The RIDDLE syndrome protein mediates a ubiquitin-dependent signaling cascade at sites of DNA damage.

By Grant S. Stewart, Stephanie Panier, Kelly Townsend, Abdallah K. Al-Hakim, N. Kolas, Edward S. Miller, Shinichiro Nakada, J. Ylanko, Signe Olivarius, Megan Mendez and 10 more. Cell, 2009

807 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/a58bb9da838d2f85493f01aa08fb78eb741c3a9f

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In Molecular Biology

1. Stephen P. Jackson
2. J. Bartek
3. S. Polo
4. J. Lukas
5. C. Lukas
6. M. Jasin
7. Rodney Rothstein
8. Yosef Shiloh

In Oncology

1. Stephen P. Jackson
2. J. Bartek
3. J. Lukas
4. S. Polo
5. C. Lukas
6. M. Jasin
7. Yosef Shiloh
8. P. Jeggo

Citations in the corpus

• RNF168 ubiquitinates K13-15 on H2A/H2AX to drive DNA damage signaling. (2012, methodology): “Two major E3 ligases are also known to take part in DDR after DSBs: RNF8, that acts upstream of RNF168 allowing its recruitment (Doil et al., 2009; Pinato et al., 2009; Stewart et al., 2009) and BRCA1, that is thought to act downstream of RNF168 (Kim et al., 2007; Sobhian et al., 2007).”
• Dynamics of DNA damage response proteins at DNA breaks: a focus on protein modifications. (2011, background): “For example, various protein– ubiquitin conjugates, including ubiquitylated histones, have been detected at sites of DNA breaks in mammalian cells (Morris and Solomon 2004; Polanowska et al. 2006; Mailand et al. 2007; Doil et al. 2009; Stewart et al. 2009).”
• 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”
• 53BP1 is a reader of the DNA damage-induced H2A Lys15 ubiquitin mark (2013, neutral): “Class switching to IgG1 was assayed in 53BP1 murine primary B cells complemented with 53BP1 (1-1711) and mutants thereof by retroviral delivery.”
• 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”
• RNF168 binds and amplifies ubiquitin conjugates on damaged chromosomes to allow accumulation of repair proteins. (2009, neutral): “Thus, constitutive phosphorylation of the S-D-T clusters by Casein kinase 2 generates binding sites for the FHA and BRCT domains of NBS1, a core component of the MRE11-NBS1-RAD50 nuclease complex (Melander et al., 2008; Spycher et al., 2008 ).”
• 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”