A role for cell-cycle-regulated histone H3 lysine 56 acetylation in the DNA damage response
By H. Masumoto, D. Hawke, Ryuji Kobayashi, Alain Verreault. Nature, 2005
612 citations recorded by the source corpus.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/c9f694d8c64aea42a70cd1846fbe6134ae5b2416
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Citations in the corpus
- Acetyl-CoA Induces Cell Growth and Proliferation by Promoting the Acetylation of Histones at Growth Genes (2011, background): “These data confirm that H3K56 acetylation occurs during S phase and as a function of the cell cycle (Masumoto et al., 2005; Xu et al., 2005).”
- Histone Tails and the H3 αN Helix Regulate Nucleosome Mobility and Stability (2007, background): “Widespread acetylation of H3 at K56 has been found to occur during S phase in budding yeast (35, 43, 49, 60).”
- Chromatin replication and epigenome maintenance (2012, background): “In budding yeast, H3K56ac is present on most new histones incorporated into chromati”
- Epigenetic inheritance during the cell cycle (2009, background): “In budding yeast, new H3 is acetylated at residue K56 (H3K56ac), which regulates the nucleosome assembly that is dependent on CAF1 and the yeast-specific histone chaperone Rtt106 (Ref”
- Chromatin challenges during DNA replication and repair. (2007, neutral): “In addition to N-terminal tail acetylation, newly synthesized histones are acetylated at lysine 56 of H3 and lysine 91 within the globular domain of H4 prior to their incorporation into chromatin (Masumoto et al., 2005; Ye et al., 2005; Zhou et al., 2006).”
- Surviving the breakup: the DNA damage checkpoint. (2006, background): “Acetylation of histone H3 lysine 56 (H3-K56Ac) may also promote DNA accessibility in chromatin, though in this case the relevant targets appear to be repair rather than checkpoint proteins (91).”
- Covalent modifications of histones during development and disease pathogenesis (2007, background): “For example, acetylation of Lys56 on histone H3 is dispensable for transcription but required for genome stabilit”