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Ncr1-CreERT2 Mouse Model
| Strain Name | C57BL/6NMcl- Ncr1<sup>tm1(P2A-CreERT2)</sup>/MCL |
|---|---|
| Editing Type | Knock-In |
| Gene Name | Ncr1/Natural cytotoxicity triggering receptor 1 |
| Gene Synonyms | NKp46, Ly94 |
| Strain Background | C57BL/6N |
| NCBI No. | Gene ID: 17079 / MGI: 1333806 |
- Studies on NK cell development and maturation
- Research on NK cell antiviral immunity
- Research on tumor immune surveillance and immunotherapy
- Research on ILC1 biological functions
- Research on NKp46-positive ILC3 and mucosal immunity
- Research on innate lymphoid cell lineage tracing
- Conditional modification of genes in NKp46-positive cells
This line was generated by precisely inserting a P2A-CreERT2 expression cassette at the end of the murine Ncr1 coding sequence, immediately before the stop codon. Ncr1 and CreERT2 are co-expressed from the same open reading frame; during translation, P2A mediates ribosomal skipping, such that the upstream NKp46 protein and the downstream CreERT2 recombinase are produced as independent proteins rather than a full NKp46-CreERT2 fusion protein [1]. CreERT2 consists of Cre recombinase fused to a mutated estrogen receptor ligand-binding domain; upon tamoxifen administration, CreERT2 translocates into the nucleus and mediates loxP recombination, enabling temporally controlled genetic modification [2].
Ncr1 encodes the natural cytotoxicity receptor NKp46. The inducible Cre system driven by Ncr1 regulatory elements can be used to label NKp46-positive cell populations, including conventional NK cells, a subset of tissue-resident NK cells, ILC1s, and NKp46-positive ILC3s [3]. Therefore, when Ncr1-P2A-CreERT2 mice are crossed with mice carrying floxed alleles or Cre-dependent reporter genes, and tamoxifen is administered at the appropriate time, conditional gene knockout, knock-in, or lineage tracing can be performed in Ncr1-positive cells and their progeny at the time of induction.
References
- Donnelly MLL, Luke G, Mehrotra A, et al. Analysis of the aphthovirus 2A/2B polyprotein “cleavage” mechanism indicates not a proteolytic reaction, but a novel translational effect: a putative ribosomal “skip”. J Gen Virol. 2001;82(Pt 5):1013-1025.
- Feil R, Wagner J, Metzger D, Chambon P. Regulation of Cre recombinase activity by mutated estrogen receptor ligand-binding domains. Biochem Biophys Res Commun. 1997;237(3):752-757.
- Nabekura T, Lanier LL. Tracking the fate of antigen-specific versus cytokine-activated natural killer cells after cytomegalovirus infection. J Exp Med. 2016;213(12):2745-2758.
- Endogenous Expression Drive: CreERT2 expression is controlled by endogenous Ncr1 regulatory elements.
- Independent Protein Expression: P2A mediates separate expression of NKp46 and CreERT2.
- Temporal Control: Cre-mediated loxP recombination initiates upon tamoxifen induction.
- NKp46-Positive Cell Coverage: Suitable for studies on NK cells, ILC1s, and NKp46-positive ILC3s.
- Conditional Genetic Manipulation: Compatible with floxed alleles or Cre-dependent reporter systems.
FAQ
Game-changing benefits？
While competitors highlight germline efficiency gains, shorter timelines and enhanced 3Rs animal welfare benefits for their technologies, these are merely incremental improvements over traditional approaches. In sharp contrast, our proprietary technology delivers fully pure, homogeneous lineages—every single cell of the mice is derived exclusively from totipotent ES cells, with guaranteed 100% germline transmission efficiency. To experience these unparalleled benefits firsthand, enquire about your custom mouse model project with us or order embryos for in-house validation at your facility.
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