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Updated: Mar 17, 2026

Direct Restart of a Replication Fork Stalled by a Head-On RNA Polymerase
Published on: April 29, 2010
TRAIP regulates replication fork recovery and progression via PCNA
Wanjuan Feng1, Yingying Guo2, Jun Huang3
1School of Biomedical Sciences, LKS Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong S.A.R., China; Centre for Cancer Research, LKS Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong S.A.R., China.
Researchers identified TRAIP (RNF206) as a novel protein that interacts with PCNA to aid DNA replication fork recovery during cellular stress. This discovery highlights TRAIP-PCNA interactions in maintaining genome stability.
Area of Science:
- Molecular Biology
- Cell Biology
- Genetics
Background:
- Proliferating Cell Nuclear Antigen (PCNA) is crucial for DNA replication and repair.
- Understanding the regulation of DNA replication forks under stress is vital for genome stability.
Purpose of the Study:
- To identify novel PCNA-interacting factors involved in mammalian replicative stress responses.
- To elucidate the role of TRAIP (RNF206) in DNA replication fork recovery.
Main Methods:
- Co-immunoprecipitation to identify PCNA-interacting proteins.
- Cellular localization studies using microscopy.
- Analysis of replication fork progression and chromosome stability in TRAIP-deficient cells.
Main Results:
- TRAIP (RNF206) was identified as a novel PCNA-interacting protein.
- TRAIP localizes to nucleoli and translocates to stalled replication forks upon stress.
- TRAIP interacts with PCNA via a conserved PIP box.
- Inactivation of TRAIP or its PCNA interaction impairs replication fork recovery and leads to chromosome instability.
Conclusions:
- TRAIP is a key component of the mammalian replicative stress response network.
- The TRAIP-PCNA interaction is critical for the recovery of stalled DNA replication forks.
- TRAIP-PCNA axis plays a significant role in maintaining genome integrity.
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