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  1. Article ; Online: Hyperphosphorylated tau self-assembles into amorphous aggregates eliciting TLR4-dependent responses

    Jonathan X. Meng / Yu Zhang / Dominik Saman / Arshad M. Haider / Suman De / Jason C. Sang / Karen Brown / Kun Jiang / Jane Humphrey / Linda Julian / Eric Hidari / Steven F. Lee / Gabriel Balmus / R. Andres Floto / Clare E. Bryant / Justin L. P. Benesch / Yu Ye / David Klenerman

    Nature Communications, Vol 13, Iss 1, Pp 1-

    2022  Volume 16

    Abstract: In this work, the authors report that hyperphosphorylated recombinant tau spontaneously assembles into small, amorphous aggregates, which disrupt membranes and induce Toll-like receptor 4-dependent responses in human macrophages. ...

    Abstract In this work, the authors report that hyperphosphorylated recombinant tau spontaneously assembles into small, amorphous aggregates, which disrupt membranes and induce Toll-like receptor 4-dependent responses in human macrophages.
    Keywords Science ; Q
    Language English
    Publishing date 2022-05-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: CLONAL EVOLUTION OF A MOUSE METASTATIC HEMANGIOSARCOMA

    Marius Carlan / Andreea Flavia Carlan / Gabriel Balmus

    Analele Ştiinţifice Ale Universităţii Alexandru Ioan Cuza din Iași,Sectiunea II A : Genetica si Biologie Moleculara , Vol 5, Iss

    2004  Volume 1

    Keywords Genetics ; QH426-470 ; Biology (General) ; QH301-705.5 ; Science ; Q
    Language English
    Publishing date 2004-08-01T00:00:00Z
    Publisher Alexandru Ioan Cuza University of Iasi
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: A Genome-Wide Association Study for Regulators of Micronucleus Formation in Mice

    Rebecca E. McIntyre / Jérôme Nicod / Carla Daniela Robles-Espinoza / John Maciejowski / Na Cai / Jennifer Hill / Ruth Verstraten / Vivek Iyer / Alistair G. Rust / Gabriel Balmus / Richard Mott / Jonathan Flint / David J. Adams

    G3: Genes, Genomes, Genetics, Vol 6, Iss 8, Pp 2343-

    2016  Volume 2354

    Abstract: In mammals the regulation of genomic instability plays a key role in tumor suppression and also controls genome plasticity, which is important for recombination during the processes of immunity and meiosis. Most studies to identify regulators of genomic ... ...

    Abstract In mammals the regulation of genomic instability plays a key role in tumor suppression and also controls genome plasticity, which is important for recombination during the processes of immunity and meiosis. Most studies to identify regulators of genomic instability have been performed in cells in culture or in systems that report on gross rearrangements of the genome, yet subtle differences in the level of genomic instability can contribute to whole organism phenotypes such as tumor predisposition. Here we performed a genome-wide association study in a population of 1379 outbred Crl:CFW(SW)-US_P08 mice to dissect the genetic landscape of micronucleus formation, a biomarker of chromosomal breaks, whole chromosome loss, and extranuclear DNA. Variation in micronucleus levels is a complex trait with a genome-wide heritability of 53.1%. We identify seven loci influencing micronucleus formation (false discovery rate <5%), and define candidate genes at each locus. Intriguingly at several loci we find evidence for sexual dimorphism in micronucleus formation, with a locus on chromosome 11 being specific to males.
    Keywords Micronuclei ; genomic instability ; genome-wide association study (GWAS) ; Outbred mice ; genetic mapping ; Genetics ; QH426-470 ; Biology (General) ; QH301-705.5 ; Science ; Q
    Subject code 572
    Language English
    Publishing date 2016-08-01T00:00:00Z
    Publisher Genetics Society of America
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Specific Roles of XRCC4 Paralogs PAXX and XLF during V(D)J Recombination

    Chloé Lescale / Hélène Lenden Hasse / Andrew N. Blackford / Gabriel Balmus / Joy J. Bianchi / Wei Yu / Léa Bacoccina / Angélique Jarade / Christophe Clouin / Rohan Sivapalan / Bernardo Reina-San-Martin / Stephen P. Jackson / Ludovic Deriano

    Cell Reports, Vol 16, Iss 11, Pp 2967-

    2016  Volume 2979

    Abstract: Paralog of XRCC4 and XLF (PAXX) is a member of the XRCC4 superfamily and plays a role in nonhomologous end-joining (NHEJ), a DNA repair pathway critical for lymphocyte antigen receptor gene assembly. Here, we find that the functions of PAXX and XLF in V( ... ...

    Abstract Paralog of XRCC4 and XLF (PAXX) is a member of the XRCC4 superfamily and plays a role in nonhomologous end-joining (NHEJ), a DNA repair pathway critical for lymphocyte antigen receptor gene assembly. Here, we find that the functions of PAXX and XLF in V(D)J recombination are masked by redundant joining activities. Thus, combined PAXX and XLF deficiency leads to an inability to join RAG-cleaved DNA ends. Additionally, we demonstrate that PAXX function in V(D)J recombination depends on its interaction with Ku. Importantly, we show that, unlike XLF, the role of PAXX during the repair of DNA breaks does not overlap with ATM and the RAG complex. Our findings illuminate the role of PAXX in V(D)J recombination and support a model in which PAXX and XLF function during NHEJ repair of DNA breaks, whereas XLF, the RAG complex, and the ATM-dependent DNA damage response promote end joining by stabilizing DNA ends.
    Keywords V(D)J recombination ; DNA repair ; NHEJ ; PAXX ; XLF ; XRCC4 ; Biology (General) ; QH301-705.5
    Subject code 612
    Language English
    Publishing date 2016-09-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: ATM orchestrates the DNA-damage response to counter toxic non-homologous end-joining at broken replication forks

    Gabriel Balmus / Domenic Pilger / Julia Coates / Mukerrem Demir / Matylda Sczaniecka-Clift / Ana C. Barros / Michael Woods / Beiyuan Fu / Fengtang Yang / Elisabeth Chen / Matthias Ostermaier / Tatjana Stankovic / Hannes Ponstingl / Mareike Herzog / Kosuke Yusa / Francisco Munoz Martinez / Stephen T. Durant / Yaron Galanty / Petra Beli /
    David J. Adams / Allan Bradley / Emmanouil Metzakopian / Josep V. Forment / Stephen P. Jackson

    Nature Communications, Vol 10, Iss 1, Pp 1-

    2019  Volume 18

    Abstract: Mutations in the ATM tumor suppressor gene confer hypersensitivity to DNA-damaging chemotherapeutic agents. Here, the authors provide evidence that these hypersensitivities reflect a crucial role for ATM at damaged replication forks being to prevent ... ...

    Abstract Mutations in the ATM tumor suppressor gene confer hypersensitivity to DNA-damaging chemotherapeutic agents. Here, the authors provide evidence that these hypersensitivities reflect a crucial role for ATM at damaged replication forks being to prevent toxic DNA end-joining leading to chromosome fusions and cell death.
    Keywords Science ; Q
    Language English
    Publishing date 2019-01-01T00:00:00Z
    Publisher Nature Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article ; Online: ATM orchestrates the DNA-damage response to counter toxic non-homologous end-joining at broken replication forks

    Gabriel Balmus / Domenic Pilger / Julia Coates / Mukerrem Demir / Matylda Sczaniecka-Clift / Ana C. Barros / Michael Woods / Beiyuan Fu / Fengtang Yang / Elisabeth Chen / Matthias Ostermaier / Tatjana Stankovic / Hannes Ponstingl / Mareike Herzog / Kosuke Yusa / Francisco Munoz Martinez / Stephen T. Durant / Yaron Galanty / Petra Beli /
    David J. Adams / Allan Bradley / Emmanouil Metzakopian / Josep V. Forment / Stephen P. Jackson

    Nature Communications, Vol 10, Iss 1, Pp 1-

    2019  Volume 18

    Abstract: Mutations in the ATM tumor suppressor gene confer hypersensitivity to DNA-damaging chemotherapeutic agents. Here, the authors provide evidence that these hypersensitivities reflect a crucial role for ATM at damaged replication forks being to prevent ... ...

    Abstract Mutations in the ATM tumor suppressor gene confer hypersensitivity to DNA-damaging chemotherapeutic agents. Here, the authors provide evidence that these hypersensitivities reflect a crucial role for ATM at damaged replication forks being to prevent toxic DNA end-joining leading to chromosome fusions and cell death.
    Keywords Science ; Q
    Language English
    Publishing date 2019-01-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article ; Online: Targeting of NAT10 enhances healthspan in a mouse model of human accelerated aging syndrome

    Gabriel Balmus / Delphine Larrieu / Ana C. Barros / Casey Collins / Monica Abrudan / Mukerrem Demir / Nicola J. Geisler / Christopher J. Lelliott / Jacqueline K. White / Natasha A. Karp / James Atkinson / Andrea Kirton / Matt Jacobsen / Dean Clift / Raphael Rodriguez / Sanger Mouse Genetics Project / David J. Adams / Stephen P. Jackson

    Nature Communications, Vol 9, Iss 1, Pp 1-

    2018  Volume 14

    Abstract: Hutchinson-Gilford Progeria Syndrome is characterized by premature aging with cardiovascular disease being the main cause of death. Here the authors show that inhibition of the NAT10 enzyme enhances cardiac function and fitness, and reduces age-related ... ...

    Abstract Hutchinson-Gilford Progeria Syndrome is characterized by premature aging with cardiovascular disease being the main cause of death. Here the authors show that inhibition of the NAT10 enzyme enhances cardiac function and fitness, and reduces age-related phenotypes in a mouse model of premature aging.
    Keywords Science ; Q
    Language English
    Publishing date 2018-04-01T00:00:00Z
    Publisher Nature Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  8. Article ; Online: Targeting of NAT10 enhances healthspan in a mouse model of human accelerated aging syndrome

    Gabriel Balmus / Delphine Larrieu / Ana C. Barros / Casey Collins / Monica Abrudan / Mukerrem Demir / Nicola J. Geisler / Christopher J. Lelliott / Jacqueline K. White / Natasha A. Karp / James Atkinson / Andrea Kirton / Matt Jacobsen / Dean Clift / Raphael Rodriguez / Sanger Mouse Genetics Project / David J. Adams / Stephen P. Jackson

    Nature Communications, Vol 9, Iss 1, Pp 1-

    2018  Volume 14

    Abstract: Hutchinson-Gilford Progeria Syndrome is characterized by premature aging with cardiovascular disease being the main cause of death. Here the authors show that inhibition of the NAT10 enzyme enhances cardiac function and fitness, and reduces age-related ... ...

    Abstract Hutchinson-Gilford Progeria Syndrome is characterized by premature aging with cardiovascular disease being the main cause of death. Here the authors show that inhibition of the NAT10 enzyme enhances cardiac function and fitness, and reduces age-related phenotypes in a mouse model of premature aging.
    Keywords Science ; Q
    Language English
    Publishing date 2018-04-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

    Full text online

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