A5109142945- Coenzyme Q10 studies and effects
- DNA Repair Mechanisms
- Carcinogens and Genotoxicity Assessment
- Mitochondrial Function and Pathology
- Mycotoxins in Agriculture and Food
- CRISPR and Genetic Engineering
- Advanced Glycation End Products research
- Photosynthetic Processes and Mechanisms
- Adipose Tissue and Metabolism
- Genomics, phytochemicals, and oxidative stress
- Redox biology and oxidative stress
- RNA regulation and disease
- Epigenetics and DNA Methylation
- Diet and metabolism studies
- Acute Lymphoblastic Leukemia research
- Hearing, Cochlea, Tinnitus, Genetics
- Sesame and Sesamin Research
- RNA Interference and Gene Delivery
- RNA and protein synthesis mechanisms
- Metabolism and Genetic Disorders
- Protist diversity and phylogeny
- Plant Pathogens and Resistance
- Cardiovascular Syncope and Autonomic Disorders
- Molecular Biology Techniques and Applications
- Escherichia coli research studies
Oregon Health & Science University
2013-2025
Rosalind Franklin University of Medicine and Science
2007
Duke Medical Center
1969
Endogenously formed reactive oxygen species continuously damage cellular constituents including DNA. These challenges, coupled with exogenous exposure to agents that generate species, are both associated normal aging processes and linked cardiovascular disease, cancer, cataract formation, fatty liver disease. Although not all of these diseases have been definitively shown originate from mutations in nuclear DNA or mitochondrial DNA, repair oxidized, saturated, ring-fragmented bases via the...
Oxidative damage to DNA is mainly repaired via base excision repair, a pathway that catalyzed by glycosylases such as 8-oxoguanine glycosylase (OGG1). While OGG1 has been implicated in maintaining genomic integrity and preventing tumorigenesis, we report novel role for altering cellular whole body energy homeostasis. OGG1-deficient (Ogg1(-/-)) mice have increased adiposity hepatic steatosis following exposure high-fat diet (HFD), compared wild-type (WT) animals. Ogg1(-/-) animals also higher...
Abstract Obesity and related metabolic pathologies represent a significant public health concern. is associated with increased oxidative stress that damages genomic mitochondrial DNA. Oxidatively-induced lesions in both DNA pools are repaired via the base-excision repair pathway, initiated by glycosylases such as 8-oxoguanine glycosylase (OGG1). Global deletion of OGG1 common polymorphisms render mice humans susceptible to disease. However, relative contribution this phenotype unknown. Here,...
Significance Human dietary exposures to aflatoxin in some of the most populated and underdeveloped portions world are a major contributing factor formation human hepatocellular carcinomas (HCCs) that account for over 700,000 deaths annually. Although genomic signatures aflatoxin-driven carcinogenesis G:C T:A point mutations arising from bypass aflatoxin-induced DNA adducts, maintenance genome stability has been generally attributed nucleotide excision repair. However, we present three lines...
The DNA repair enzyme NEIL1 is a glycosylase that involved in the first step of base excision (BER) oxidatively induced damage. exhibits strong preference for 4,6-diamino-5-formamidopyrimidine (FapyAde) and 2,6-diamino-4-hydroxy-5-formamidopyrimidine (FapyGua) from with no specificity 8-hydroxyguanine (8-OH-Gua). In this study, we report on significant accumulation (5'R)-8,5'-cyclo-2'-deoxyadenosine (R-cdA) (5'S)-8,5'-cyclo-2'-deoxyadenosine (S-cdA) liver neil1(-/-) mice were not exposed to...
Exposure to chronic and acute oxidative stress is correlated with many human diseases, including, but not limited to, cancer, heart disease, diabetes, obesity. In addition cellular lipids proteins, can result in damage DNA bases, especially mitochondrial DNA. We previously described the development of spontaneous late-onset obesity, hepatic steatosis, hyperinsulinemia, hyperleptinemia mice that are deficient glycosylase nei-like 1 (NEIL1), which initiates base excision repair several...
Dietary exposure to aflatoxin B1 (AFB1) is a significant contributor the incidence of hepatocellular carcinomas globally. AFB1 leads formation AFB1-N7-guanine (AFB1-N7-Gua) and two diastereomers imidazole ring-opened 8,9-dihydro-8-(2,6-diamino-4-oxo-3,4-dihydropyrimid-5-yl-formamido)-9-hydroxyaflatoxin (AFB1-FapyGua) in DNA. These adducts lead G → T transversion mutations with adduct being more mutagenic than cationic species. Accurate measurement these three as biomarkers DNA urine will...
<p>Background trinucleotide context counts</p>
<div>Abstract<p>Dietary exposure to aflatoxin B<sub>1</sub> (AFB<sub>1</sub>) is a risk factor for the development of hepatocellular carcinomas. Following metabolic activation, AFB<sub>1</sub> reacts with guanines form covalent DNA adducts, which induce high-frequency G > T transversions. The molecular signature associated these mutational events aligns single-base substitution 24 (SBS24) in Catalog Somatic Mutations Cancer database....
<p>Mutation frequencies in the Chr13 and Chr19 targets</p>
<p>Proportions of mutations in transcribed, un-transcribed, bidirectional and non-transcribed regions</p>
<p>Spontaneous mutation subtypes</p>
<p>Proportion of mutation subtypes</p>
<p>Mutation frequencies in target regions aflatoxin-exposed mice</p>
<p>Read depth across genomic targets</p>
<p>Heatmap of cosine similarity scores</p>
<p>Trinucleotide mutation spectra in aflatoxin-exposed mice</p>
<p>Locations and regions of targets</p>
<p>Assay performance metrics</p>
<p>Cosine similarity scores</p>
<p>Frequency of total mutations, SBS, insertions, deletions and MBS</p>
<p>Mutation frequencies of multiple nucleotide variants, deletions and insertions</p>
<p>Mutation frequencies in target regions unexposed mice</p>
<p>Trinucleotide mutation spectra in unexposed mice</p>