Formation of MacroH2A-containing senescence-associated heterochromatin foci and senescence driven by ASF1a and HIRA.

By Rugang Zhang, Maxim V Poustovoitov, Xiao-feng Ye, H. Santos, Wei Chen, S. Daganzo, J. Erzberger, I. Serebriiskii, Adrian A. Canutescu, Roland L. Dunbrack and 4 more. Developmental Cell, 2005

712 citations recorded by the source corpus.

Subfields: Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/ea31a7febaf021c0fe4f77f45e93507ae628e8a9

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Citations in the corpus

Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors. (2005, background): “…mechanisms are as yet unknown, the senescence response appears to result in a reorganization of chromatin, at least some aspects of which require pRB activity (Jacobs et al., 1999; Leung et al., 2001; Bandyopadhyay et al., 2002; Itahana et al., 2003; Narita et al., 2003; Zhang et al., 2003, 2005).”
A Versatile Viral System for Expression and Depletion of Proteins in Mammalian Cells (2009, methodology): “The insertion of an shRNA cassette in the 39 LTR of the pQCXIP plasmid was previously used successfully [48].”
Structure, dynamics and functions of promyelocytic leukaemia nuclear bodies (2007, background): “and also that they participate in establishing condensed chromatin in senescing cell”
Cellular senescence: when bad things happen to good cells (2007, background): “Is oncogene-induced senescence distinct from chromatin or telomere/damage-induced senescence? Perhaps not; for example, oncogenic RAS induces p16 and the formation of SAHF”
Epigenetics and aging (2016, background): “For a long time, SAHFhave been perceived as another difference between the aging process and replicative senescence (43).”
Senescence-messaging secretome: SMS-ing cellular stress (2009, background): “57 ) and requires the chromatin regulators ASF1A and HIRA”
Cellular senescence and its effector programs (2014, background): “For example, upon the induction of senescence in HDFs, senescenceassociated heterochromatic foci (SAHFs) become readily visible as distinct DAPI-dense foci, the formation of which is typically dependent on the Rb pathway (Narita et al. 2003).”
Outcome of a Workshop on Applications of Protein Models in Biomedical Research (2009, background): “As an example, collaboration between experimental biologists and molecular modelers at the Fox Chase Cancer Center was aimed at understanding different phenotypes of overexpression of the chromatin remodeling protein ASF1a in humans (Tang et al., 2006; Zhang et al., 2005).”
Cellular senescence and tumor suppressor gene p16 (2011, background): “Oncogene-mediated premature senescence is a tumor suppressor mechanism that has been well described in the RAS activated MAP kinase pathway.(19,91,92) The Ets family of tran-”
The essence of senescence. (2010, background): “RNAi depletion of either ASF1A or HMGA1 (a SAHF component) leads to a partial bypass of senescence (Zhang et al. 2005; Narita et al. 2006).”
Accumulation of senescent cells in mitotic tissue of aging primates. (2007, background): “SAHF formation is driven by the chromatin regulators HIRA and ASF1a (Zhang et al., 2005) which promote the accumulation of heterochromatin proteins such as lysine 9 methylated histone H3 (Me-K9H3), the histone H2A variant macroH2A (Zhang et al., 2005), and HP1α, β and γ (Narita et al., 2003).”