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  1. Article ; Online: Utilization of Host Cell Chromosome Conformation by Viral Pathogens: Knowing When to Hold and When to Fold.

    Majumder, Kinjal / Morales, Abigail J

    Frontiers in immunology

    2021  Volume 12, Page(s) 633762

    Abstract: Though viruses have their own genomes, many depend on the nuclear environment of their hosts for replication and survival. A substantial body of work has therefore been devoted to understanding how viral and eukaryotic genomes interact. Recent advances ... ...

    Abstract Though viruses have their own genomes, many depend on the nuclear environment of their hosts for replication and survival. A substantial body of work has therefore been devoted to understanding how viral and eukaryotic genomes interact. Recent advances in chromosome conformation capture technologies have provided unprecedented opportunities to visualize how mammalian genomes are organized and, by extension, how packaging of nuclear DNA impacts cellular processes. Recent studies have indicated that some viruses, upon entry into host cell nuclei, produce factors that alter host chromatin topology, and thus, impact the 3D organization of the host genome. Additionally, a variety of distinct viruses utilize host genome architectural factors to advance various aspects of their life cycles. Indeed, human gammaherpesviruses, known for establishing long-term reservoirs of latent infection in B lymphocytes, utilize 3D principles of genome folding to package their DNA and establish latency in host cells. This manipulation of host epigenetic machinery by latent viral genomes is etiologically linked to the onset of B cell oncogenesis. Small DNA viruses, by contrast, are tethered to distinct cellular sites that support virus expression and replication. Here, we briefly review the recent findings on how viruses and host genomes spatially communicate, and how this impacts virus-induced pathology.
    Language English
    Publishing date 2021-03-25
    Publishing country Switzerland
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2021.633762
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Targeting the Achievement Gap: Strategies Toward Removing Inequities in Undergraduate Immunology Education.

    Riestra, Angelica M / Morales, Abigail J / Mercer, Frances

    Frontiers in immunology

    2019  Volume 10, Page(s) 2906

    Abstract: A diverse student body enriches the classroom with lived experiences, varied skillsets, community and cultural knowledge, resiliency, and altruistic interests, all critical attributes that benefit both the classroom and the STEM field at large. However, ... ...

    Abstract A diverse student body enriches the classroom with lived experiences, varied skillsets, community and cultural knowledge, resiliency, and altruistic interests, all critical attributes that benefit both the classroom and the STEM field at large. However, a persistent disparity in academic and educational attainment exists between under-represented minority (URM) and non-URM students in STEM fields. This achievement gap discourages talented URM students from entering STEM professions, threatening the potential, expertise, and perspective of these professions. Here we describe the factors that contribute to the achievement gap and present strategies, utilized in our Immunology classrooms, for combating each factor. We discuss project-based learning pedagogy to give students increased agency and feelings of empowerment. We also highlight concrete practices to foster students' science identities and sense of community, factors that highly promote STEM retention. The dynamic subject of Immunology provides myriad opportunities to implement a curriculum committed to equity, as we outline below.
    MeSH term(s) Allergy and Immunology/education ; Education, Medical, Undergraduate ; Female ; Humans ; Male ; Minority Groups ; Social Conditions
    Language English
    Publishing date 2019-12-11
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2019.02906
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: DNA damage responses in murine Pre-B cells with genetic deficiencies in damage response genes.

    Innes, Cynthia L / Hesse, Jill E / Morales, Abigail J / Helmink, Beth A / Schurman, Shepherd H / Sleckman, Barry P / Paules, Richard S

    Cell cycle (Georgetown, Tex.)

    2019  Volume 19, Issue 1, Page(s) 67–83

    Abstract: DNA damage can be generated in multiple ways from genotoxic and physiologic sources. Genotoxic damage is known to disrupt cellular functions and is lethal if not repaired properly. We compare the transcriptional programs activated in response to ... ...

    Abstract DNA damage can be generated in multiple ways from genotoxic and physiologic sources. Genotoxic damage is known to disrupt cellular functions and is lethal if not repaired properly. We compare the transcriptional programs activated in response to genotoxic DNA damage induced by ionizing radiation (IR) in abl pre-B cells from mice deficient in DNA damage response (DDR) genes
    MeSH term(s) Animals ; Cell Cycle/genetics ; Cell Cycle/radiation effects ; Cell Cycle Checkpoints/genetics ; DNA Damage/genetics ; Gene Expression Regulation/radiation effects ; Genotype ; Mice ; Precursor Cells, B-Lymphoid/immunology ; Precursor Cells, B-Lymphoid/metabolism ; Precursor Cells, B-Lymphoid/radiation effects ; Radiation, Ionizing ; Signal Transduction ; Transcription, Genetic/radiation effects
    Language English
    Publishing date 2019-11-22
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural
    ZDB-ID 2146183-1
    ISSN 1551-4005 ; 1538-4101 ; 1554-8627
    ISSN (online) 1551-4005
    ISSN 1538-4101 ; 1554-8627
    DOI 10.1080/15384101.2019.1693118
    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)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article ; Online: A type I IFN-dependent DNA damage response regulates the genetic program and inflammasome activation in macrophages.

    Morales, Abigail J / Carrero, Javier A / Hung, Putzer J / Tubbs, Anthony T / Andrews, Jared M / Edelson, Brian T / Calderon, Boris / Innes, Cynthia L / Paules, Richard S / Payton, Jacqueline E / Sleckman, Barry P

    eLife

    2017  Volume 6

    Abstract: Macrophages produce genotoxic agents, such as reactive oxygen and nitrogen species, that kill invading pathogens. Here we show that these agents activate the DNA damage response (DDR) kinases ATM and DNA-PKcs through the generation of double stranded ... ...

    Abstract Macrophages produce genotoxic agents, such as reactive oxygen and nitrogen species, that kill invading pathogens. Here we show that these agents activate the DNA damage response (DDR) kinases ATM and DNA-PKcs through the generation of double stranded breaks (DSBs) in murine macrophage genomic DNA. In contrast to other cell types, initiation of this DDR depends on signaling from the type I interferon receptor. Once activated, ATM and DNA-PKcs regulate a genetic program with diverse immune functions and promote inflammasome activation and the production of IL-1β and IL-18. Indeed, following infection with
    MeSH term(s) Animals ; DNA Breaks, Double-Stranded ; DNA Damage ; Gene Expression Regulation ; Immunity, Innate ; Inflammasomes/metabolism ; Interferon Type I/metabolism ; Listeria monocytogenes/immunology ; Macrophages/immunology ; Mice ; Protein Kinases/metabolism
    Chemical Substances Inflammasomes ; Interferon Type I ; Protein Kinases (EC 2.7.-)
    Language English
    Publishing date 2017-03-31
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2687154-3
    ISSN 2050-084X ; 2050-084X
    ISSN (online) 2050-084X
    ISSN 2050-084X
    DOI 10.7554/eLife.24655
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: High-Throughput Screening Approach for Identifying Compounds That Inhibit Nonhomologous End Joining.

    Bredemeyer, Andrea L / Edwards, Bruce S / Haynes, Mark K / Morales, Abigail J / Wang, Yinan / Ursu, Oleg / Waller, Anna / Sklar, Larry A / Sleckman, Barry P

    SLAS discovery : advancing life sciences R & D

    2017  Volume 23, Issue 7, Page(s) 624–633

    Abstract: DNA double-strand breaks (DSBs) are repaired primarily by homologous recombination (HR) or nonhomologous end joining (NHEJ). Compounds that modulate HR have shown promise as cancer therapeutics. The V(D)J recombination reaction, which assembles antigen ... ...

    Abstract DNA double-strand breaks (DSBs) are repaired primarily by homologous recombination (HR) or nonhomologous end joining (NHEJ). Compounds that modulate HR have shown promise as cancer therapeutics. The V(D)J recombination reaction, which assembles antigen receptor genes in lymphocytes, is initiated by the introduction of DNA DSBs at two recombining gene segments by the RAG endonuclease, followed by the NHEJ-mediated repair of these DSBs. Here, using HyperCyt automated flow cytometry, we develop a robust high-throughput screening (HTS) assay for NHEJ that utilizes engineered pre-B-cell lines where the V(D)J recombination reaction can be induced and monitored at a single-cell level. This approach, novel in processing four 384-well plates at a time in parallel, was used to screen the National Cancer Institute NeXT library to identify compounds that inhibit V(D)J recombination and NHEJ. Assessment of cell light scattering characteristics at the primary HTS stage (83,536 compounds) enabled elimination of 60% of apparent hits as false positives. Although all the active compounds that we identified had an inhibitory effect on RAG cleavage, we have established this as an approach that could identify compounds that inhibit RAG cleavage or NHEJ using new chemical libraries.
    MeSH term(s) DNA Breaks, Double-Stranded/drug effects ; DNA End-Joining Repair/drug effects ; Dose-Response Relationship, Drug ; Drug Discovery/methods ; Flow Cytometry ; High-Throughput Screening Assays ; Homologous Recombination ; Humans ; Molecular Structure ; Precursor Cells, B-Lymphoid/immunology ; Precursor Cells, B-Lymphoid/metabolism ; V(D)J Recombination
    Language English
    Publishing date 2017-12-12
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2885123-7
    ISSN 2472-5560 ; 2472-5552
    ISSN (online) 2472-5560
    ISSN 2472-5552
    DOI 10.1177/2472555217746324
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4911: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  6. Article ; Online: Deficiency of XLF and PAXX prevents DNA double-strand break repair by non-homologous end joining in lymphocytes.

    Hung, Putzer J / Chen, Bo-Ruei / George, Rosmy / Liberman, Caleb / Morales, Abigail J / Colon-Ortiz, Pedro / Tyler, Jessica K / Sleckman, Barry P / Bredemeyer, Andrea L

    Cell cycle (Georgetown, Tex.)

    2016  Volume 16, Issue 3, Page(s) 286–295

    Abstract: Non-homologous end joining (NHEJ) is a major DNA double-strand break (DSB) repair pathway that functions in all phases of the cell cycle. NHEJ repairs genotoxic and physiological DSBs, such as those generated by ionizing radiation and during V(D)J ... ...

    Abstract Non-homologous end joining (NHEJ) is a major DNA double-strand break (DSB) repair pathway that functions in all phases of the cell cycle. NHEJ repairs genotoxic and physiological DSBs, such as those generated by ionizing radiation and during V(D)J recombination at antigen receptor loci, respectively. DNA end joining by NHEJ relies on the core factors Ku70, Ku80, XRCC4, and DNA Ligase IV. Additional proteins also play important roles in NHEJ. The XRCC4-like factor (XLF) participates in NHEJ through its interaction with XRCC4, and XLF deficiency in humans leads to immunodeficiency and increased sensitivity to ionizing radiation. However, XLF is dispensable for NHEJ-mediated DSB repair during V(D)J recombination in murine lymphocytes, where it may have redundant functions with other DSB repair factors. Paralog of XRCC4 and XLF (PAXX) is a recently identified NHEJ factor that has structural similarity to XRCC4 and XLF. Here we show that PAXX is also dispensable for NHEJ during V(D)J recombination and during the repair of genotoxic DSBs in lymphocytes. However, a combined deficiency of PAXX and XLF blocks NHEJ with a severity comparable to that observed in DNA Ligase IV-deficient cells. Similar to XLF, PAXX interacts with Ku through its C-terminal region, and mutations that disrupt Ku binding prevent PAXX from promoting NHEJ in XLF-deficient lymphocytes. Our findings suggest that the PAXX and XLF proteins may have redundant functions during NHEJ.
    MeSH term(s) Animals ; B-Lymphocytes/metabolism ; DNA Breaks, Double-Stranded ; DNA End-Joining Repair ; DNA Repair ; DNA-Binding Proteins/chemistry ; DNA-Binding Proteins/deficiency ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Mice ; Mutant Proteins/metabolism ; Protein Domains ; V(D)J Recombination
    Chemical Substances DNA-Binding Proteins ; Mutant Proteins ; XLF protein, mouse
    Language English
    Publishing date 2016-11-10
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2146183-1
    ISSN 1551-4005 ; 1538-4101 ; 1554-8627
    ISSN (online) 1551-4005
    ISSN 1538-4101 ; 1554-8627
    DOI 10.1080/15384101.2016.1253640
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text 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)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

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