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  1. Article ; Online: ERCC1-XPF endonuclease-positioned to cut.

    Schärer, Orlando D

    The EMBO journal

    2017  Volume 36, Issue 14, Page(s) 1993–1995

    MeSH term(s) DNA Repair ; DNA-Binding Proteins/genetics ; Endonucleases ; Humans ; Proteins
    Chemical Substances DNA-Binding Proteins ; Proteins ; Endonucleases (EC 3.1.-)
    Language English
    Publishing date 2017--14
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 586044-1
    ISSN 1460-2075 ; 0261-4189
    ISSN (online) 1460-2075
    ISSN 0261-4189
    DOI 10.15252/embj.201797489
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1808: Show issues Location:
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    Zs.MG 100: Show issues

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  2. Article ; Online: Repair, Removal, and Shutdown: It All Hinges on RNA Polymerase II Ubiquitylation.

    Son, Kook / Schärer, Orlando D

    Cell

    2020  Volume 180, Issue 6, Page(s) 1039–1041

    Abstract: Two papers, by Nakazawa and Vidaković, show how ubiquitylation of a single lysine residue in RNA polymerase II serves as a master switch to regulate transcription, RNA polymerase II degradation, and transcription-coupled nucleotide excision repair in ... ...

    Abstract Two papers, by Nakazawa and Vidaković, show how ubiquitylation of a single lysine residue in RNA polymerase II serves as a master switch to regulate transcription, RNA polymerase II degradation, and transcription-coupled nucleotide excision repair in response to DNA damage.
    MeSH term(s) DNA Damage ; DNA Repair ; RNA Polymerase II ; Transcription, Genetic ; Ubiquitination
    Chemical Substances RNA Polymerase II (EC 2.7.7.-)
    Language English
    Publishing date 2020-03-22
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2020.02.053
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1167: Show issues Location:
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  3. Article ; Online: Development of Comprehensive Ultraperformance Liquid Chromatography-High-Resolution Mass Spectrometry Assays to Quantitate Cisplatin-Induced DNA-DNA Cross-Links.

    Groehler, Arnold S / Maratova, Asema / Dao, Nhat Mai / Mahkmut, Anuar / Schärer, Orlando D

    Chemical research in toxicology

    2023  Volume 36, Issue 6, Page(s) 822–837

    Abstract: Cisplatin (CP) is a common antitumor drug that is used to treat many solid tumors. The activity of CP is attributed to the formation of DNA-DNA cross-links, which consist of 1,2-intra-, 1,3-intra-, and interstrand cross-links. To better understand how ... ...

    Abstract Cisplatin (CP) is a common antitumor drug that is used to treat many solid tumors. The activity of CP is attributed to the formation of DNA-DNA cross-links, which consist of 1,2-intra-, 1,3-intra-, and interstrand cross-links. To better understand how each intrastrand cross-link contributes to the activity of CP, we have developed comprehensive ultraperformance liquid chromatography-selective ion monitoring (UPLC-SIM) assays to quantify 1,2-GG-, 1,2-AG-, 1,3-GCG-, and 1,3-GTG-intrastrand cross-links. The limit of quantitation for the developed assays ranged from 5 to 50 fmol or as low as 6 cross-links per 10
    MeSH term(s) Cisplatin/pharmacology ; DNA Adducts ; DNA/chemistry ; Chromatography, Liquid ; Mass Spectrometry ; DNA Repair ; Cross-Linking Reagents/chemistry
    Chemical Substances Cisplatin (Q20Q21Q62J) ; DNA Adducts ; DNA (9007-49-2) ; Cross-Linking Reagents
    Language English
    Publishing date 2023-05-19
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 639353-6
    ISSN 1520-5010 ; 0893-228X
    ISSN (online) 1520-5010
    ISSN 0893-228X
    DOI 10.1021/acs.chemrestox.2c00308
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2320: Show issues Location:
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  4. Article ; Online: The complexity and regulation of repair of alkylation damage to nucleic acids.

    Tsao, Ning / Schärer, Orlando D / Mosammaparast, Nima

    Critical reviews in biochemistry and molecular biology

    2021  Volume 56, Issue 2, Page(s) 125–136

    Abstract: DNA damaging agents have been a cornerstone of cancer therapy for nearly a century. The discovery of many of these chemicals, particularly the alkylating agents, are deeply entwined with the development of poisonous materials originally intended for use ... ...

    Abstract DNA damaging agents have been a cornerstone of cancer therapy for nearly a century. The discovery of many of these chemicals, particularly the alkylating agents, are deeply entwined with the development of poisonous materials originally intended for use in warfare. Over the last decades, their anti-proliferative effects have focused on the specific mechanisms by which they damage DNA, and the factors involved in the repair of such damage. Due to the variety of aberrant adducts created even for the simplest alkylating agents, numerous pathways of repair are engaged as a defense against this damage. More recent work has underscored the role of RNA damage in the cellular response to these agents, although the understanding of their role in relation to established DNA repair pathways is still in its infancy. In this review, we discuss the chemistry of alkylating agents, the numerous ways in which they damage nucleic acids, as well as the specific DNA and RNA repair pathways which are engaged to counter their effects.
    MeSH term(s) Alkylating Agents/toxicity ; Alkylation/drug effects ; Animals ; DNA/chemistry ; DNA/genetics ; DNA Damage/drug effects ; DNA Repair/drug effects ; Humans ; RNA/chemistry ; RNA/genetics
    Chemical Substances Alkylating Agents ; RNA (63231-63-0) ; DNA (9007-49-2)
    Language English
    Publishing date 2021-01-12
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1000977-2
    ISSN 1549-7798 ; 1381-3455 ; 1040-9238
    ISSN (online) 1549-7798
    ISSN 1381-3455 ; 1040-9238
    DOI 10.1080/10409238.2020.1869173
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1024: Show issues Location:
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  5. Article ; Online: New Synthetic Analogs of Nitrogen Mustard DNA Interstrand Cross-Links and Their Use to Study Lesion Bypass by DNA Polymerases.

    Cheun, Young K / Groehler, Arnold S / Schärer, Orlando D

    Chemical research in toxicology

    2021  Volume 34, Issue 7, Page(s) 1790–1799

    Abstract: Nitrogen mustards are a widely used class of antitumor agents that exert their cytotoxic effects through the formation of DNA interstrand cross-links (ICLs). Despite being among the first antitumor agents used, the biological responses to NM ICLs remain ... ...

    Abstract Nitrogen mustards are a widely used class of antitumor agents that exert their cytotoxic effects through the formation of DNA interstrand cross-links (ICLs). Despite being among the first antitumor agents used, the biological responses to NM ICLs remain only partially understood. We have previously reported the generation of NM ICL mimics by incorporation of ICL precursors into DNA using solid-phase synthesis at defined positions, followed by a double reductive amination reaction. However, the structure of these mimics deviated from the native NM ICLs. Using further development of our approach, we report a new class of NM ICL mimics that only differ from their native counterpart by substitution of dG with 7-deaza-dG at the ICL. Importantly, this approach allows for the synthesis of diverse NM ICLs, illustrated here with a mimic of the adduct formed by chlorambucil. We used the newly generated ICLs in reactions with replicative and translesion synthesis DNA polymerase to demonstrate their stability and utility for functional studies. These new NM ICLs will allow for the further characterization of the biological responses to this important class of antitumor agents.
    MeSH term(s) Antineoplastic Agents, Alkylating/chemical synthesis ; Antineoplastic Agents, Alkylating/chemistry ; DNA/chemical synthesis ; DNA/chemistry ; DNA-Directed DNA Polymerase/chemistry ; Humans ; Intercalating Agents/chemical synthesis ; Intercalating Agents/chemistry ; Mechlorethamine/analogs & derivatives ; Mechlorethamine/chemical synthesis
    Chemical Substances Antineoplastic Agents, Alkylating ; Intercalating Agents ; Mechlorethamine (50D9XSG0VR) ; DNA (9007-49-2) ; DNA-Directed DNA Polymerase (EC 2.7.7.7)
    Language English
    Publishing date 2021-06-16
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 639353-6
    ISSN 1520-5010 ; 0893-228X
    ISSN (online) 1520-5010
    ISSN 0893-228X
    DOI 10.1021/acs.chemrestox.1c00123
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2320: Show issues Location:
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  6. Article ; Online: XPA tumor variant leads to defects in NER that sensitize cells to cisplatin.

    Blee, Alexandra M / Gallagher, Kaitlyn S / Kim, Hyun-Suk / Kim, Mihyun / Kharat, Suhas S / Troll, Christina R / D'Souza, Areetha / Park, Jiyoung / Neufer, P Drew / Schärer, Orlando D / Chazin, Walter J

    NAR cancer

    2024  Volume 6, Issue 1, Page(s) zcae013

    Abstract: Nucleotide excision repair (NER) reduces efficacy of treatment with platinum (Pt)-based chemotherapy by removing Pt lesions from DNA. Previous study has identified that missense mutation or loss of the NER genes Excision Repair Cross Complementation ... ...

    Abstract Nucleotide excision repair (NER) reduces efficacy of treatment with platinum (Pt)-based chemotherapy by removing Pt lesions from DNA. Previous study has identified that missense mutation or loss of the NER genes Excision Repair Cross Complementation Group 1 and 2 (
    Language English
    Publishing date 2024-03-18
    Publishing country England
    Document type Journal Article
    ISSN 2632-8674
    ISSN (online) 2632-8674
    DOI 10.1093/narcan/zcae013
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  7. Article ; Online: Repair, Removal, and Shutdown: It All Hinges on RNA Polymerase II Ubiquitylation

    Son, Kook / Schärer, Orlando D.

    Cell. 2020 Mar., v. 180, no. 6 p.1039-1041

    2020  

    Abstract: Two papers, by Nakazawa and Vidaković, show how ubiquitylation of a single lysine residue in RNA polymerase II serves as a master switch to regulate transcription, RNA polymerase II degradation, and transcription-coupled nucleotide excision repair in ... ...

    Abstract Two papers, by Nakazawa and Vidaković, show how ubiquitylation of a single lysine residue in RNA polymerase II serves as a master switch to regulate transcription, RNA polymerase II degradation, and transcription-coupled nucleotide excision repair in response to DNA damage.
    Keywords DNA damage ; DNA repair ; DNA-directed RNA polymerase ; lysine
    Language English
    Dates of publication 2020-03
    Size p. 1039-1041.
    Publishing place Elsevier Inc.
    Document type Article ; Online
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2020.02.053
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    Z 75/702: Show issues
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  8. Article ; Online: PARP Inhibition in Prostate Cancer With Homologous Recombination Repair Alterations.

    von Werdt, Alexander / Brandt, Laura / Schärer, Orlando D / Rubin, Mark A

    JCO precision oncology

    2021  Volume 5

    Abstract: Purpose: With the broad use of next-generation sequencing assays, it has become clear that mutations in DNA repair genes are more commonly found than previously reported. In advanced prostate cancer patients with : Methods: A systematic review was ... ...

    Abstract Purpose: With the broad use of next-generation sequencing assays, it has become clear that mutations in DNA repair genes are more commonly found than previously reported. In advanced prostate cancer patients with
    Methods: A systematic review was conducted in MEDLINE, National Library of Medicine, and ClinicalTrials.gov to identify studies published between January 1, 2016, and August 31, 2021. The search strategy incorporated terms for PARPi, BRCA, DNA damage, homologous recombination, organoids, patient-derived organoids, biomarker AND prostate cancer, breast cancer, ovarian cancer.
    Results: A total of 261 records remained after duplicate removal, 69 of which were included in the qualitative synthesis.
    Conclusion: To improve the outcome of targeted therapy and increase sensitivity of tumor detection, patients should be repeatedly screened for DNA repair gene alterations and biomarkers. Future clinical studies should explore the use of PARPi beyond
    MeSH term(s) DNA Damage/drug effects ; Humans ; Male ; Poly(ADP-ribose) Polymerase Inhibitors/metabolism ; Poly(ADP-ribose) Polymerase Inhibitors/pharmacology ; Prostatic Neoplasms/drug therapy ; Prostatic Neoplasms/genetics ; Recombinational DNA Repair/genetics
    Chemical Substances Poly(ADP-ribose) Polymerase Inhibitors
    Language English
    Publishing date 2021-10-22
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Systematic Review
    ISSN 2473-4284
    ISSN (online) 2473-4284
    DOI 10.1200/PO.21.00152
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Nucleotide excision repair leaves a mark on chromatin: DNA damage detection in nucleosomes.

    Apelt, Katja / Lans, Hannes / Schärer, Orlando D / Luijsterburg, Martijn S

    Cellular and molecular life sciences : CMLS

    2021  Volume 78, Issue 24, Page(s) 7925–7942

    Abstract: Global genome nucleotide excision repair (GG-NER) eliminates a broad spectrum of DNA lesions from genomic DNA. Genomic DNA is tightly wrapped around histones creating a barrier for DNA repair proteins to access DNA lesions buried in nucleosomal DNA. The ... ...

    Abstract Global genome nucleotide excision repair (GG-NER) eliminates a broad spectrum of DNA lesions from genomic DNA. Genomic DNA is tightly wrapped around histones creating a barrier for DNA repair proteins to access DNA lesions buried in nucleosomal DNA. The DNA-damage sensors XPC and DDB2 recognize DNA lesions in nucleosomal DNA and initiate repair. The emerging view is that a tight interplay between XPC and DDB2 is regulated by post-translational modifications on the damage sensors themselves as well as on chromatin containing DNA lesions. The choreography between XPC and DDB2, their interconnection with post-translational modifications such as ubiquitylation, SUMOylation, methylation, poly(ADP-ribos)ylation, acetylation, and the functional links with chromatin remodelling activities regulate not only the initial recognition of DNA lesions in nucleosomes, but also the downstream recruitment and necessary displacement of GG-NER factors as repair progresses. In this review, we highlight how nucleotide excision repair leaves a mark on chromatin to enable DNA damage detection in nucleosomes.
    MeSH term(s) Animals ; Chromatin/chemistry ; Chromatin/genetics ; DNA Damage ; DNA Repair ; DNA Repair Enzymes/genetics ; DNA Repair Enzymes/metabolism ; Humans ; Nucleosomes/physiology ; Protein Processing, Post-Translational
    Chemical Substances Chromatin ; Nucleosomes ; DNA Repair Enzymes (EC 6.5.1.-)
    Language English
    Publishing date 2021-11-03
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 1358415-7
    ISSN 1420-9071 ; 1420-682X
    ISSN (online) 1420-9071
    ISSN 1420-682X
    DOI 10.1007/s00018-021-03984-7
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 195: Show issues Location:
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  10. Article ; Online: Trabectedin derails transcription-coupled nucleotide excision repair to induce DNA breaks in highly transcribed genes.

    Son, Kook / Takhaveev, Vakil / Mor, Visesato / Yu, Hobin / Dillier, Emma / Zilio, Nicola / Püllen, Nikolai J L / Ivanov, Dmitri / Ulrich, Helle D / Sturla, Shana J / Schärer, Orlando D

    Nature communications

    2024  Volume 15, Issue 1, Page(s) 1388

    Abstract: Most genotoxic anticancer agents fail in tumors with intact DNA repair. Therefore, trabectedin, anagent more toxic to cells with active DNA repair, specifically transcription-coupled nucleotide excision repair (TC-NER), provides therapeutic opportunities. ...

    Abstract Most genotoxic anticancer agents fail in tumors with intact DNA repair. Therefore, trabectedin, anagent more toxic to cells with active DNA repair, specifically transcription-coupled nucleotide excision repair (TC-NER), provides therapeutic opportunities. To unlock the potential of trabectedin and inform its application in precision oncology, an understanding of the mechanism of the drug's TC-NER-dependent toxicity is needed. Here, we determine that abortive TC-NER of trabectedin-DNA adducts forms persistent single-strand breaks (SSBs) as the adducts block the second of the two sequential NER incisions. We map the 3'-hydroxyl groups of SSBs originating from the first NER incision at trabectedin lesions, recording TC-NER on a genome-wide scale. Trabectedin-induced SSBs primarily occur in transcribed strands of active genes and peak near transcription start sites. Frequent SSBs are also found outside gene bodies, connecting TC-NER to divergent transcription from promoters. This work advances the use of trabectedin for precision oncology and for studying TC-NER and transcription.
    MeSH term(s) Humans ; Trabectedin ; Excision Repair ; Neoplasms ; Transcription, Genetic ; Precision Medicine ; DNA Repair ; DNA Damage ; DNA/genetics ; Nucleotides ; DNA Breaks
    Chemical Substances Trabectedin (ID0YZQ2TCP) ; DNA (9007-49-2) ; Nucleotides
    Language English
    Publishing date 2024-02-15
    Publishing country England
    Document type Journal Article
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-024-45664-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

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