RNF8 ubiquitylates histones at DNA double-strand breaks and promotes assembly of repair proteins.

By Niels Mailand, Simon Bekker-Jensen, Helene Faustrup, Fredrik Melander, J. Bartek, C. Lukas, J. Lukas. Cell, 2007

1,237 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/f00b76a3c3c7279de64c83806dae784771a953a9

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. Stephen P. Jackson
2. J. Bartek
3. S. Polo
4. J. Lukas
5. M. Jasin
6. L. Zou
7. Alexandre Maréchal
8. C. Lukas

In Oncology

1. Stephen P. Jackson
2. S. Polo
3. J. Bartek
4. J. Lukas
5. L. Zou
6. Alexandre Maréchal
7. C. Lukas
8. Michael B. Yaffe

Citations in the corpus

• The RIDDLE syndrome protein mediates a ubiquitin-dependent signaling cascade at sites of DNA damage. (2009, neutral): “recruitment of the RAP80-ABRA1-BRCA1 complex and the accumulation of 53BP1 at sites of DNA damage (Huen et al., 2007; Kolas et al., 2007; Mailand et al., 2007; Sakasai and Tibbetts, 2008; Wang and Elledge, 2007).”
• RNF168 ubiquitinates K13-15 on H2A/H2AX to drive DNA damage signaling. (2012, background): “Previous studies have shown that both RNF8 and RNF168 are active toward isolated purified histone proteins (Doil et al., 2009; Mailand et al., 2007; Pinato et al., 2009).”
• Mitotic homologous recombination maintains genomic stability and suppresses tumorigenesis (2010, neutral): “The heterodimer UBC13–RNF8 (ubiquitin-conjugating enzyme 13–RING finger protein 8) carries out Lys63 polyubiquitylation of H2A”
• An ATM-Dependent Transcriptional Silencing Program is Transmitted Through Chromatin in Cis to DNA Double Strand Breaks (2010, background): “Specifically, the E3 ubiquitin ligases RNF8 and RNF168 effect the formation of lysine 63-linked polyubiquitin (K63Ub) chains on damaged chromatin, including on histones H2A and H2AX, in an ATM-dependent manner (Doil et al., 2009; Huen et al., 2007; Kolas et al., 2007; Mailand et al., 2007; Stewart e”
• Repair of strand breaks by homologous recombination. (2013, background): “Its accumulation and H2AX phosphorylation (gH2AX) signal the recruitment of MDC1 (Stucki et al. 2005), which in turn recruits 53BP1 (Luijsterburg and van Attikum 2012) and then the E3 ubiquitin ligases, RNF8, RNF168, and BRCA1 (Huen et al. 2007; Kolas et al. 2007; Mailand et al. 2007; Wang and Elled”
• The DNA damage response: ten years after. (2007, background): “…E3 ubiquitin ligase, Ubc13-Rnf8, which ubiquitinates H2AX and possibly other proteins to then recruit 53BP1 and the Brca1 ‘‘A complex’’ (Huen et al., 2007; Kolas et al., 2007; Mailand et al., 2007; Wang and Elledge, 2007), the latter through the UIM domains of its Rap80 component (Petrini, 2007).”
• RNF168 binds and amplifies ubiquitin conjugates on damaged chromosomes to allow accumulation of repair proteins. (2009, positive): “To this end, we tested, by an in vivo ubiquitylation assay, whether RNF168 can target various histones (Mailand et al., 2007) and found that RNF168 efficiently ubiquitylated H2A and H2AX, but not H2B or H3 (Figure 5C).”
• Dynamics of DNA damage response proteins at DNA breaks: a focus on protein modifications. (2011, methodology): “…include the checkpoint mediators 53BP1, BRCA1, and PTIP (Pax2 transactivation domain interaction protein) (Huen et al. 2007; Kolas et al. 2007; Mailand et al. 2007; Wang and Elledge 2007; Doil et al. 2009; Gong et al. 2009; Stewart et al. 2009; Wu et al. 2009a,b); the ubiquitin ligase RAD18,…”
• DNA damage sensing by the ATM and ATR kinases. (2013, background): “3B) (Huen et al. 2007; Kim et al. 2007a,b; Kolas et al. 2007; Mailand et al. 2007; Sobhian et al. 2007; Wang and Elledge 2007; Wang et al. 2007; Doil et al. 2009; Galanty et al. 2009; Morris et al. 2009; Stewart 2009; Bekker-Jensen et al. 2010; Meerang et al. 2011; Mattiroli et al. 2012).”
• RNF8 transduces the DNA-damage signal via histone ubiquitylation and checkpoint protein assembly. (2007, background): “In the accompanying paper, in addition to H2AX, H2A has also been shown to be a substrate of RNF8 (Mailand et al., 2007).”
• The age of crosstalk: phosphorylation, ubiquitination, and beyond. (2007, background): “molecules to which MDC1 is bound; ubiquitinated H2AX then recruits RAP80 through a UIM interaction, and finally the BRCA1/BARD1 E3 ligase, bound via its BRCT repeats tophosphorylated Ccdc98/Abraxas, isrecruited toRAP80, resulting in additional local histone ubiquitination (Huen et al., 2007; Mailan”