimize formaldehyde-mediated DNA lesions. Our investigation revealed that nucleotide excision repair and homologous recombination have major roles in cellular tolerance to formaldehyde, while mutations in the Fanconi anemia, translesion synthesis, and base excision repair pathways also render cells sensitive to formaldehyde. We also demonstrate that loss of Wss1 or Wss2, proteases involved in the removal of DNA-protein crosslinks, sensitizes cells to formaldehyde and leads to replication defects. These results suggest that formaldehyde generates a variety of DNA lesions, including interstrand crosslinks, DNA-protein crosslinks, and base adducts. Thus, our genetic studies provide a framework for future investigation regarding health effects resulting from formaldehyde exposure.
    MeSH term(s) DNA Damage ; DNA Repair ; DNA Replication ; Fanconi Anemia Complementation Group Proteins/genetics ; Fanconi Anemia Complementation Group Proteins/metabolism ; Formaldehyde/adverse effects ; Formaldehyde/toxicity ; Homologous Recombination ; Respiratory Hypersensitivity ; Schizosaccharomyces/drug effects ; Schizosaccharomyces/genetics ; Schizosaccharomyces/metabolism
    Chemical Substances Fanconi Anemia Complementation Group Proteins ; Formaldehyde (1HG84L3525)
    Language English
    Publishing date 2020-02-07
    Publishing country United States
    Document type Journal Article
    ZDB-ID 282876-5
    ISSN 1432-0983 ; 0172-8083
    ISSN (online) 1432-0983
    ISSN 0172-8083
    DOI 10.1007/s00294-020-01057-z
    Database MEDical Literature Analysis and Retrieval System OnLINE

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