MDC1 is a mediator of the mammalian DNA damage checkpoint
By G. Stewart, Bin Wang, C. Bignell, A. Taylor, Stephen J. Elledge. Nature, 2003
952 citations recorded by the source corpus.
Subfields: Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/48ffc60e99ce1929af9d3627c648e8f094449dc5
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Citations in the corpus
- Living on a break: cellular senescence as a DNA-damage response (2008, background): “Crucial to the establishment of this positive feedback loop are mediator of DNA-damage checkpoint 1 ( MDC1”
- DNA damage sensing by the ATM and ATR kinases. (2013, background): “Through its BRCT domains, Mdc1 directly binds to phosphorylated H2AX (known asgH2AX) and is required for full-sized gH2AX foci formation (Stewart et al. 2003; Lee et al. 2005; Stucki et al. 2005).”
- γ-H2AX in recognition and signaling of DNA double-strand breaks in the context of chromatin (2008, background): “While 53BP1 can be targeted to damaged chromatin by the above mechanism, its efficient accumulation and sustained retention withinDSB-containing chromatin requires g-H2AX andMDC1 (64,65,72,77,83).”
- Phosphorylation of BLM, Dissociation from Topoisomerase IIIα, and Colocalization with γ-H2AX after Topoisomerase I-Induced Replication Damage (2005, background): “MDC1 silencing has been demonstrated to abrogate the phosphorylation of H2AX as well as BRCA1, DNA-PK, and Chk1 and the formation of foci containing Nbs1, 53BP1, and BRCA1 (42, 43, 61).”
- Phosphorylation-dependent assembly of DNA damage response systems and the central roles of TOPBP1 (2021, background): “However, subsequent studies demonstrated that γH2AX is a direct participant in recruitment of repair factors, and interacts directly with MDC1 [7]; via specific binding of its C-terminal”
- Pathways of apoptotic and non-apoptotic death in tumour cells (2004, background): “Cells that lack MDC1 are sensitive to ionizing radiation and show a G2-checkpoint defec”