Abstract
Left unrepaired, the myriad types of damage that can occur in genomic DNA pose a serious threat to the faithful transmission of the correct complement of genetic material. Defects in DNA damage signaling and repair result in genomic instability, a hallmark of cancer, and often cause lethality, underlining the importance of these processes in the cell and whole organism. The past decade has seen huge advances in our understanding of how the signal transduction pathways triggered by DNA damage radically alter cell behavior. In contrast, it is still unclear how primary DNA damage is detected and how this interfaces with signal transduction and DNA repair proteins.
Keywords
DNA damageDNA repairGenome instabilitySignal transductionDNABiologyCell biologygenomic DNAGeneticsComputational biology
Affiliated Institutions
Related Publications
Stabilization of stalled DNA replication forks by the BRCA2 breast cancer susceptibility protein
How dividing mammalian cells overcome blocks to DNA replication by DNA damage, depleted nucleotide pools, or template-bound proteins is unclear. Here, we show that the response ...
Cell cycle checkpoint signaling through the ATM and ATR kinases
The genomes of eukaryotic cells are under continuous assault by environmental agents (e.g., UV light and reactive chemicals) as well as the byproducts of normal intracellular me...
The cGAS–cGAMP–STING pathway connects DNA damage to inflammation, senescence, and cancer
Detection of microbial DNA is an evolutionarily conserved mechanism that alerts the host immune system to mount a defense response to microbial infections. However, this detecti...
Molecular Mechanisms of Mammalian DNA Repair and the DNA Damage Checkpoints
▪ Abstract DNA damage is a relatively common event in the life of a cell and may lead to mutation, cancer, and cellular or organismic death. Damage to DNA induces several cellul...
p53 and its 14 kDa C-terminal domain recognize primary DNA damage in the form of insertion/deletion mismatches
Insertion/deletion (IDL) mismatches in DNA are lesions consisting of extra bases on one strand. Here, the binding of p53 and its 14 kDa C-terminal domain to DNAs containing one ...
Publication Info
- Year
- 2002
- Type
- review
- Volume
- 297
- Issue
- 5581
- Pages
- 547-551
- Citations
- 690
- Access
- Closed
External Links
Social Impact
Altmetric
PlumX Metrics
Social media, news, blog, policy document mentions
Citation Metrics
690
OpenAlex
Cite This
John Rouse,
Stephen P. Jackson
(2002).
Interfaces Between the Detection, Signaling, and Repair of DNA Damage.
Science
, 297
(5581)
, 547-551.
https://doi.org/10.1126/science.1074740
Identifiers
- DOI
- 10.1126/science.1074740