Homozygous Pdzk1tm1Dls knock-out mice exhibit decreased HDL receptor scavenger receptor B-I levels.
Dr. David L. Silver, Albert Einstein College of Medicine
Mice homozygous for this targeted mutation are viable and fertile. Liver tissue from homozygous mutant mice lacks endogenous protein expression. Homozygotes, but not heterozygotes, have significantly decreased (~85-95%) hepatic high density lipoprotein (HDL) receptor scavenger receptor B-I (SR-BI) levels. This decrease is further exacerbated following diet supplementation with the PPAR-alpha activator fenofibrate. These mice may be useful in studies of cardiovascular health and atherosclerosis, lipid metabolism, SR-B1 regulation, kidney function, as well as kidney transporter (e.g. urate transporter) regulation and liver organic anion transport.
A targeting vector was designed to replace exon 1 and part of intron 1 of the endogenous gene with a neomycin resistance cassette. This construct was electroporated into 129S6/SvEvTac-derived CSL3 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6J blastocysts. Chimeric mice were bred with C57BL/6J to generate heterozygous mice on this mixed B6;129S6 genetic background. Heterozygotes were then bred together for many generations prior to arrival at The Jackson Laboratory.
|Allele Name||targeted mutation 1, David L Silver|
|Allele Type||Targeted (Null/Knockout)|
|Gene Symbol and Name||Pdzk1, PDZ domain containing 1|
|Strain of Origin||129S6/SvEvTac|
|Molecular Note||Exon 1, containing the ATG, and part of intron 1 were replaced by neomycin resistance cassette. Western blot of mutant liver lysates confirmed absence of protein.|
|Mutations Made By|| |
Dr. David Silver, Albert Einstein College of Medicine
When maintaining a live colony, homozygous mice may be bred together.
When using the PDZK1 KO mouse strain in a publication, please cite the originating article(s) and include JAX stock #006208 in your Materials and Methods section.