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Decreased cADPR and increased NAD+ in the Cd38-/- mouse
Genevieve S Young1, Elena Choleris, Frances E Lund
1Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ont., Canada N1G 3W1. gyoung01@uoguelph.ca
Biochemical and Biophysical Research Communications
|June 6, 2006
Summary
CD38 enzyme activity regulates calcium signaling molecule cyclic ADP-ribose (cADPR) levels. Studies in Cd38 knockout mice reveal reduced cADPR and increased NAD(+) levels, demonstrating CD38
Area of Science:
- Biochemistry
- Cellular Biology
- Physiology
Background:
- CD38 is a glycoprotein catalyzing cyclic ADP-ribose (cADPR) formation from nicotinamide adenine dinucleotide (NAD(+)).
- cADPR acts as an intracellular calcium signaling molecule.
- Previous studies indicated variability in cADPR levels.
Purpose of the Study:
- To investigate the role of CD38 in regulating cADPR and NAD(+) levels.
- To refine the measurement of cADPR using a modified fluorimetric cycling assay.
- To demonstrate the relationship between CD38 and NAD(+) metabolism.
Main Methods:
- Utilized a modified fluorimetric cycling assay to measure cADPR levels.
- Analyzed cADPR and NAD(+) concentrations in brain, lung, and kidney tissues.
- Compared levels in wild-type and Cd38 knockout (Cd38(-/-)) mice.
Main Results:
- Reported significantly decreased cADPR levels in the brain and lung of Cd38(-/-) mice.
- Observed significantly reduced inter-individual variation in cADPR levels compared to previous studies.
- Demonstrated significant increases in brain, lung, and kidney NAD(+) levels in Cd38(-/-) mice.
Conclusions:
- CD38 plays a crucial role in regulating intracellular cADPR levels.
- The modified assay provides more precise measurements of cADPR, suggesting tighter regulatory control.
- Established a direct link between CD38 activity and NAD(+) homeostasis.
