Abstract
G2E3 attenuating replicative stress.
Highlights
Cancer cells generally display an increased level of replicative stress
This initial observation led to the discovery of numerous ubiquitin-dependent factors essential for DNA damage response, DNA repair, and DNA replication
We found that DNA damage triggers a profound reduction in G2E3 levels [3]
Summary
Cancer cells generally display an increased level of replicative stress. Strategies to exploit this phenomenon by further increasing replicative stress include the use of conventional DNA-damaging chemotherapeutics, and the targeted inhibition of damage response signaling [1]. Interfering with the ubiquitin signaling system leads to dysfunctional DNA damage response.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have