ArticleCurrent genomics2015
DNA secondary structure at chromosomal fragile sites in human disease.
Article in Current genomics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 57 citations in OpenAlex.
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- Sequencing and characterizing short tandem repeats in the human genome.Nature reviews. Genetics · 2024Review
- DNA fragility at topologically associated domain boundaries is promoted by alternative DNA secondary structure and topoisomerase II activity.Nucleic acids research · 2024Article
- A Unifying Hypothesis for the Genome Dynamics Proposed to Underlie Neuropsychiatric Phenotypes.Genes · 2024Review
- Optical Mapping: Detecting Genomic Resistance Cassettes in MRSA.ACS omega · 2024Article
- Molecular characterization of TCF3::PBX1 chromosomal breakpoints in acute lymphoblastic leukemia and their use for measurable residual disease assessment.Scientific reports · 2023Article
- Post- and Pre-Radiolabeling Assays forBiochemistry · 2023Article
- Dynamic alternative DNA structures in biology and disease.Nature reviews. Genetics · 2023Review
- The remodeling of Z-DNA in the mammalian germ line.Biochemical Society transactions · 2022Article
- Hallmarks of DNA replication stress.Molecular cell · 2022Review
- Fragile sites, chromosomal lesions, tandem repeats, and disease.Frontiers in genetics · 2022Review
- Consequences and Resolution of Transcription-Replication Conflicts.Life (Basel, Switzerland) · 2021Review
- Dysregulation of hsa-miR-34a and hsa-miR-449a leads to overexpression of PACS-1 and loss of DNA damage response (DDR) in cervical cancer.The Journal of biological chemistry · 2020Article
- An Epigenetics-Based Hypothesis of Autoantigen Development in Systemic Lupus Erythematosus.Epigenomes · 2020Review
- Article
- Journal Current Genomics: News and Editorial Prospects.Current genomics · 2019Article
- Review
- ERCC1/XPF Is Important for Repair of DNA Double-Strand Breaks Containing Secondary Structures.iScience · 2019Article
- SSB1/SSB2 Proteins Safeguard B Cell Development by Protecting the Genomes of B Cell Precursors.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
DNA has the ability to form a variety of secondary structures that can interfere with normal cellular processes, and many of these structures have been associated with neurological diseases and cancer. Secondary structure-forming sequences are often found at chromosomal fragile sites, which are hotspots for sister chromatid exchange, chromosomal translocations, and deletions. Structures formed at fragile sites can lead to instability by disrupting normal cellular processes such as DNA replication and transcription. The instability caused by disruption of replication and transcription can lead to DNA breakage, resulting in gene rearrangements and deletions that cause disease. In this review, we discuss the role of DNA secondary structure at fragile sites in human disease.
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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.