ArticleDNA repair2016
Enhanced sensitivity of Neil1
Article in DNA repair, 2016. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Photoreactive Properties of Melanin Obtained from Human Induced Pluripotent Stem Cell-Derived Melanocytes.International journal of molecular sciences · 2025Article
- Role of NEIL1 in genome maintenance.DNA repair · 2025Review
- DNA repair and disease: insights from the human DNA glycosylase NEIL family.Experimental & molecular medicine · 2025Review
- Spontaneous allelic variant in deafness-blindness gene Ush1g resulting in an expanded phenotype.Genes, brain, and behavior · 2023Article
- Article
- Three Classes of Antioxidant Defense Systems and the Development of Postmenopausal Osteoporosis.Frontiers in physiology · 2022Review
- Mono- and biallelic germline variants of DNA glycosylase genes in colon adenomatous polyposis families from two continents.Frontiers in oncology · 2022Article
- Heritable pattern of oxidized DNA base repair coincides with pre-targeting of repair complexes to open chromatin.Nucleic acids research · 2021Article
- Modulation of UVB-induced Carcinogenesis by Activation of Alternative DNA Repair Pathways.Scientific reports · 2018Article
- OGG1-DNA interactions facilitate NF-κB binding to DNA targets.Scientific reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Oxidative stress and reactive oxygen species (ROS)-induced DNA base damage are thought to be central mediators of UV-induced carcinogenesis and skin aging. However, increased steady-state levels of ROS-induced DNA base damage have not been reported after chronic UV exposure. Accumulation of ROS-induced DNA base damage is governed by rates of lesion formation and repair. Repair is generally performed by Base Excision Repair (BER), which is initiated by DNA glycosylases, such as 8-oxoguanine glycosylase and Nei-Endonuclease VIII-Like 1 (NEIL1). In the current study, UV light (UVB) was used to elicit protracted low-level ROS challenge in wild-type (WT) and Neil1
Indexed as
Identifiers
What OpenQuestion holds
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.