ReviewOxidative medicine and cellular longevity2014
Human AP endonuclease 1: a potential marker for the prediction of environmental carcinogenesis risk.
Review in Oxidative medicine and cellular longevity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 20 citations in OpenAlex.
- RETRACTED: Identification of Redox-Sensitive Transcription Factors as Markers of Malignant Pleural Mesothelioma.Cancers · 2021Article
- The Base Excision Repair Pathway in the NematodeFrontiers in cell and developmental biology · 2020Review
- Lamin A/C promotes DNA base excision repair.Nucleic acids research · 2019Article
- Functionalized biochar-supported magnetic MnFeRSC advances · 2018Article
- Configurational and Conformational Equilibria of NChemical research in toxicology · 2018Article
- Lead facilitates foci formation in a Balb/c-3T3 two-step cell transformation model: role of Ape1 function.Environmental science and pollution research international · 2018Article
- Genomic Approach to Understand the Association of DNA Repair with Longevity and Healthy Aging Using Genomic Databases of Oldest-Old Population.Oxidative medicine and cellular longevity · 2018Review
- Altered Secretory Activity of APE1/Ref-1 D148E Variants Identified in Human Patients With Bladder Cancer.International neurourology journal · 2016Article
- Redox regulation of genome stability by effects on gene expression, epigenetic pathways and DNA damage/repair.Redox biology · 2015Review
- Mitochondrial Oxidative Stress, Mitochondrial DNA Damage and Their Role in Age-Related Vascular Dysfunction.International journal of molecular sciences · 2015Review
- Nivolumab Therapy for SynchronousCase reports in oncologyArticle
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human apurinic/apyrimidinic endonuclease 1 (APE1) functions mainly in DNA repair as an enzyme removing AP sites and in redox signaling as a coactivator of various transcription factors. Based on these multifunctions of APE1 within cells, numerous studies have reported that the alteration of APE1 could be a crucial factor in development of human diseases such as cancer and neurodegeneration. In fact, the study on the combination of an individual's genetic make-up with environmental factors (gene-environment interaction) is of great importance to understand the development of diseases, especially lethal diseases including cancer. Recent reports have suggested that the human carcinogenic risk following exposure to environmental toxicants is affected by APE1 alterations in terms of gene-environment interactions. In this review, we initially outline the critical APE1 functions in the various intracellular mechanisms including DNA repair and redox regulation and its roles in human diseases. Several findings demonstrate that the change in expression and activity as well as genetic variability of APE1 caused by environmental chemical (e.g., heavy metals and cigarette smoke) and physical carcinogens (ultraviolet and ionizing radiation) is likely associated with various cancers. These enable us to ultimately suggest APE1 as a vital marker for the prediction of environmental carcinogenesis risk.
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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.