B6.129S-Lipg^tm1Tq/J

Stock number: 005681
Product name: LIPG-
Research areas: Cardiovascular Research, Cell Biology Research

Description

These Lipg knock-out mice exhibit increased fasting plasma levels of total cholesterol, high-density lipoprotein (HDL) cholesterol, and phospholipids. They are suitable for use in cholesterol-related studies.

Detailed description

Homozygous mice are viable and do not display any behavioral or histological defects. Although homozygotes are fertile, the donating investigator reports decreased fecundity. Northern blot analysis showed no endogenous gene expression in lung, liver, kidney, spleen, or aorta. Homozygotes have increased fasting plasma levels of total cholesterol, high-density lipoprotein (HDL) cholesterol, and phospholipids compared to wild type. Mutant mouse plasma apoA-I is increased while heparin-releasable phospholipase activity is impaired. Homozygous null mice have decreased arterial endothelium monocyte adhesion. This mutant can be used in studies of lipoprotein metabolism, atherosclerotic vascular disease, and other cholesterol-related studies.

Development

A targeting vector containing a neomycin resistance gene was used to replace exon 1 of the endogenous gene. The construct was electroporated into 129S6/SvEv-derived TL-1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts. A resulting chimeric male was backcrossed to a C57BL/6J female. Heterozygous pups were bred to C57BL/6J for at least six generations before being interbred.

Allele

Symbol: Lipg^tm1Tq
Name: targeted mutation 1, Thomas Quertermous
MGI accession ID: MGI:2450672
Generation method: Targeted
Attributes: Null/Knockout
Synonyms: LIPG^-
Marker symbol: Lipg
Marker name: lipase, endothelial
Marker synonyms: 3110013K01Rik; EDL; EL; endothelial lipase; lipase; mEDL; PRO719
Chromosome: 18
Strain of origin: 129S6/SvEvTac
Molecular note: The gene was disrupted by insertion of a neomycin resistance cassette into exon 1 via homologous recombination. Absence of gene expression in homozygous mutant animals was confirmed by Northern blot analysis of lung, kidney, aorta, liver, and heart.