ArticleOncogenesis2020
The HLTF-PARP1 interaction in the progression and stability of damaged replication forks caused by methyl methanesulfonate.
Article in Oncogenesis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- The SWI/SNF-related protein SMARCA3 is a histone H3K23 ubiquitin ligase that regulates H3K9me3 in cancer.Molecular cell · 2025Article
- Epidemiology, pathophysiology and clinical aspects of Hepatocellular Carcinoma in MAFLD patients.Hepatology international · 2024Review
- Exo1 cooperates with Tel1/ATM in promoting recombination events at DNA replication forks.iScience · 2024Article
- HLTF disrupts Cas9-DNA post-cleavage complexes to allow DNA break processing.Nature communications · 2024Article
- APLF facilitates interstrand DNA crosslink repair and replication fork protection to confer cisplatin resistance.Nucleic acids research · 2024Article
- MBD1 protects replication fork stability by recruiting PARP1 and controlling transcription-replication conflicts.Cancer gene therapy · 2024Article
- Ethanol induces replication fork stalling and membrane stress in immortalized laryngeal cells.iScience · 2023Article
- Article
- PARP1 recruits DNA translocases to restrain DNA replication and facilitate DNA repair.PLoS genetics · 2022Article
- Hydroxyurea-The Good, the Bad and the Ugly.Genes · 2021Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
Abstract
Human HLTF participates in the lesion-bypass mechanism through the fork reversal structure, known as template switching of post-replication repair. However, the mechanism by which HLTF promotes the replication progression and fork stability of damaged forks remains unclear. Here, we identify a novel protein-protein interaction between HLTF and PARP1. The depletion of HLTF and PARP1 increases chromosome breaks, further reduces the length of replication tracks, and concomitantly increases the number of stalled forks after methyl methanesulfonate treatment according to a DNA fiber analysis. The progression of replication also depends on BARD1 in the presence of MMS treatment. By combining 5-ethynyl-2'-deoxyuridine with a proximity ligation assay, we revealed that the HLTF, PARP1, and BRCA1/BARD1/RAD51 proteins were initially recruited to damaged forks. However, prolonged stalling of damaged forks results in fork collapse. HLTF and PCNA dissociate from the collapsed forks, with increased accumulation of PARP1 and BRCA1/BARD1/RAD51 at the collapsed forks. Our results reveal that HLTF together with PARP1 and BARD1 participates in the stabilization of damaged forks, and the PARP1-BARD1 interaction is further involved in the repair of collapse forks.
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.