MDC1 maintains genomic stability by participating in the amplification of ATM-dependent DNA damage signals.

By Zhenkun Lou, Katherine Minter-Dykhouse, S. Franco, M. Gostissa, Melissa A Rivera, Arkady Celeste, J. Manis, J. V. van Deursen, A. Nussenzweig, T. Paull and 2 more. Molecules and Cells, 2006

693 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/f691585ea98dacc70d5365b998bd1cfd2cf11e01

How researchers see this paper

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In Cancer Research

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

In Molecular Biology

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

Citations in the corpus

• Dynamics of DNA damage response proteins at DNA breaks: a focus on protein modifications. (2011, background): “…lacking H2AX, RNF8, or 53BP1, and, to a lesser extent, MDC1, have class switch recombination defects that would have profound impacts on animal viability in natural environments (Petersen et al. 2001; Celeste et al. 2002; Ward et al. 2004; Lou et al. 2006; L Li et al. 2010; Santos et al. 2010).”
• RNF8 ubiquitylates histones at DNA double-strand breaks and promotes assembly of repair proteins. (2007, positive): “Finally, chromatin retention of BRCA1 is also regulated by MDC1 (Bekker-Jensen et al., 2006; Lou et al., 2003 ) and requires at least two additional proteins, RAP80 and ABRA1 (Kim et al., 2007; Sobhian et al., 2007; Wang et al., 2007; Yan et al., 2007).”
• Mechanism and regulation of class switch recombination. (2008, background): “CSR in cultured mdc1−/− B cells is only mildly reduced, to about 50%–70% of wild-type B cells (167).”
• DNA damage sensing by the ATM and ATR kinases. (2013, background): “Autophosphorylation of ATM has been implicated in Mdc1 binding (Lou et al. 2006).”
• RNF8 transduces the DNA-damage signal via histone ubiquitylation and checkpoint protein assembly. (2007, background): “A positive feedback loop has been proposed in which ATM/ATR concentrates at g-H2AX-containing double-strand breaks via MDC1 to further phosphorylate adjacent H2AX molecules and amplify the DNA-damage signal (Lou et al., 2006; Stucki et al., 2005).”