ArticleNucleic acids research2014
Strand invasion by HLTF as a mechanism for template switch in fork rescue.
Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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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.
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Who cites it
42 citing papers in PubMed, 63 citations in OpenAlex.
- Elucidating HLTF-Mediated DNA Fork Remodeling via Native Mass Spectrometry.Journal of the American Chemical Society · 2026Article
- Article
- SHPRH together with the Ube2D family of enzymes directly ubiquitinates PCNA at Lys164 in vitro.PloS one · 2026Article
- Recurrent DNA nicks drive massive expansions of (GAA)Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- HLTF resolves G4s and promotes G4-induced replication fork slowing to maintain genome stability.Molecular cell · 2024Article
- PARP1 recruits DNA translocases to restrain DNA replication and facilitate DNA repair.PLoS genetics · 2022Article
- DNA Sequence Specificity Reveals a Role of the HLTF HIRAN Domain in the Recognition of Trinucleotide Repeats.Biochemistry · 2022Article
- Rad5 participates in lesion bypass through its Rev1-binding and ubiquitin ligase domains, but not through its helicase function.Frontiers in molecular biosciences · 2022Article
- Making Choices: DNA Replication Fork Recovery Mechanisms.Seminars in cell & developmental biology · 2021Review
- The HLTF-PARP1 interaction in the progression and stability of damaged replication forks caused by methyl methanesulfonate.Oncogenesis · 2020Article
- Time for remodeling: SNF2-family DNA translocases in replication fork metabolism and human disease.DNA repair · 2020Review
- The Human RAD5 Homologs, HLTF and SHPRH, Have Separate Functions in DNA Damage Tolerance Dependent on The DNA Lesion Type.Biomolecules · 2020Article
- iDamage: a method to integrate modified DNA into the yeast genome.Nucleic acids research · 2019Article
- A tough row to hoe: when replication forks encounter DNA damage.Biochemical Society transactions · 2018Review
- Homologous Recombination: To Fork and Beyond.Genes · 2018Review
- Regulation of HLTF-mediated PCNA polyubiquitination by RFC and PCNA monoubiquitination levels determines choice of damage tolerance pathway.Nucleic acids research · 2018Article
- Ubiquitylation at the Fork: Making and Breaking Chains to Complete DNA Replication.International journal of molecular sciences · 2018Review
- The HIRAN domain of helicase-like transcription factor positions the DNA translocase motor to drive efficient DNA fork regression.The Journal of biological chemistry · 2018Article
- Functions of SMARCAL1, ZRANB3, and HLTF in maintaining genome stability.Critical reviews in biochemistry and molecular biology · 2017Review
- The identification of FANCD2 DNA binding domains reveals nuclear localization sequences.Nucleic acids research · 2017Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stalling of replication forks at unrepaired DNA lesions can result in discontinuities opposite the damage in the newly synthesized DNA strand. Translesion synthesis or facilitating the copy from the newly synthesized strand of the sister duplex by template switching can overcome such discontinuities. During template switch, a new primer-template junction has to be formed and two mechanisms, including replication fork reversal and D-loop formation have been suggested. Genetic evidence indicates a major role for yeast Rad5 in template switch and that both Rad5 and its human orthologue, Helicase-like transcription factor (HLTF), a potential tumour suppressor can facilitate replication fork reversal. This study demonstrates the ability of HLTF and Rad5 to form a D-loop without requiring ATP binding and/or hydrolysis. We also show that this strand-pairing activity is independent of RAD51 in vitro and is not mechanistically related to that of another member of the SWI/SNF family, RAD54. In addition, the 3'-end of the invading strand in the D-loop can serve as a primer and is extended by DNA polymerase. Our data indicate that HLTF is involved in a RAD51-independent D-loop branch of template switch pathway that can promote repair of gaps formed during replication of damaged DNA.
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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.