Nucleases in homologous recombination as targets for cancer therapy
Jazyk angličtina Země Anglie, Velká Británie Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem, přehledy
PubMed
24928444
DOI
10.1016/j.febslet.2014.06.010
PII: S0014-5793(14)00464-5
Knihovny.cz E-zdroje
- Klíčová slova
- Cancer therapy, Genomic integrity, Homologous recombination, Inhibitor, Nuclease,
- MeSH
- cílená molekulární terapie MeSH
- deoxyribonukleasy antagonisté a inhibitory genetika metabolismus MeSH
- enzymy opravy DNA antagonisté a inhibitory genetika metabolismus MeSH
- homologní rekombinace * MeSH
- inhibitory enzymů farmakologie terapeutické užití MeSH
- lidé MeSH
- nádory farmakoterapie enzymologie genetika MeSH
- rekombinační oprava DNA * MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- přehledy MeSH
- Názvy látek
- deoxyribonukleasy MeSH
- enzymy opravy DNA MeSH
- inhibitory enzymů MeSH
Genomic DNA is constantly challenged from endogenous as well as exogenous sources. The DNA damage response (DDR) mechanism has evolved to combat these challenges and ensure genomic integrity. In this review, we will focus on repair of DNA double-strand breaks (DSB) by homologous recombination and the role of several nucleases and other recombination factors as suitable targets for cancer therapy. Their inactivation as well as overexpression have been shown to sensitize cancer cells by increasing toxicity to DNA-damaging agents and radiation or to be responsible for resistance of cancer cells. These factors can also be used in targeted cancer therapy by taking advantage of specific genetic abnormalities of cancer cells that are not present in normal cells and that result in cancer cell lethality.
Citace poskytuje Crossref.org
MUS81 cleaves TOP1-derived lesions and other DNA-protein cross-links
Esc2 promotes Mus81 complex-activity via its SUMO-like and DNA binding domains