ArticleBMC molecular biology2007
Manipulation of cell cycle progression can counteract the apparent loss of correction frequency following oligonucleotide-directed gene repair.
Article in BMC molecular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- Genome editing outcomes reveal mycobacterial NucS participates in a short-patch repair of DNA mismatches.Nucleic acids research · 2024Article
- Genome Editing Outcomes Reveal Mycobacterial NucS Participates in a Short-Patch Repair of DNA Mismatches.bioRxiv : the preprint server for biology · 2023Article
- Transient inhibition of p53 enhances prime editing and cytosine base-editing efficiencies in human pluripotent stem cells.Nature communications · 2022Article
- Relaxed chromatin induced by histone deacetylase inhibitors improves the oligonucleotide-directed gene editing in plant cells.Journal of plant research · 2018Article
- Combinatorial gene editing in mammalian cells using ssODNs and TALENs.Scientific reports · 2014Article
- Article
- Proliferation of genetically modified human cells on electrospun nanofiber scaffolds.Molecular therapy. Nucleic acids · 2012Article
- Oligonucleotide delivery by nucleofection does not rescue the reduced proliferation phenotype of gene-edited cells.Nucleic acid therapeutics · 2012Article
- DNA damage response pathway and replication fork stress during oligonucleotide directed gene editing.Molecular therapy. Nucleic acids · 2012Article
- Progress and prospects: oligonucleotide-directed gene modification in mouse embryonic stem cells: a route to therapeutic application.Gene therapy · 2011Review
- Article
- DNA breakage associated with targeted gene alteration directed by DNA oligonucleotides.Mutation research · 2009Article
- Progress and prospects: targeted gene alteration (TGA).Gene therapy · 2007Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundSingle-stranded oligonucleotides (ssODN) are used routinely to direct specific base alterations within mammalian genomes that result in the restoration of a functional gene. Despite success with the technique, recent studies have revealed that following repair events, correction frequencies decrease as a function of time, possibly due to a sustained activation of damage response signals in corrected cells that lead to a selective stalling. In this study, we use thymidine to slow down the replication rate to enhance repair frequency and to maintain substantial levels of correction over time.
resultsFirst, we utilized thymidine to arrest cells in G1 and released the cells into S phase, at which point specific ssODNs direct the highest level of correction. Next, we devised a protocol in which cells are maintained in thymidine following the repair reaction, in which the replication is slowed in both corrected and non-corrected cells and the initial correction frequency is retained. We also present evidence that cells enter a senescence state upon prolonged treatment with thymidine but this passage can be avoided by removing thymidine at 48 hours.
conclusionTaken together, we believe that thymidine may be used in a therapeutic fashion to enable the maintenance of high levels of treated cells bearing repaired genes.
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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.