Homozygous Apoa2tm1Bres knockout mice exhibit reductions in HDL cholesterol levels and in HDL particle size.
Dr. Jan L. Breslow, Rockefeller University
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.
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 Name||targeted mutation 1, Jan L Breslow|
|Allele Type||Targeted (Null/Knockout)|
|Allele Synonym(s)||apoA-II -|
|Gene Symbol and Name||Apoa2, apolipoprotein A-II|
|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.|
|Mutations Made By|| |
Dr. Jan Breslow, Rockefeller University
When maintaining a live colony, homozygous mice are bred together.
When using the apoA-II KO mouse strain in a publication, please cite the originating article(s) and include JAX stock #006258 in your Materials and Methods section.