These Apoa4 knock-out mice show low levels of plasma cholesterol, free fatty acids, and both high density and very low density lipoproteins.
Dr. Jan L. Breslow, Rockefeller University
Mice homozygous for this targeted mutation are viable and fertile with no protein detectable in plasma, liver, or intestinal tissues. Homozygotes have decreased plasma levels of cholesterol, free fatty acids, and high density (HDL) and very low density lipoprotein (VLDL). These mice may be useful in studies of lipid metabolism, atherosclerosis, heart disease, appetite regulation, intestinal lipid absorption, or inflammatory bowel disease.
A targeting vector was designed to replace exon 1 of the endogenous gene 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-IV -|
|Gene Symbol and Name||Apoa4, apolipoprotein A-IV|
|Strain of Origin||129S4/SvJae|
|Molecular Note||A 1.1kb genomic fragment containing exon 1 and intron 1 was replaced with a neomycin selection cassette. No transcript was detectable in northern blot analysis on intestinal RNA from homozygous mice, and western blot analysis demonstrated that no stable protein was detectable in plasma of homozygous mice.|
|Mutations Made By|| |
Dr. Jan Breslow, Rockefeller University
When maintaining a live colony, homozygous mice are bred together.
When using the apoA-IV KO mouse strain in a publication, please cite the originating article(s) and include JAX stock #006404 in your Materials and Methods section.