Apoe Knockout Mice
Apoe Knockout Mice - Related Videos
09:56
Improved Genome Editing via Oviductal Nucleic Acids Delivery-based In Vivo Electroporation Technique for Knockout Mice Generation
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2025
The efficiency of the Improved Genome Editing via Oviductal Nucleic Acids Delivery (I-GONAD) method is comparable to traditional microinjection, which requires zygote collection from donor females and transfer to pseudo-pregnant females. This protocol demonstrates its effectiveness by introducing CRISPR/Cas9-induced mutations into the ROSA26 locus on chromosome 6.
05:47
A Modified Surgical Model of Hind Limb Ischemia in ApoE-/- Mice using a Miniature Incision
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Cited by 3 •
2021
This article demonstrates an efficient surgical approach to establish acute ischemia in mice with a small incision. This approach can be applied by most research groups without any laboratory upgrades.
10:59
Production of Apolipoprotein C-III Knockout Rabbits using Zinc Finger Nucleases
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Cited by 32 •
2013
Recent development in gene targeting tools makes production of knockout (KO) rabbits possible. In the present work, we generated five Apolipoprotein (Apo) C-III KO rabbits using Zinc Finger Nucleases (ZFN). This work demonstrated that ZFN is a highly efficient method to produce KO rabbits.
04:13
CRISPR Concatemer-Mediated Multiple Gene Knockout: A Technique to Simultaneously Knockout Multiple Genes by Non-Homologous End-Joining Pathway in Mouse Intestinal Cells
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2025
This video describes a gene knockout technique using a CRISPR-concatemer to simultaneously knock out multiple genes in cultured mouse intestinal organoid cells. This method is used to knock out a diseased gene and to elucidate the function of a gene and its paralogues.
01:11
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase
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2026
Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
FAQs
Loss of ApoE disrupts the transport and clearance of lipid-rich lipoprotein particles from the blood, so remnant particles are not efficiently removed. This changes the animals’ plasma lipid environment and creates conditions that favor plaque formation. The model therefore links a defined defect in lipoprotein processing with downstream vascular disease, helping researchers study how lipid imbalance contributes to atherosclerosis.
Because these mice already have impaired remnant clearance, adding dietary fat and cholesterol intensifies the lipid burden associated with plaque development. Diet consequently acts as an environmental variable that can alter disease progression rather than merely serving as background nutrition. Researchers can use this contrast to examine how inherited susceptibility and dietary exposure jointly influence atherosclerotic risk.
Apoe knockout mice allow investigators to examine lipid metabolism alongside vascular inflammation and plaque development in the same disease setting. This is important because cardiovascular disease is not represented only by elevated plasma cholesterol; the model supports investigation of how altered lipid handling relates to inflammatory vascular changes and progressive atherosclerosis.
Studies commonly examine plasma cholesterol, plaque formation or progression, and vascular inflammation. Together, these outcomes show how the ApoE-related lipid defect is expressed systemically and in blood vessels. Tracking them helps investigators assess disease severity and determine whether a genetic, dietary, or therapeutic intervention changes the cardiovascular phenotype.
Researchers compare disease-related outcomes in animals exposed to a candidate lipid-lowering or anti-atherosclerotic therapy, using the model’s spontaneous plaque phenotype as a test setting. Changes in plasma cholesterol, plaque development, or vascular inflammation can help indicate whether an intervention affects relevant features of cardiovascular disease.
A researcher would choose this model when the study requires spontaneous atherosclerotic disease together with elevated plasma cholesterol and a manipulable dietary context. It is especially relevant for questions about lipid metabolism, plaque development, vascular inflammation, or cardiovascular therapies, rather than investigations unrelated to lipid-driven vascular disease.