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]

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Summary

Introduction

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.

Results
Conclusion

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