The DNA damage response: putting checkpoints in perspective

By Bin-Bing S. Zhou, Stephen J. Elledge. Nature, 2000

3,406 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/b2d859279f087d0ba53ccc0876b0656ba068e117

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Citations in the corpus

Regulation of DNA replication fork progression through damaged DNA by the Mec1/Rad53 checkpoint (2001, background): “jpg" NDATA ITEM> ]> The checkpoint kinase proteins Mec1 and Rad53 are required in the budding yeast, Saccharomyces cerevisiae , to maintain cell viability in the presence of drugs causing damage to DNA or arrest of DNA replication fork”
Conserved modes of recruitment of ATM, ATR and DNA-PKcs to sites of DNA damage (2005, background): “These groups comprise sensor proteins that recognize damaged DNA directly or indirectly, transducer proteins—typically PIKKs such as ATM, ATR and DNA-PKcs—that relay and amplify the damage signal, and effector proteins that control cell cycle progression, chromatin restructuring and DNA repai”
DNA helicases Sgs1 and BLM promote DNA double-strand break resection. (2008, background): “To survive DSB exposure and maximize genome stability, cells possess a complex machinery to detect DSBs, signal their presence, and mediate their repair (Zhou and Elledge 2000; Rouse and Jackson 2002; Lisby and Rothstein 2004; Wyman and Kanaar 2006).”
The DNA Damage Response: Making it safe to play with knives (2010, background): “These include the determination to undergo apoptosis or enter terminal differentiation through senescence, the activation of heightened immune surveillance, DNA damage prophylaxis through tanning, as well as DNA repair itself (Cui et al., 2007; Gasser and Raulet, 2006; Zhou and Elledge, 2000).”
Genome maintenance mechanisms for preventing cancer (2001, background): “The cell-cycle machinery somehow senses genome injury and arrests at specific checkpoints in G1, S, G2 and M to allow repair of lesions before they are converted into permanent mutations (reviewed in ref”
Organelle-specific initiation of cell death pathways (2001, background): “The nuclear DNA damage response Nuclear DNA damage is one of the best-studied initiators of apoptosis (reviewed in ref”
Cellular response to hyperosmotic stresses. (2007, background): “The cell cycle arrest that is associated with most other causes of DNA damage provides a lull in DNA replication during which the DNA can be repaired (345).”
Stems cells and the pathways to aging and cancer. (2008, background): “This may result from the fact that the cellular machinery responsible for eliciting DNA-damage responses for repair, growth arrest, or apoptosis is so intimately linked to cell-cycle progression and cell-cycle-dependent checkpoint control mechanisms (reviewed in Zhou and Elledge, 2000).”
Cell cycle checkpoint signaling through the ATM and ATR kinases. (2001, background): “For more information regarding the yeast ATM/ATR homologs, or a more global overview of cell-cycle checkpoints, the reader is referred to several recent reviews (Elledge 1996; Weinert 1997; Lowndes and Murguia 2000; Tibbetts and Abraham 2000; Zhou and Elledge 2000).”
p53-deficient cells rely on ATM- and ATR-mediated checkpoint signaling through the p38MAPK/MK2 pathway for survival after DNA damage. (2007, background): “The ATM/Chk2 pathway responds primarily to DNA double-strand breaks (DSBs), while the ATR/Chk1 pathway is activated by bulky DNA lesions, and following replication fork collapse during S phase (Zhou and Elledge, 2000).”