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Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type- and insult-dependent manner, and follow expression of p16 (ink4a)

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    SYSNO ASEP0356108
    Document TypeJ - Journal Article
    R&D Document TypeJournal Article
    Subsidiary JČlánek ve WOS
    TitleSenescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type- and insult-dependent manner, and follow expression of p16 (ink4a)
    Author(s) Košař, Martin (UMG-J)
    Bartkova, J. (DK)
    Hubáčková, Soňa (UMG-J) RID
    Hodný, Zdeněk (UMG-J) RID
    Lukas, J. (DK)
    Bártek, Jiří (UMG-J) RID
    Source TitleCell Cycle. - : Taylor & Francis - ISSN 1538-4101
    Roč. 10, č. 3 (2011), s. 457-468
    Number of pages12 s.
    Languageeng - English
    CountryUS - United States
    Keywordsgenotoxic and replicative stress ; senescence-associated heterochromatin foci ; DNA damage response
    Subject RIVEB - Genetics ; Molecular Biology
    R&D ProjectsGA204/08/1418 GA ČR - Czech Science Foundation (CSF)
    GA301/08/0353 GA ČR - Czech Science Foundation (CSF)
    CEZAV0Z50520514 - UMG-J (2005-2011)
    UT WOS000286827100023
    DOI10.4161/cc.10.3.14707
    AnnotationPrimary human fibroblasts undergoing oncogene-induced or replicative senescence are known to form senescence-associated heterochromatin foci (SAHF), nuclear DNA domains stained densely by DAPI and enriched for histone modifications including lysine9-trimethylated histone H3. While cellular senescence occurs also in premalignant human lesions, it is unclear how universal SAHF formation is among various cell types, under diverse stresses and whether SAHF occur in vivo. Here, we report that human primary fibroblasts and primary keratinocytes undergoing replicative senescence or premature senescence induced by oncogenic H-Ras, diverse chemotherapeutics and bacterial cytolethal distending toxin, show differential capacity to form SAHF indicating that unlike the widely present DNA damage response marker γH2AX, SAHF is not a common feature of cellular senescence.
    WorkplaceInstitute of Molecular Genetics
    ContactNikol Škňouřilová, nikol.sknourilova@img.cas.cz, Tel.: 241 063 217
    Year of Publishing2011
Number of the records: 1  

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