Chromosomal stability and the DNA double-stranded break connection

By D. Gent, Jan H. J. Hoeijmakers, Roland Kanaar. Nature reviews genetics, 2001

1,300 citations recorded by the source corpus.

Subfields: Cancer Research, Cell Biology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/fe12b5960eded1340809ea6629a661724f4170a7

How researchers see this paper

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In Cancer Research

1. Yosef Shiloh
2. Alan Ashworth
3. Michael J Hendzel
4. I. H. Ismail
5. J. Bartek

In Cell Biology

1. K. Gudmundsdottir
2. Yosef Shiloh
3. Alan Ashworth
4. D. Slade
5. M. Radman

In Molecular Biology

1. K. Gudmundsdottir
2. O. Fernández-Capetillo
3. Yosef Shiloh
4. Alan Ashworth
5. Michael J Hendzel
6. Thomas Helleday
7. I. H. Ismail
8. D. Slade

Citations in the corpus

• Structure of the Ku heterodimer bound to DNA and its implications for double-strand break repair (2001, background): “jpg" NDATA ITEM> ]> Damage to DNA in the form of double-strand breaks (DSBs) compromises the integrity of cells, and defects in DSB repair processes can lead to chromosomal translocations, loss of growth control and cance”
• Biological consequences of radiation-induced DNA damage: relevance to radiotherapy. (2013, background): “Homologous recombination provides greater repair fidelity than NHEJ, the latter being the major pathway to repair prompt DSB throughout all phases of the cell cycle (reviewed in [33,34]).”
• DNA double-strand break repair: from mechanistic understanding to cancer treatment. (2007, background): “However, the opposite effect has been observed in several non-homologous end joining mouse models [110,111].”
• ATM and related protein kinases: safeguarding genome integrity (2003, background): “This is especially true for the response to highly cytotoxic DNA lesions, such as double-strand breaks (DSBs”
• Histone H2AX phosphorylation is dispensable for the initial recognition of DNA breaks (2003, background): “This may explain why H2AX −/− mice exhibit a relatively mild phenotype, compared with mice carrying targeted deletion of the DNA damage signalling–repair proteins ATR, Brca1, M–R–N or Rad51 (ref”
• The γ‐H2A.X: Is it just a surrogate marker of double‐strand breaks or much more? (2008, background): “This process requires both replication coupled and replication-uncoupled mechanisms [Vermaak et al., 2003].”
• Regulation and mechanisms of mammalian double-strand break repair (2003, background): “Studies of both knockout mice and repair-deficient cultured cells suggest that disruption of any factor involved in HRR results in chromosomal instability and (for those defects that are not lethal) cancer predisposition (Thompson and Schild, 2001; van Gent et al., 2001).”