Apoe Knockout mouse — liver specific context
Apoe is the mouse ortholog of human APOE and encodes a 299 residue exchangeable apolipoprotein whose amino-terminal four-helix bundle presents the receptor binding surface for LDLR, LRP1 and heparan sulfate proteoglycans, while the carboxy-terminal domain mediates lipid binding and self-association, together directing clearance of chylomicron remnants and VLDL and controlling brain lipid and amyloid beta handling. Mouse Apoe resembles human APOE4 at the domain interaction level and lacks the human isoform series, so targeted replacement knockins carrying human APOE2, APOE3 or APOE4 coding sequence under the endogenous promoter are the only honest platform for isoform-dependent questions in Alzheimer disease, and they are routinely crossed to amyloid or tau models. Conventional null mice develop marked hypercholesterolemia and spontaneous atherosclerosis on chow, which remains the workhorse cardiovascular readout. Because Apoe and Apoj partially overlap in glial lipid transport, interpret CNS phenotypes with that in mind, and select humanized alleles when testing isoform-selective or ASO based therapeutics.
Whole body loss of Apoe gives the clearest readout when the question is whether the gene is required at all. Follow up tissue work can still move to a conditional allele if lethality or compensation appears. For liver work, plan Cre specificity, reporter crosses, and baseline phenotyping before you scale.
Catalog options
A conventional knockout answers whether the gene is required broadly. When liver is the organ of interest, a global null can still be informative if viability is acceptable and you want the simplest genotype. If the null is harsh, a floxed allele with a regional Cre is the safer long term platform.
| Model | Type | Category | Availability | Catalog # | |
|---|---|---|---|---|---|
| Apoe-KO(2) | Knockout | KO/CKO mice, disease model mice | live | KO 190565 | Inquire |
Designing a Apoe Knockout allele
A whole-locus null remains the most productive single allele here, but be clear about what it models. Hypercholesterolemia in these mice is driven by failure of remnant and VLDL clearance rather than LDL excess, so lesion composition and lipoprotein distribution differ from familial hypercholesterolemia, where an Ldlr null is the better comparator. Delete all four exons rather than interrupting exon 3, since truncated amino-terminal fragments retain some receptor binding and complicate interpretation. Keep the line congenic on C57BL/6 because atherosclerosis susceptibility is strongly strain dependent, and decide up front whether chow-fed spontaneous lesions or Western diet acceleration fits the timeline. When using the null as a sensitized background for a second gene, run a lipid-matched control, since many downstream phenotypes track plasma cholesterol rather than ApoE itself. Score en face aortic lesion area, aortic root sections, FPLC profiles, and hippocampal synaptic markers.
Pricing and quotes
The Apoe Knockout lines listed above are catalog models. Send us the catalog number and our team confirms current availability, pricing, and whether the line ships cryopreserved or live.
If your study needs a Apoe allele configuration that is not listed above, our scientific team designs and generates it. Model generation quotes return in about twenty four hours with milestones for genotyping, QC, and dispatch.
FAQ
What Apoe Knockout mouse models are available?
When Apoe Knockout lines are in catalog, we ship from inventory. If your configuration is not listed, we design the allele to order. Common paths include conditional knockout, constitutive knockout, humanized, knockin, and transgenic options, with documented germline transmission and United States QC.
Is Apoe knockout embryonic lethal in mice?
It depends on background and allele design. Some Apoe germline knockouts are viable. Others need conditional alleles or mixed backgrounds. We review publications and our own experience, then recommend floxed versus null before you commit.
Which Cre driver is best for liver specific focused experiments?
Driver choice depends on onset timing, recombination efficiency, and known leak. We map your organ and cell type to a short list of proven Cre lines, then talk through reporter crosses and controls. Your note points to liver specific, so we start driver selection there.
Do you ship live Apoe animals?
When catalog lines are live, we ship with health certificates and QC documentation. If your exact combo is not listed, we quote a generation project with cryo or live dispatch depending on cohort timing and geography.
How do I request a quote for Apoe?
Use the catalog inquire buttons or the request quote form. Include your allele goal, Cre plan if any, strain background, and cohort size. A PhD led team responds with pricing, milestones, and the fastest path to experimental animals.
Citations
- Loss of SPRR3 in ApoE-/- mice leads to atheroma vulnerability through Akt dependent and independent effects in VSMCs
- NK Cell Maturation and Cytotoxicity Are Controlled by the Intramembrane Aspartyl Protease SPPL3
- Group X secretory phospholipase A(2) augments angiotensin II-induced inflammatory responses and abdominal aortic aneurysm formation in apoE-deficient mice.