B6;129S4-Apoa2^tm1Bres/J

Stock number: 006258
Product name: apoA-II KO
Research areas: Cardiovascular Research, Diabetes and Obesity Research, Metabolism Research, Research Tools

Description

Homozygous Apoa2^tm1Bres knockout mice exhibit reductions in HDL cholesterol levels and in HDL particle size.

Detailed description

Mice homozygous for this targeted mutation are viable and fertile. Homozygous mice have no detectable transcripts in liver tissues and the high density lipoprotein (HDL) particle size is reduced. Homozygotes have decreased plasma levels of HDL cholesterol and free fatty acids in both fed and fasted states. In addition, the plasma concentration of fasting glucose and insulin is decreased. These mice may be useful in studies of lipid metabolism, atherosclerosis, heart disease, insulin resistance and diabetes.

Development

A targeting vector was designed to almost completely remove the four exons of the endogenous gene and replace them with a neomycin resistance gene. This construct was electroporated into 129S4/SvJae-derived J1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6J blastocysts. Chimeric mice were bred with C57BL/6J and the resulting heterozygous offspring were bred together for many generations prior to arrival at The Jackson Laboratory.

Allele

Symbol: Apoa2^tm1Bres
Name: targeted mutation 1, Jan L Breslow
MGI accession ID: MGI:2157148
Generation method: Targeted
Attributes: Null/Knockout
Synonyms: apoA-II -
Marker symbol: Apoa2
Marker name: apolipoprotein A-II
Marker synonyms: Alp-2; Apoa-2; APOAII; Apo-AII; ApoA-II; Hdl-1
Chromosome: 1
Strain of origin: 129S4/SvJae
Molecular note: A genomic fragment containing exons 1-3 and part of exon 4 was replaced with a neomycin selection cassette. Northern blot analysis on total liver RNA demonstrated that the transcript was not detectable in homozygous mice, and the encoded protein was not detected in HDL isolates of plasma derived from homozygous mice.