RNF168 binds and amplifies ubiquitin conjugates on damaged chromosomes to allow accumulation of repair proteins.

By C. Doil, Niels Mailand, Simon Bekker-Jensen, Patrice Ménard, D. Larsen, Rainer Pepperkok, Jan Ellenberg, Stephanie Panier, D. Durocher, J. Bartek and 2 more. Cell, 2009

972 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/45d26dd447c4daef4946c4521ae8e1e6d0704d65

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In Genetics

1. Christoph Sommer
2. Stephen P. Jackson
3. Ian D. Hickson
4. M. Jasin
5. Daniel Gerlich
6. D. G. Gibson

In Molecular Biology

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

Citations in the corpus

• The DNA Damage Response: Making it safe to play with knives (2010, background): “The E3 ubiquitin ligase RNF168 then binds these chains through its motifs interacting with ubiquitin (MIU) to stimulate K63 ubiquitination (Doil et al., 2009; Stewart et al., 2009).”
• 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).”
• 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”
• CellCognition: time-resolved phenotype annotation in high-throughput live cell imaging (2010, methodology): “Indeed, imaging-based RNAi and chemical-compound screening has become an important discovery tool for the identification of new gene function, for example, in the regulation of DNA damage and repai”
• 53BP1 nuclear bodies form around DNA lesions generated by mitotic transmission of chromosomes under replication stress (2011, background): “RESULTS 53BP1 nuclear bodies mark spontaneous DNA lesions in a subset of cells Among the reasons that drew our attention to endogenous DNA damage were recurrent report”
• Histone Modifications and Cancer. (2016, background): “The HR pathway involves polyubiquitination of H2A or H2AX at Lys63 by the RNF8 and RNF168 ubiquitin ligases at sites of DNA DSBs, acting to recruit DNA repair factors, such as BRCA1 (Doil et al. 2009; Campbell et al. 2012).”
• More than just a focus: The chromatin response to DNA damage and its role in genome integrity maintenance (2011, background): “Experiments with antibodies specific to distinct ubiquitin chains revealed that DNA-damage-flanking chromatin is enriched in Lys 63-linked ubiquitin polymer”
• 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”
• Homologous recombination and human health: the roles of BRCA1, BRCA2 and associated proteins (2015, background): “The BRCA1-A complex targets BRCA1 to ubiquitin conjugates at DSBs, which are critical for DNA-damage signaling and repair (Huen et al. 2007; Doil et al. 2009).”