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  • 1
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    H2AX prevents CtIP-mediated DNA end resection and aberrant repair in G1-phase lymphocytes (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-12-17
    Description: DNA double-strand breaks (DSBs) are generated by the recombination activating gene (RAG) endonuclease in all developing lymphocytes as they assemble antigen receptor genes. DNA cleavage by RAG occurs only at the G1 phase of the cell cycle and generates two hairpin-sealed DNA (coding) ends that require nucleolytic opening before their repair by classical non-homologous end-joining (NHEJ). Although there are several cellular nucleases that could perform this function, only the Artemis nuclease is able to do so efficiently. Here, in vivo, we show that in murine cells the histone protein H2AX prevents nucleases other than Artemis from processing hairpin-sealed coding ends; in the absence of H2AX, CtIP can efficiently promote the hairpin opening and resection of DNA ends generated by RAG cleavage. This CtIP-mediated resection is inhibited by gamma-H2AX and by MDC-1 (mediator of DNA damage checkpoint 1), which binds to gamma-H2AX in chromatin flanking DNA DSBs. Moreover, the ataxia telangiectasia mutated (ATM) kinase activates antagonistic pathways that modulate this resection. CtIP DNA end resection activity is normally limited to cells at post-replicative stages of the cell cycle, in which it is essential for homology-mediated repair. In G1-phase lymphocytes, DNA ends that are processed by CtIP are not efficiently joined by classical NHEJ and the joints that do form frequently use micro-homologies and show significant chromosomal deletions. Thus, H2AX preserves the structural integrity of broken DNA ends in G1-phase lymphocytes, thereby preventing these DNA ends from accessing repair pathways that promote genomic instability.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3150591/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3150591/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Helmink, Beth A -- Tubbs, Anthony T -- Dorsett, Yair -- Bednarski, Jeffrey J -- Walker, Laura M -- Feng, Zhihui -- Sharma, Girdhar G -- McKinnon, Peter J -- Zhang, Junran -- Bassing, Craig H -- Sleckman, Barry P -- A125195/PHS HHS/ -- AI074953/AI/NIAID NIH HHS/ -- AI47829/AI/NIAID NIH HHS/ -- CA136470/CA/NCI NIH HHS/ -- CA21765/CA/NCI NIH HHS/ -- NS37956/NS/NINDS NIH HHS/ -- P01 CA096832/CA/NCI NIH HHS/ -- P01 CA096832-08/CA/NCI NIH HHS/ -- R01 AI047829/AI/NIAID NIH HHS/ -- R01 AI047829-13/AI/NIAID NIH HHS/ -- R01 AI074953/AI/NIAID NIH HHS/ -- R01 AI074953-04/AI/NIAID NIH HHS/ -- R01 CA136470/CA/NCI NIH HHS/ -- R01 CA136470-04/CA/NCI NIH HHS/ -- R01 NS037956/NS/NINDS NIH HHS/ -- R01 NS037956-12/NS/NINDS NIH HHS/ -- R21 ES019779/ES/NIEHS NIH HHS/ -- R21 ES019779-02/ES/NIEHS NIH HHS/ -- T32 D007499/PHS HHS/ -- England -- Nature. 2011 Jan 13;469(7329):245-9. doi: 10.1038/nature09585. Epub 2010 Dec 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Immunology, Washington University School of Medicine, St Louis, Missouri 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21160476" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ataxia Telangiectasia Mutated Proteins ; Carrier Proteins/*metabolism ; Cell Cycle Proteins/*metabolism ; Cell Line, Transformed ; Chromatin/metabolism ; *DNA Breaks, Double-Stranded ; *DNA Repair ; DNA-Binding Proteins/metabolism ; Endonucleases ; *G1 Phase ; *Gene Rearrangement, B-Lymphocyte/genetics ; Genomic Instability ; Histones/deficiency/genetics/*metabolism ; Intracellular Signaling Peptides and Proteins/metabolism ; Lymphocytes/cytology/*metabolism ; Mice ; Nuclear Proteins ; Precursor Cells, B-Lymphoid/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Recombination, Genetic/genetics ; Substrate Specificity ; Tumor Suppressor Proteins/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    The Preservation Potential of Coastal Coseismic and Tsunami Evidence Observed Following the 2012 Mw 7.8 Haida Gwaii Thrust Earthquake (2015)
    Seismological Society of America (SSA)
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    Publication Date: 2015-05-01
    Description: We describe near-field coseismic and tsunami evidence collected following the 28 October 2012 M w  7.8 thrust earthquake that occurred offshore western Haida Gwaii, British Columbia, and discuss factors that influence its extent and preservation potential. Observations indicate minor geomorphic and sedimentological impacts on the rugged and unpopulated west coast of the islands, despite widespread coastal coseismic subsidence (~0.5 m), triggered landslides, and tsunami waves exceeding 3 m in runup (maximum 13 m) along ~230 km of coastline. Evidence left by the tsunami was minimal, likely because it occurred during a low tide that restricted its onshore reach, its flow depth, and its capacity to entrain and transport significant amounts of clastic sediment, sources of which are minimal or absent on the dominantly steep, rocky coastline. It is unlikely that subaerial evidence of coseismic subsidence and tsunami inundation will be recognizably recorded in the coastal stratigraphy of western Haida Gwaii, due to the relatively small magnitude of subsidence, a lack of suitable coastal environments such as tidal marshes to record paleoelevation differences, sedimentation rates that are too low to bury a paleoseismic or paleotsunami record, and long-term relative sea level fall leading to erosion and bioturbation. A higher preservation potential is likely for tsunami deposits in coastal lakes, ponds, and bogs, as well as coseismic slope failure deposits offshore, in lakes and in sheltered fjords. Our findings imply that large tsunamigenic earthquakes are likely undersampled in the paleoseismic record of Haida Gwaii and of other plate margins with similar characteristics.
    Print ISSN: 0037-1106
    Electronic ISSN: 1943-3573
    Topics: Geosciences , Physics
    Published by Seismological Society of America (SSA)
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  • 3
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    Ataxia telangiectasia mutated (Atm) and DNA-PKcs kinases have overlapping activities during chromosomal signal joint formation [Immunology] (2011)
    National Academy of Sciences
    Details
    Publication Date: 2011-02-02
    Description: Lymphocyte antigen receptor gene assembly occurs through the process of V(D)J recombination, which is initiated when the RAG endonuclease introduces DNA DSBs at two recombining gene segments to form broken DNA coding end pairs and signal end pairs. These paired DNA ends are joined by proteins of the nonhomologous end-joining (NHEJ) pathway of DSB repair to form a coding joint and signal joint, respectively. RAG DSBs are generated in G1-phase developing lymphocytes, where they activate the ataxia telangiectasia mutated (Atm) and DNA-PKcs kinases to orchestrate diverse cellular DNA damage responses including DSB repair. Paradoxically, although Atm and DNA-PKcs both function during coding joint formation, Atm appears to be dispensible for signal joint formation; and although some studies have revealed an activity for DNA-PKcs during signal joint formation, others have not. Here we show that Atm and DNA-PKcs have overlapping catalytic activities that are required for chromosomal signal joint formation and for preventing the aberrant resolution of signal ends as potentially oncogenic chromosomal translocations.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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