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  1. Article: The regulation of DNA end resection by chromatin response to DNA double strand breaks.

    Chen, Bo-Ruei / Sleckman, Barry P

    Frontiers in cell and developmental biology

    2022  Volume 10, Page(s) 932633

    Abstract: DNA double-strand breaks (DSBs) constantly arise upon exposure to genotoxic agents and during physiological processes. The timely repair of DSBs is important for not only the completion of the cellular functions involving DSBs as intermediates, but also ... ...

    Abstract DNA double-strand breaks (DSBs) constantly arise upon exposure to genotoxic agents and during physiological processes. The timely repair of DSBs is important for not only the completion of the cellular functions involving DSBs as intermediates, but also the maintenance of genome stability. There are two major pathways dedicated to DSB repair: homologous recombination (HR) and non-homologous end joining (NHEJ). The decision of deploying HR or NHEJ to repair DSBs largely depends on the structures of broken DNA ends. DNA ends resected to generate extensive single-strand DNA (ssDNA) overhangs are repaired by HR, while those remaining blunt or minimally processed can be repaired by NHEJ. As the generation and repair of DSB occurs within the context of chromatin, the resection of broken DNA ends is also profoundly affected by the state of chromatin flanking DSBs. Here we review how DNA end resection can be regulated by histone modifications, chromatin remodeling, and the presence of ssDNA structure through altering the accessibility to chromatin and the activity of pro- and anti-resection proteins.
    Language English
    Publishing date 2022-07-15
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2022.932633
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  2. Article ; Online: A Whole Genome CRISPR/Cas9 Screening Approach for Identifying Genes Encoding DNA End-Processing Proteins.

    Chen, Bo-Ruei / Sleckman, Barry P

    Methods in molecular biology (Clifton, N.J.)

    2022  Volume 2444, Page(s) 15–27

    Abstract: DNA double-strand breaks (DSBs) are mainly repaired by homologous recombination (HR) and non-homologous end joining (NHEJ). The choice of HR or NHEJ is dictated in part by whether the broken DNA ends are resected to generate extended single-stranded DNA ( ...

    Abstract DNA double-strand breaks (DSBs) are mainly repaired by homologous recombination (HR) and non-homologous end joining (NHEJ). The choice of HR or NHEJ is dictated in part by whether the broken DNA ends are resected to generate extended single-stranded DNA (ssDNA) overhangs, which are quickly bound by the trimeric ssDNA binding complex RPA, the first step of HR. Here we describe a series of protocols for generating Abelson murine leukemia virus-transformed pre-B cells (abl pre-B cells) with stably integrated inducible Cas9 that can be used to identify and study novel pathways regulating DNA end processing. These approaches involve gene inactivation by CRISPR/Cas9, whole genome guide RNA (gRNA) library-mediated screen, and flow cytometry-based detection of chromatin-bound RPA after DNA damage.
    MeSH term(s) Animals ; CRISPR-Cas Systems/genetics ; DNA ; DNA Breaks, Double-Stranded ; DNA End-Joining Repair ; Mice ; RNA, Guide, CRISPR-Cas Systems/genetics
    Chemical Substances RNA, Guide, CRISPR-Cas Systems ; DNA (9007-49-2)
    Language English
    Publishing date 2022-03-10
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-0716-2063-2_2
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  3. Article ; Online: A Flow Cytometry-Based Method for Analyzing DNA End Resection in G

    Chen, Bo-Ruei / Tyler, Jessica K / Sleckman, Barry P

    Bio-protocol

    2022  Volume 12, Issue 10, Page(s) e4413

    Abstract: DNA double strand breaks (DSBs) constantly arise in cells during normal cellular processes or upon exposure to genotoxic agents, and are repaired mostly by homologous recombination (HR) and non-homologous end joining (NHEJ). One key determinant of DNA ... ...

    Abstract DNA double strand breaks (DSBs) constantly arise in cells during normal cellular processes or upon exposure to genotoxic agents, and are repaired mostly by homologous recombination (HR) and non-homologous end joining (NHEJ). One key determinant of DNA DSB repair pathway choice is the processing of broken DNA ends to generate single strand DNA (ssDNA) overhangs, a process termed DNA resection. The generation of ssDNA overhangs commits DSB repair through HR and inhibits NHEJ. Therefore, DNA resection must be carefully regulated to avoid mis-repaired or persistent DSBs. Accordingly, many approaches have been developed to monitor ssDNA generation in cells to investigate genes and pathways that regulate DNA resection. Here we describe a flow cytometric approach measuring the levels of replication protein A (RPA) complex, a high affinity ssDNA binding complex composed of three subunits (RPA70, RPA32, and RPA14 in mammals), on chromatin after DNA DSB induction to assay DNA resection. This flow cytometric assay requires only conventional flow cytometers and can easily be scaled up to analyze a large number of samples or even for genetic screens of pooled mutants on a genome-wide scale. We adopt this assay in G
    Language English
    Publishing date 2022-05-20
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2833269-6
    ISSN 2331-8325 ; 2331-8325
    ISSN (online) 2331-8325
    ISSN 2331-8325
    DOI 10.21769/BioProtoc.4413
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  4. Article ; Online: At the intersection of DNA damage and immune responses.

    Bednarski, Jeffrey J / Sleckman, Barry P

    Nature reviews. Immunology

    2019  Volume 19, Issue 4, Page(s) 231–242

    Abstract: DNA damage occurs on exposure to genotoxic agents and during physiological DNA transactions. DNA double-strand breaks (DSBs) are particularly dangerous lesions that activate DNA damage response (DDR) kinases, leading to initiation of a canonical DDR ( ... ...

    Abstract DNA damage occurs on exposure to genotoxic agents and during physiological DNA transactions. DNA double-strand breaks (DSBs) are particularly dangerous lesions that activate DNA damage response (DDR) kinases, leading to initiation of a canonical DDR (cDDR). This response includes activation of cell cycle checkpoints and engagement of pathways that repair the DNA DSBs to maintain genomic integrity. In adaptive immune cells, programmed DNA DSBs are generated at precise genomic locations during the assembly and diversification of lymphocyte antigen receptor genes. In innate immune cells, the production of genotoxic agents, such as reactive nitrogen molecules, in response to pathogens can also cause genomic DNA DSBs. These DSBs in adaptive and innate immune cells activate the cDDR. However, recent studies have demonstrated that they also activate non-canonical DDRs (ncDDRs) that regulate cell type-specific processes that are important for innate and adaptive immune responses. Here, we review these ncDDRs and discuss how they integrate with other signals during immune system development and function.
    MeSH term(s) Adaptive Immunity/immunology ; Animals ; Cell Cycle Checkpoints/immunology ; DNA/immunology ; DNA Breaks, Double-Stranded ; DNA Damage/immunology ; Humans ; Immunity, Innate/immunology
    Chemical Substances DNA (9007-49-2)
    Language English
    Publishing date 2019-02-18
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2062776-2
    ISSN 1474-1741 ; 1474-1733
    ISSN (online) 1474-1741
    ISSN 1474-1733
    DOI 10.1038/s41577-019-0135-6
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    Zs.A 5565: Show issues Location:
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  5. Article ; Online: A Path(way) to Keeping Your Synapses on an Even Keel.

    Ryan, Timothy A / Sleckman, Barry P

    Neuron

    2018  Volume 100, Issue 5, Page(s) 1013–1014

    Abstract: In this issue of Neuron, Harris et al. (2018) show that a signal transduction pathway normally exploited by the innate immune system in recognizing foreign agents plays a critical role in controlling a synapse's ability to maintain stability in the ... ...

    Abstract In this issue of Neuron, Harris et al. (2018) show that a signal transduction pathway normally exploited by the innate immune system in recognizing foreign agents plays a critical role in controlling a synapse's ability to maintain stability in the efficacy of synaptic transmission over both rapid and prolonged timescales.
    MeSH term(s) Immunity, Innate ; Neurons ; Synapses ; Synaptic Transmission ; Synaptic Vesicles
    Language English
    Publishing date 2018-12-19
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 808167-0
    ISSN 1097-4199 ; 0896-6273
    ISSN (online) 1097-4199
    ISSN 0896-6273
    DOI 10.1016/j.neuron.2018.11.033
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    Zs.A 2496: Show issues Location:
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    Zs.MG 92: Show issues

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  6. Article ; Online: DNA damage responses: beyond double-strand break repair.

    Bredemeyer, Andrea L / Sleckman, Barry P

    Current biology : CB

    2015  Volume 25, Issue 1, Page(s) R45–6

    Abstract: The RAG endonuclease generates DNA double strand breaks during antigen receptor gene assembly, an essential process for B- and T-lymphocyte development. However, a recent study reveals that RAG endonuclease activity affects natural killer cell function, ... ...

    Abstract The RAG endonuclease generates DNA double strand breaks during antigen receptor gene assembly, an essential process for B- and T-lymphocyte development. However, a recent study reveals that RAG endonuclease activity affects natural killer cell function, demonstrating that such double strand breaks, and the responses they elicit, may have broad cellular effects.
    MeSH term(s) Animals ; DNA-Binding Proteins/metabolism ; Homeodomain Proteins/metabolism ; Killer Cells, Natural/immunology
    Chemical Substances DNA-Binding Proteins ; Homeodomain Proteins
    Language English
    Publishing date 2015-01-05
    Publishing country England
    Document type Comment ; Journal Article
    ZDB-ID 1071731-6
    ISSN 1879-0445 ; 0960-9822
    ISSN (online) 1879-0445
    ISSN 0960-9822
    DOI 10.1016/j.cub.2014.11.024
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    Zs.A 3208: Show issues Location:
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  7. Article: Ribosome biosynthesis and Hedgehog activity are cooperative actionable signaling mechanisms in breast cancer following radiotherapy.

    Metge, Brandon J / Alsheikh, Heba A / Chen, Dongquan / Elhamamsy, Amr R / Hinshaw, Dominique C / Chen, Bo-Ruei / Sleckman, Barry P / Samant, Rajeev S / Shevde, Lalita A

    NPJ precision oncology

    2023  Volume 7, Issue 1, Page(s) 61

    Abstract: Hyperactivated ribosome biosynthesis is attributed to a need for elevated protein synthesis that accommodates cell growth and division, and is characterized by nucleomorphometric alterations and increased nucleolar counts. Ribosome biogenesis is ... ...

    Abstract Hyperactivated ribosome biosynthesis is attributed to a need for elevated protein synthesis that accommodates cell growth and division, and is characterized by nucleomorphometric alterations and increased nucleolar counts. Ribosome biogenesis is challenged when DNA-damaging treatments such as radiotherapy are utilized. Tumor cells that survive radiotherapy form the basis of recurrence, tumor progression, and metastasis. In order to survive and become metabolically revitalized, tumor cells need to reactivate RNA Polymerase I (RNA Pol I) to synthesize ribosomal RNA, an integral component of ribosomes. In this study, we showed that following radiation therapy, tumor cells from breast cancer patients demonstrate activation of a ribosome biosynthesis signature concurrent with enrichment of a signature of Hedgehog (Hh) activity. We hypothesized that GLI1 activates RNA Pol I in response to irradiation and licenses the emergence of a radioresistant tumor population. Our work establishes a novel role for GLI1 in orchestrating RNA Pol I activity in irradiated breast cancer cells. Furthermore, we present evidence that in these irradiated tumor cells, Treacle ribosome biogenesis factor 1 (TCOF1), a nucleolar protein that is important in ribosome biogenesis, facilitates nucleolar translocation of GLI1. Inhibiting Hh activity and RNA Pol I activity disabled the outgrowth of breast cancer cells in the lungs. As such, ribosome biosynthesis and Hh activity present as actionable signaling mechanisms to enhance the effectiveness of radiotherapy.
    Language English
    Publishing date 2023-06-28
    Publishing country England
    Document type Journal Article
    ISSN 2397-768X
    ISSN 2397-768X
    DOI 10.1038/s41698-023-00410-y
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  8. Article ; Online: ATM deficiency: revealing the pathways to cancer.

    Tubbs, Anthony T / Sleckman, Barry P

    Cell cycle (Georgetown, Tex.)

    2014  Volume 13, Issue 19, Page(s) 2992

    MeSH term(s) Animals ; Caenorhabditis elegans/genetics ; Caenorhabditis elegans/metabolism ; Caenorhabditis elegans Proteins/genetics ; Caenorhabditis elegans Proteins/metabolism ; Cell Cycle Proteins/genetics ; Cyclin B/metabolism ; Cytoplasmic Dyneins/metabolism ; Humans ; Nuclear Proteins/genetics
    Chemical Substances Caenorhabditis elegans Proteins ; Cell Cycle Proteins ; Cyclin B ; Nuclear Proteins ; Cytoplasmic Dyneins (EC 3.6.4.2)
    Language English
    Publishing date 2014-12-08
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2146183-1
    ISSN 1551-4005 ; 1538-4101 ; 1554-8627
    ISSN (online) 1551-4005
    ISSN 1538-4101 ; 1554-8627
    DOI 10.4161/15384101.2014.959849
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  9. Article ; Online: The histone chaperone ASF1 regulates the activation of ATM and DNA-PKcs in response to DNA double-strand breaks.

    Huang, Ting-Hsiang / Shen, Zih-Jie / Sleckman, Barry P / Tyler, Jessica K

    Cell cycle (Georgetown, Tex.)

    2018  Volume 17, Issue 12, Page(s) 1413–1424

    Abstract: The Ataxia-telangiectasia mutated (ATM) kinase and the DNA-dependent protein kinase catalytic subunit (DNA-PKcs) are activated by DNA double-strand breaks (DSBs). These DSBs occur in the context of chromatin but how chromatin influences the activation of ...

    Abstract The Ataxia-telangiectasia mutated (ATM) kinase and the DNA-dependent protein kinase catalytic subunit (DNA-PKcs) are activated by DNA double-strand breaks (DSBs). These DSBs occur in the context of chromatin but how chromatin influences the activation of these kinases is not known. Here we show that loss of the replication-dependent chromatin assembly factors ASF1A/B or CAF-1 compromises ATM activation, while augmenting DNA-PKcs activation, in response to DNA DSBs. Cells deficient in ASF1A/B or CAF-1 exhibit reduced histone H4 lysine 16 acetylation (H4K16ac), a histone mark known to promote ATM activation. ASF1A interacts with the histone acetyl transferase, hMOF that mediates H4K16ac. ASF1A depletion leads to increased recruitment of DNA-PKcs to DSBs. We propose normal chromatin assembly and H4K16ac during DNA replication is required to regulate ATM and DNA-PKcs activity in response to the subsequent induction of DNA DSBs.
    MeSH term(s) Acetylation ; Ataxia Telangiectasia Mutated Proteins/genetics ; Cell Cycle Proteins/genetics ; Cell Line, Tumor ; Chromatin/genetics ; DNA/genetics ; DNA Breaks, Double-Stranded ; DNA Replication/genetics ; DNA-Activated Protein Kinase/genetics ; HCT116 Cells ; HeLa Cells ; Histone Chaperones/genetics ; Histones/genetics ; Humans ; Molecular Chaperones ; Nuclear Proteins/genetics ; Signal Transduction/genetics
    Chemical Substances ASF1A protein, human ; Cell Cycle Proteins ; Chromatin ; Histone Chaperones ; Histones ; Molecular Chaperones ; Nuclear Proteins ; DNA (9007-49-2) ; ATM protein, human (EC 2.7.11.1) ; Ataxia Telangiectasia Mutated Proteins (EC 2.7.11.1) ; DNA-Activated Protein Kinase (EC 2.7.11.1) ; PRKDC protein, human (EC 2.7.11.1)
    Language English
    Publishing date 2018-07-25
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2146183-1
    ISSN 1551-4005 ; 1538-4101 ; 1554-8627
    ISSN (online) 1551-4005
    ISSN 1538-4101 ; 1554-8627
    DOI 10.1080/15384101.2018.1486165
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  10. Article ; Online: The RNF8 and RNF168 Ubiquitin Ligases Regulate Pro- and Anti-Resection Activities at Broken DNA Ends During Non-Homologous End Joining.

    Chen, Bo-Ruei / Wang, Yinan / Shen, Zih-Jie / Bennett, Amelia / Hindi, Issa / Tyler, Jessica K / Sleckman, Barry P

    DNA repair

    2021  Volume 108, Page(s) 103217

    Abstract: The RING-type E3 ubiquitin ligases RNF8 and RNF168 recruit DNA damage response (DDR) factors to chromatin flanking DNA double strand breaks (DSBs) including 53BP1, which protects DNA ends from resection during DNA DSB repair by non-homologous end joining ...

    Abstract The RING-type E3 ubiquitin ligases RNF8 and RNF168 recruit DNA damage response (DDR) factors to chromatin flanking DNA double strand breaks (DSBs) including 53BP1, which protects DNA ends from resection during DNA DSB repair by non-homologous end joining (NHEJ). Deficiency of RNF8 or RNF168 does not lead to demonstrable NHEJ defects, but like deficiency of 53BP1, the combined deficiency of XLF and RNF8 or RNF168 leads to diminished NHEJ in lymphocytes arrested in G
    MeSH term(s) DNA/metabolism ; DNA End-Joining Repair ; DNA Repair ; DNA-Binding Proteins/metabolism ; Tumor Suppressor p53-Binding Protein 1/metabolism ; Ubiquitin/metabolism ; Ubiquitin-Protein Ligases/metabolism ; Ubiquitination
    Chemical Substances DNA-Binding Proteins ; Tumor Suppressor p53-Binding Protein 1 ; Ubiquitin ; DNA (9007-49-2) ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
    Language English
    Publishing date 2021-09-01
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2071608-4
    ISSN 1568-7856 ; 1568-7864
    ISSN (online) 1568-7856
    ISSN 1568-7864
    DOI 10.1016/j.dnarep.2021.103217
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