Increased peripheral lipid clearance in an animal model of amyotrophic lateral sclerosis
Open Access
- 1 July 2007
- journal article
- Published by Elsevier in Journal of Lipid Research
- Vol. 48 (7) , 1571-1580
- https://doi.org/10.1194/jlr.m700017-jlr200
Abstract
No abstract availableKeywords
All Related Versions
This publication has 39 references indexed in Scilit:
- Gene transfer demonstrates that muscle is not a primary target for non-cell-autonomous toxicity in familial amyotrophic lateral sclerosisProceedings of the National Academy of Sciences, 2006
- Molecular biology of amyotrophic lateral sclerosis: insights from geneticsNature Reviews Neuroscience, 2006
- Triglyceride-rich lipoprotein metabolism in unique VLDL receptor, LDL receptor, and LRP triple-deficient miceJournal of Lipid Research, 2005
- The R6/2 transgenic mouse model of Huntington's disease develops diabetes due to deficient β-cell mass and exocytosisHuman Molecular Genetics, 2005
- The VLDL receptor plays a major role in chylomicron metabolism by enhancing LPL-mediated triglyceride hydrolysisJournal of Lipid Research, 2004
- Up‐regulation of mitochondrial uncoupling protein 3 reveals an early muscular metabolic defect in amyotrophic lateral sclerosisThe FASEB Journal, 2003
- The Enzymes, Regulation, and Genetics of Bile Acid SynthesisAnnual Review of Biochemistry, 2003
- Very Low Density Lipoprotein (VLDL) Receptor-deficient Mice Have Reduced Lipoprotein Lipase ActivityJournal of Biological Chemistry, 2002
- Gastrointestinal dysfunction in amyotrophic lateral sclerosisAmyotrophic Lateral Sclerosis, 2000
- Mutations in Cu/Zn superoxide dismutase gene are associated with familial amyotrophic lateral sclerosisNature, 1993