Research Models
APOE3 knock-in (Cornell)
Species: Mouse
Genes: APOE
Modification: APOE: Knock-In
Disease Relevance: Alzheimer's Disease
Strain Name: N/A
Genetic Background: C57BL/6J
Availability: Available through Li Gan. Requestors must complete a standard MTA with Weill Cornell Medicine.
These knock-in mice express human APOE3 under the control of mouse regulatory elements. Thus far, these mice have been used as controls for studies of the effects of the APOE Christchurch mutation (Naguib et al., 2025). (See APOE3Ch (Cornell) and APOE3Ch (Cornell) x PS19.)
Modification details
Human APOE3 cDNA with a poly A tail was inserted immediately upstream of the ATG start codon of the mouse Apoe gene. Expression of human APOE3 is controlled by the mouse Apoe promoter and regulatory elements, and the mouse Apoe gene is inactivated.
Last Updated: 21 Aug 2025
References
Mutations Citations
Research Models Citations
Paper Citations
- Naguib S, Lopez-Lee C, Torres ER, Lee SI, Zhu J, Zhu D, Ye P, Norman K, Zhao M, Wong MY, Ambaw YA, Muñoz-Castañeda R, Wang W, Patel T, Bhagwat M, Norinsky R, Mok SA, Walther TC, Farese RV Jr, Luo W, Sinha SC, Wu Z, Fan L, Gong S, Gan L. The R136S mutation in the APOE3 gene confers resilience against tau pathology via inhibition of the cGAS-STING-IFN pathway. Immunity. 2025 Jun 18; Epub 2025 Jun 18 PubMed.
Further Reading
No Available Further Reading
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