Lessons learned from the mouse model of short-chain acyl-CoA dehydrogenase deficiency.
The SCAD deficient mouse model has been useful to investigate mechanisms of deficient fatty acid oxidation disease in human patients. This mouse model has been thoroughly characterized and is readily available from the Jackson Laboratory. Using the new technologies of gene-knockout mouse modeling, we envisage developing additional members of the acyl-CoA dehydrogenase family of enzyme deficiencies in mice and furthering our understanding of fatty acid metabolism in health and disease.
Wood
P A
PA
Department of Comparative Medicine, School of Medicine, University of Alabama at Birmingham 35294-0019, USA.
Kelly-Kurtz
C L
CL
Hinsdale
M E
ME
Hamm
D A
DA
Rhead
W J
WJ
D042964:Acyl-CoA Dehydrogenase; D044944:Acyl-CoA Dehydrogenases / Q000172:deficiency* / Q000235:genetics* / Q000378:metabolism; D000818:Animals; D004195:Disease Models, Animal; D005091:Exons; D006801:Humans; D007438:Introns; D008052:Lipid Metabolism, Inborn Errors / Q000201:enzymology* / Q000235:genetics; D051379:Mice; D008815:Mice, Inbred Strains; D018345:Mice, Knockout; D017384:Sequence Deletion
D044944:Acyl-CoA Dehydrogenases; D042964:Acyl-CoA Dehydrogenase