Aging and kinase kinetics of Y77E11.A and Y17G7B.10 in C. Elegans
Location
Ballroom
Start Date
4-12-2019 9:00 AM
End Date
4-12-2019 2:30 PM
Poster Number
18
Faculty Sponsor’s Department
Biomedical Sciences
Name of Project's Faculty Sponsor
Dr. Patrick Bradshaw
Type
Poster: Competitive
Project's Category
Stress Response, Alzheimers Disease
Abstract or Artist's Statement
Aging and kinase kinetics of Y77E11.A and Y17G7B.10 in C. Elegans
Jacob Goodlaxson, Department of Biomedical Sciences, College of Medicine, East Tennessee State University, Johnson City, TN.
The free radical theory of aging suggests that free radical induced oxidative damage may play a role in the pathogenesis of age-related neurological diseases. The reduced form of nicotinamide adenine dinucleotide phosphate (NADPH) protects against redox stress by providing reducing equivalents to antioxidants such as glutathione and thioredoxin. A measurement of the kinase kinetics of nicotinamide adenine dinucleotide demonstrated a decline in the rate of conversion from NAD into NADP. A homeostatic relationship of NADPH and NADP+ in mitochondria and cytosol may prevent the progression of aging due to the amelioration of the reactive oxygen species (ROS), and other charged particles. The NAPD+ cation is the chief acceptor of negatively charged particles which ionize and create free radical ions. Two previously uncharacterized proteins, Y77E11.A (NADK1) and Y17G7B.10 (NADK2), were studied for their possible kinetic role in producing and maintaining NADPH levels. The roles of NADK1 and NADK2 were determined by taking whole worm lysates of Caenorhabditis elegans deficient of these proteins, followed by supplementation with NAD, then monitoring of NADP levels. These two proteins were statistically important in the conversion of NAD to NADP+. These NADK’s displayed statistically significant reduction in NADP production which could lead to more redox stress. This research indicates that pro-longevity therapies should aim to maintain elevated levels of NADPH and NADP+ to hinder the aging process.
Aging and kinase kinetics of Y77E11.A and Y17G7B.10 in C. Elegans
Ballroom
Aging and kinase kinetics of Y77E11.A and Y17G7B.10 in C. Elegans
Jacob Goodlaxson, Department of Biomedical Sciences, College of Medicine, East Tennessee State University, Johnson City, TN.
The free radical theory of aging suggests that free radical induced oxidative damage may play a role in the pathogenesis of age-related neurological diseases. The reduced form of nicotinamide adenine dinucleotide phosphate (NADPH) protects against redox stress by providing reducing equivalents to antioxidants such as glutathione and thioredoxin. A measurement of the kinase kinetics of nicotinamide adenine dinucleotide demonstrated a decline in the rate of conversion from NAD into NADP. A homeostatic relationship of NADPH and NADP+ in mitochondria and cytosol may prevent the progression of aging due to the amelioration of the reactive oxygen species (ROS), and other charged particles. The NAPD+ cation is the chief acceptor of negatively charged particles which ionize and create free radical ions. Two previously uncharacterized proteins, Y77E11.A (NADK1) and Y17G7B.10 (NADK2), were studied for their possible kinetic role in producing and maintaining NADPH levels. The roles of NADK1 and NADK2 were determined by taking whole worm lysates of Caenorhabditis elegans deficient of these proteins, followed by supplementation with NAD, then monitoring of NADP levels. These two proteins were statistically important in the conversion of NAD to NADP+. These NADK’s displayed statistically significant reduction in NADP production which could lead to more redox stress. This research indicates that pro-longevity therapies should aim to maintain elevated levels of NADPH and NADP+ to hinder the aging process.