ArticleActa biochimica et biophysica Sinica2022
PRIMPOL competes with RAD51 to resolve G-quadruplex-induced replication stress via its interaction with RPA.
Article in Acta biochimica et biophysica Sinica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- RPA exhaustion activates SLFN11 to eliminate cells with heightened replication stress.Nature cell biology · 2026Article
- How DNA secondary structures drive replication fork instability.DNA repair · 2025Review
- Accurate DNA Synthesis Across 8-Oxoadenine by Human PrimPol.International journal of molecular sciences · 2025Article
- Role of Oxidative Stress in the Occurrence, Development, and Treatment of Breast Cancer.Antioxidants (Basel, Switzerland) · 2025Review
- DNA synthesis across DNA hairpins by human PrimPol.DNA repair · 2024Article
- Human CST complex restricts excessive PrimPol repriming upon UV induced replication stress by suppressing p21.Nucleic acids research · 2024Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PRIMPOL (primase-polymerase) is a recently discovered DNA primase-polymerase involved in DNA damage tolerance and replication stress response in eukaryotic cells. However, the detailed mechanism of the PRIMPOL response to replication stress remains elusive. Here, we demonstrate that replication-related factors, including replication protein A (RPA), regulate the accumulation of PRIMPOL in subnuclear foci in response to replication stress induced by replication inhibitors. Moreover, PRIMPOL works at G-quadruplexes (G4s) in human cells to resolve the replication stress induced by G4s. The formation of PRIMPOL foci persists throughout the cell cycle. We further demonstrate that PRIMPOL competes with RAD51 to resolve G4-induced replication stress. In conclusion, our results provide novel insight into the mechanism of PRIMPOL in G4s to resolve replication stress and competition between PRIMPOL (repriming)- and RAD51 (fork reversal)-mediated pathways, which indicates a new strategy to improve the tumor response to DNA-damaging chemotherapy by targeting the PRIMPOL pathway.
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Registered trials
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