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The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.

A novel endothelial-derived lipase that modulates HDL metabolism

Jaye, Michael, Lynch, Kevin J., Krawiec, John, Marchadier, Dawn, Maugeais, Cyrille, Doan, Kim, South, Victoria, Amin, Dilip, Perrone, Mark, Rader, Daniel J.·1999·Nature Genetics
DOI 10.1038/7766
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Abstract

High-density lipoprotein (HDL) cholesterol levels are inversely associated with risk of atherosclerotic cardiovascular disease. At least 50% of the variation in HDL cholesterol levels is genetically determined, but the genes responsible for variation in HDL levels have not been fully elucidated. Lipoprotein lipase (LPL) and hepatic lipase (HL), two members of the triacylglyerol (TG) lipase family, both influence HDL metabolism and the HL (LIPC) locus has been associated with variation in HDL cholesterol levels in humans. We describe here the cloning and in vivo functional analysis of a new member of the TG lipase family. In contrast to other family members, this new lipase is synthesized by endothelial cells in vitro and thus has been termed endothelial lipase (encoded by the LIPG gene). EL is expressed in vivo in organs including liver, lung, kidney and placenta, but not in skeletal muscle. In contrast to LPL and HL, EL has a lid of only 19 residues. EL has substantial phospholipase activity, but less triglyceride lipase activity. Overexpression of EL in mice reduced plasma concentrations of HDL cholesterol and its major protein apolipoprotein A-I. The endothelial expression, enzymatic profile and in vivo effects of EL suggest that it may have a role in lipoprotein metabolism and vascular biology.

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Crossref · 10.1038/7766

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2 of 2 references verified0 citation errors · 0 not checkable

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  • EL belongs to the same lipase family as LPL, but targets phospholipids on the shell of high-density lipoproteins (HDL), leading to decreased HDL levels.

    “EL belongs to the same lipase family as LPL, but targets phospholipids on the shell of high-density lipoproteins (HDL), leading to decreased HDL levels (119–122).”

    From Regulation of lipoprotein metabolism by ANGPTL3, ANGPTL4, and ANGPTL8 (2021) · cites this paper as [119]

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Research works printed but not linked: 25

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Metadata

Authors
Jaye, M., Lynch, K. J., Krawiec, J., Marchadier, D., Maugeais, C., Doan, K., South, V., Amin, D., Perrone, M., & Rader, D. J.
Venue
Nature Genetics
Publisher
Springer Science and Business Media LLC
Published
1999-04
Volume
21
Issue
4
Pages
424-428
ISSN
  • 1061-4036
  • 1546-1718
DOI
10.1038/7766
Cited by
427
References
2
Language
en
Licence
www.springer.com/tdm (tdm)

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