Perspectives on PARPs in S Phase
Language English Country England, Great Britain Media print-electronic
Document type Journal Article, Review
Grant support
27322
Cancer Research UK - United Kingdom
PubMed
31036342
DOI
10.1016/j.tig.2019.03.008
PII: S0168-9525(19)30054-X
Knihovny.cz E-resources
- Keywords
- DNA replication stress, DNA strand break repair, Okazaki fragment, PARP1, PARP2, poly(ADP-ribose),
- MeSH
- Enzyme Activation MeSH
- Molecular Targeted Therapy MeSH
- Humans MeSH
- Multigene Family MeSH
- Disease Susceptibility MeSH
- Genomic Instability MeSH
- DNA Repair MeSH
- Poly(ADP-ribose) Polymerase Inhibitors pharmacology therapeutic use MeSH
- Poly(ADP-ribose) Polymerases genetics metabolism MeSH
- DNA Damage MeSH
- Cell Proliferation MeSH
- Antineoplastic Agents pharmacology therapeutic use MeSH
- DNA Replication MeSH
- S Phase physiology MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Review MeSH
- Names of Substances
- Poly(ADP-ribose) Polymerase Inhibitors MeSH
- Poly(ADP-ribose) Polymerases MeSH
- Antineoplastic Agents MeSH
Accurate copying of DNA during S phase is essential for genome stability and cell viability. During genome duplication, the progression of the DNA replication machinery is challenged by limitations in nucleotide supply and physical barriers in the DNA template that include naturally occurring DNA lesions and secondary structures that are difficult to replicate. To ensure correct and complete replication of the genome, cells have evolved several mechanisms that protect DNA replication forks and thus maintain genome integrity and stability during S phase. One class of enzymes that have recently emerged as important in this process, and therefore as promising targets in anticancer therapy, are the poly(ADP-ribose) polymerases (PARPs). We review here the roles of these enzymes during DNA replication as well as their impact on genome stability and cellular viability in normal and cancer cells.
References provided by Crossref.org
Dispensability of HPF1 for cellular removal of DNA single-strand breaks
Emetine blocks DNA replication via proteosynthesis inhibition not by targeting Okazaki fragments
PARP inhibition impedes the maturation of nascent DNA strands during DNA replication
Neuronal enhancers are hotspots for DNA single-strand break repair
Pathogenic ARH3 mutations result in ADP-ribose chromatin scars during DNA strand break repair