Characterization of rare NEIL1 variants found in East Asian populations

Minko, Irina G.; Vartanian, Vladimir; Tozaki, Naoto N.; Linde, Oskar K.; Coşkun, Sanem Hoşbaş; Coşkun, Erdem; Qu, Chunfeng; He, Huan; Xu, Chungui; Chen, Taoyang; Song, Qianqian; Jiao, Yuchen; Stone, Michael P.; Egli, Martin; Dizdaroğlu, Miral; McCullough, Amanda K.; Lloyd, R. Stephen

doi:10.1016/j.dnarep.2019.05.001

Cited by 12 publications

(30 citation statements)

References 38 publications

(45 reference statements)

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“…However, it is now well established that exposure to aflatoxins induces various epigenetic changes in repair genes that impedes BER. For example, hypermethylation of the promoter of NEIL1 (Nei Like 1) gene coding for a DNA glycosylase (NEIL1), which plays a key role in BER, was recently shown to reduce the excision efficiency in AFB1-FAPy adducts by transcriptional repression of the gene [39]. The repair of AFB1-FAPy lesions may be further restricted in humans due to the widespread polymorphic variants producing catalytically inactive NEIL1 enzyme [40].…”

Section: Genetic Polymorphism and Increased Mutagenicity Of Aflatoxinsmentioning

confidence: 99%

Chronic and Acute Toxicities of Aflatoxins: Mechanisms of Action

Benkerroum

2020

IJERPH

316

214

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There are presently more than 18 known aflatoxins most of which have been insufficiently studied for their incidence, health-risk, and mechanisms of toxicity to allow effective intervention and control means that would significantly and sustainably reduce their incidence and adverse effects on health and economy. Among these, aflatoxin B1 (AFB1) has been by far the most studied; yet, many aspects of the range and mechanisms of the diseases it causes remain to be elucidated. Its mutagenicity, tumorigenicity, and carcinogenicity—which are the best known—still suffer from limitations regarding the relative contribution of the oxidative stress and the reactive epoxide derivative (Aflatoxin-exo 8,9-epoxide) in the induction of the diseases, as well as its metabolic and synthesis pathways. Additionally, despite the well-established additive effects for carcinogenicity between AFB1 and other risk factors, e.g., hepatitis viruses B and C, and the hepatotoxic algal microcystins, the mechanisms of this synergy remain unclear. This study reviews the most recent advances in the field of the mechanisms of toxicity of aflatoxins and the adverse health effects that they cause in humans and animals.

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Section: Genetic Polymorphism and Increased Mutagenicity Of Aflatoxinsmentioning

confidence: 99%

Chronic and Acute Toxicities of Aflatoxins: Mechanisms of Action

Benkerroum

2020

IJERPH

316

214

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“…Expression and purification of NEIL1 enzymes were performed according to protocols initially developed for the edited NEIL1 (26,32). The current version of these protocols was recently published (24).…”

Section: Expression and Purification Of Neil1 Enzymesmentioning

confidence: 99%

“…Preparation of high-molecular DNA substrate from commercially available calf thymus DNA using a 60 Co γ-ray source was recently reported (24). DNA samples were γ-irradiated at a dose of either 5 Gy or 20 Gy.…”

Section: Preparation Of High-molecular Dna Substrate For Glycosylase Reactionsmentioning

confidence: 99%

“…For NEIL1-catalyzed reactions, aliquots of γ-irradiated DNA were supplemented with aliquots of stable isotope-labeled analogues of DNA base lesions as internal standards. Incubation of DNA samples with unedited and edited NEIL1, with subsequent analysis of the released DNA base lesions by gas chromatography-tandem mass spectrometry (GC-MS/MS) was performed as described in our prior studies (24,33). The measured levels of the excised DNA base lesions were expressed as number of lesions per 10 6 DNA bases.…”

Section: Neil1-catalyzed Reactions Using High-molecular Weight Dna Substrates and Detection Of Excised Dna Base Lesions By Gas Chromatogrmentioning

confidence: 99%

“…However, the secondary oxidation products of 8-OH-Gua, guanidinohydantoin (Gh) and its isomer, iminoallantoin, both diastereomers of spiroiminodihydantoin (Sp1 and Sp2), and two diastereomers of 5-carboxamido-5-formamido-2-iminohydantoin (R)-2Ih and (S)-2Ih have been found to be excellent substrates for NEIL1 (13)(14)(15)(16)(17)(18). Additional base damage substrates for NEIL1 that have been identified using synthetic oligodeoxynucleotide substrates include: psoralen-induced DNA crosslinks in 3-stranded structures (19), psoraleninduced 4-stranded crosslinks (20), 5-carboxylcytosine (21), methyl-FapyGua (16), amine adducts of hydantoins (22), 8,9-dihydro-8-(2,6-diamino-4-oxo-3,4-dihydropyrimid-5-ylformamido)-9-hydroxyaflatoxin B 1 (AFB 1 -FapyGua) (23,24), and nitrogen mustard-FapyGua (25).…”

Section: Introductionmentioning

confidence: 99%

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Recognition of DNA adducts by edited and unedited forms of DNA glycosylase NEIL1

et al. 2020

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Pre-mRNA encoding human NEIL1 undergoes editing by adenosine deaminase ADAR1 that converts a single adenosine to inosine, and this conversion results in an amino acid change of lysine 242 to arginine. Previous investigations of the catalytic efficiencies of the two forms of the enzyme revealed differential release of thymine glycol (ThyGly) from synthetic oligodeoxynucleotides, with the unedited form, NEIL1 K242 being ≈30-fold more efficient than the edited NEIL1 K242R. In contrast, when these enzymes were reacted with oligodeoxynucleotides containing guanidinohydantoin or spiroiminohydantoin, the edited K242R form was ≈3-fold more efficient than the unedited NEIL1. However, no prior studies have investigated the efficiencies of these two forms of NEIL1 on either high-molecular weight DNA containing multiple oxidatively-induced base damages, or oligodeoxynucleotides containing a bulky alkylated formamidopyrimidine. To understand the extent of changes in substrate recognition, γ-irradiated calf thymus DNA was treated with either edited or unedited NEIL1 and the released DNA base lesions analyzed by gas chromatography-tandem mass spectrometry. Of all *

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Risk stratification and early detection biomarkers for precision HCC screening

et al. 2022

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Hepatocellular carcinoma (HCC) mortality remains high primarily due to late diagnosis as a consequence of failed early detection. Professional societies recommend semi-annual HCC screening in at-risk patients with chronic liver disease to increase the likelihood of curative treatment receipt and improve survival. However, recent dynamic shift of HCC etiologies from viral to metabolic liver diseases has significantly increased the potential target population for the screening, whereas annual incidence rate has become substantially lower. Thus, with the contemporary HCC etiologies, the traditional screening approach might not be practical and cost-effective. HCC screening consists of (i) definition of rational at-risk population, and subsequent (ii) repeated application of early detection tests to the population at regular intervals. The suboptimal performance of the currently available HCC screening tests highlights an urgent need for new modalities and strategies to improve early HCC detection. In this review, we overview recent developments of clinical, molecular, and imaging-based tools to address the current challenge, and discuss conceptual framework and approaches of their clinical translation and implementation. These encouraging progresses are expected to transform the current "one-size-fits-all" HCC screening into

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Characterization of rare NEIL1 variants found in East Asian populations

Cited by 12 publications

References 38 publications

Chronic and Acute Toxicities of Aflatoxins: Mechanisms of Action

Chronic and Acute Toxicities of Aflatoxins: Mechanisms of Action

Recognition of DNA adducts by edited and unedited forms of DNA glycosylase NEIL1

Risk stratification and early detection biomarkers for precision HCC screening

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