RNF8 transduces the DNA-damage signal via histone ubiquitylation and checkpoint protein assembly.

By M. Huen, R. Grant, Isaac A. Manke, Kay Minn, Xiaochun Yu, Michael B. Yaffe, Junjie Chen. Cell, 2007

1,102 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/4c176d575093a5adf6869749b15b0a45b203ad1f

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Citations in the corpus

Repair of strand breaks by homologous recombination. (2013, background): “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 Elledge 2007; Doil et al. 2009; Stewart et al. 2009).”
Dynamics of DNA damage response proteins at DNA breaks: a focus on protein modifications. (2011, background): “For instance, ATM-dependent phosphorylation of MDC1 on Thr–Gln–X–Phe (TQXF) motifs creates binding sites for the FHA domain of the ubiquitin E3 ligase RNF8 (Ring finger protein 8), which in turn promotes the focal accumulation of 53BP1 and BRCA1 at DSB sites (Huen et al. 2007; Kolas et al. 2007; Mai”
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).”
An ATM-Dependent Transcriptional Silencing Program is Transmitted Through Chromatin in Cis to DNA Double Strand Breaks (2010, background): “Silence Transcription In cis to DNA Double-Strand Breaks”
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; Maila”
The DNA Damage Response: Making it safe to play with knives (2010, background): “DNA end resection is regulated by ATM through CtIP, which interacts with BRCA1 and MRN in the BRCA1-C complex (Figure 2B) (Huen et al., 2010b).”
RNF168 binds and amplifies ubiquitin conjugates on damaged chromosomes to allow accumulation of repair proteins. (2009, positive): “RNF8 catalyzes local histone ubiquitylation and thereby renders the DSB-flanking chromatin permissive to assemble additional DSB regulators such as 53BP1 and BRCA1 ( Huen et al., 2007; Kolas et al., 2007; Mailand et al., 2007; Sobhian et al., 2007; Wang et al., 2007; Wang and Elledge, 2007; Yan et ”
RNF8 ubiquitylates histones at DNA double-strand breaks and promotes assembly of repair proteins. (2007, positive): “Ourfindings, and the accompanying paper by Chen and colleagues, who reached similar conclusions ( Huen et al., 2007 [this issue of Cell]), complement the emerging role of regulatory ubiquitylations in diverse aspects of the DNAdamage response by identifying an RNF8-dependent step during the maturat”
RNF168 ubiquitinates K13-15 on H2A/H2AX to drive DNA damage signaling. (2012, methodology): “Because the E2 Ubc13 is important for the DSB pathway (Huen et al., 2007; Stewart et al., 2009; Zhao et al., 2007) and catalyzes K63 chains when complexed with the UEV cognate proteins (Hofmann and Pickart, 1999), we included this E2 in our assays.”
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).”