Histone acetylation by Trrap–Tip60 modulates loading of repair proteins and repair of DNA double-strand breaks

By Rabih Murr, J. Loizou, Yun-Gui Yang, C. Cuenin, Hai Li, Zhao-Qi Wang, Zdenko Herceg. Nature Cell Biology, 2006

631 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/7b0e5efe70a207d634aa70e125f3d2b2d6437f8f

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In Molecular Biology

1. Stephen P. Jackson
2. J. Bartek
3. S. Polo
4. J. Lukas
5. C. Lukas
6. D. Durocher
7. Michael B. Yaffe
8. Jeremy M. Stark

In Oncology

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2. J. Bartek
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4. S. Polo
5. C. Lukas
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7. Yosef Shiloh
8. P. Jeggo

Citations in the corpus

• RNF8 ubiquitylates histones at DNA double-strand breaks and promotes assembly of repair proteins. (2007, neutral): “One possibility is that RNF8, and the DSB-associated histone ubiquitylations, may also have an indirect impact on maturation of the DSB-flanking chromatin (Figure 7). In support for this indirect scenario, we noticed that genetic ablation of the TRRAP-TIP60 histone acetyltransferase (HAT) generated ”
• Human HDAC1 and HDAC2 function in the DNA-damage response to promote DNA non-homologous end-joining (2010, neutral): “Histone acetylations, together with the enzymes that mediate their addition and removal, have also been implicated in the DDR, although their modes of action are less well defined than those of histone phosphorylations and ubiquitylation”
• RNF8 transduces the DNA-damage signal via histone ubiquitylation and checkpoint protein assembly. (2007, background): “Together, our study implicates RNF8 as a novel DNA-damage-responsive protein that integrates protein phosphorylation and ubiquitylation signaling and plays a critical role in the cellular response to genotoxic stress.”
• Dynamics of DNA damage response proteins at DNA breaks: a focus on protein modifications. (2011, background): “Similarly, the recruitment of the Tip60 acetyltransferase and the deacetylase enzymes HDAC1, HDAC2, HDAC4, SIRT1, and SIRT6 has been observed at DSB sites in mammalian cells (Kao et al. 2003; Murr et al. 2006; O’Hagan et al. 2008; Oberdoerffer et al. 2008; Kaidi et al. 2010; Miller et al. 2010), and”
• RNF168 binds and amplifies ubiquitin conjugates on damaged chromosomes to allow accumulation of repair proteins. (2009, positive): “It has been shown that the TRRAP/TIP60 histone acetyltransferase facilitates 53BP1 and BRCA1 retention at the DSB sites (Murr et al., 2006), and one report suggested that TIP60 is functionally linked with histone ubiquitylations (Ikura et al.”
• Alternative-NHEJ Is a Mechanistically Distinct Pathway of Mammalian Chromosome Break Repair (2008, background): “by promoting open chromatin structures [36], and/or by”
• Chromatin challenges during DNA replication and repair. (2007, neutral): “The mammalian Tip60 complex is likewise recruited to DSBs where it acetylates H4 and H2A (Murr et al., 2006), but it remains to be tested whether it also catalyzes g -H2AX-H2B eviction.”