Methylation of histone H4 lysine 20 controls recruitment of Crb2 to sites of DNA damage.

By Steven L. Sanders, Manuela Portoso, J. Mata, J. Bähler, Robin C. Allshire, Tony Kouzarides. Cell, 2004

594 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/6d4881c6d531e36b78098764a183b35673bb852b

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Citations in the corpus

RNF8 transduces the DNA-damage signal via histone ubiquitylation and checkpoint protein assembly. (2007, background): “Given the role of histone ubiquitylation in chromatin remodeling, it is also plausible that the RNF8-dependent ubiquitylation events at the vicinity of DNA breaks may enhance the accessibility of 53BP1 to modified histones (Huyen et al., 2004; Sanders et al., 2004; Botuyan et al., 2006).”
Shelterin: the protein complex that shapes and safeguards human telomeres. (2005, unknown): “Recent work on ATM, 53BP1, and fission yeast Crb2 has suggested that a key event in the DNA damage response is a change in the nucleosomal organization at the site of DNA damage (Bakkenist and Kastan 2003; Huyen et al. 2004; Sanders et al. 2004).”
Reversal of histone lysine trimethylation by the JMJD2 family of histone demethylases. (2006, background): “Methylation at these sites has been linked to both transcriptional activation and repression, as well as DNAdamage response (Sanders et al., 2004; Zhang and Reinberg, 2001), demonstrating a widespread role for histone methylation in various aspects of chromatin biology (Martin and Zhang, 2005).”
Dynamics of DNA damage response proteins at DNA breaks: a focus on protein modifications. (2011, background): “Specifically, fission yeast Crb2 binds H4K20me2 (Sanders et al. 2004; Greeson et al. 2008) and budding yeast Rad9 binds H3K79me3 (Grenon et al. 2007), while human 53BP1 was initially reported to bind H3K79me3 and subsequently H4K20me1/2 (mono or dimethylated), which might be more physiologically rel”
How chromatin-binding modules interpret histone modifications: lessons from professional pocket pickers (2007, background): “Immunofluorescence imaging of cellular distribution showed that mammalian p53-binding protein (53BP1) and its fission yeast homolog Crb2p relocalize to double-strand breaks (DSBs) upon exposure to DNA-damaging agent”
53BP1 is a reader of the DNA damage-induced H2A Lys15 ubiquitin mark (2013, unknown): “The current models of 53BP1 recruitment to DSB sites pro-pose that H4K20 methylation is either induced or becomes available for 53BP1 binding after DNA damage 16–19 .”
The SET-domain protein superfamily: protein lysine methyltransferases (2005, background): “Kouskouti A, Scheer E, Staub A, Tora L, Talianidis I: Gene-specific modulation of TAF10 function by SET9-mediated methylation.”
Chromatin challenges during DNA replication and repair. (2007, unknown): “…addition, reduction of chromatin plasticity may be essential to inactivate the DNA-damage response by inhibiting further recruitment of checkpoint mediators that directly bind to constitutive histone marks, such as H3K79me3 and H4K20me3 (Huyen et al., 2004; Murr et al., 2006; Sanders et al., 2004).”
Surviving the breakup: the DNA damage checkpoint. (2006, background): “cerevisiae is stimulated by DNA damage but exists at a basal level in normal chromatin (123, 148, 158).”
The X-linked mental retardation gene SMCX/JARID1C defines a family of histone H3 lysine 4 demethylases. (2007, unknown): “Histone methylation has been linked to transcriptional activation and repression, as well as DNA-damage response (Sanders et al., 2004; Zhang and Reinberg, 2001).”
The diverse functions of histone lysine methylation (2005, background): “Surprisingly, deletion of SET9 — the enzyme responsible for H4-K20 methylation in this organism — does not result in defective heterochromatin formation as assayed by centromeric silencing 22 .”
Understanding the language of Lys36 methylation at histone H3 (2012, unknown): “Histone methylation is also critical for the maintenance of genomic stability, including the biological response to DSB”