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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)

  1. 1.
    0356108 - ÚMG 2011 RIV US eng J - Článek v odborném periodiku
    Košař, Martin - Bartkova, J. - Hubáčková, Soňa - Hodný, Zdeněk - Lukas, J. - Bártek, Jiří
    Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type- and insult-dependent manner, and follow expression of p16 (ink4a).
    Cell Cycle. Roč. 10, č. 3 (2011), s. 457-468. ISSN 1538-4101. E-ISSN 1551-4005
    Grant CEP: GA ČR GA204/08/1418; GA ČR GA301/08/0353
    Výzkumný záměr: CEZ:AV0Z50520514
    Klíčová slova: genotoxic and replicative stress * senescence-associated heterochromatin foci * DNA damage response
    Kód oboru RIV: EB - Genetika a molekulární biologie
    Impakt faktor: 5.359, rok: 2011

    Primary 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.
    Trvalý link: http://hdl.handle.net/11104/0194721

     
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