Csf1r-P2A-CreERT2 Mouse Model
| Starin Name | C57BL/6N‑Csf1r<sup>tm1(P2A‑CreERT2)</sup> |
|---|---|
| Strain Background | C57BL/6N |
Applications
- Myeloid‑Cell–Mediated Immunity: Conditional knockout in macrophages, monocytes, and MDSCs to study innate immune activation, antigen presentation, and immunosuppressive polarization.
- Tumor Microenvironment (TME) & TAM Research: Macrophage‑specific gene manipulation to investigate tumor‑associated macrophage (TAM) function, CSF‑1R–dependent survival, and combination immuno‑oncology (anti‑CSF‑1R + anti‑PD‑1/PD‑L1).
- Bone Metabolism & Osteoclast Biology: Osteoclast‑specific gene deletion to model osteoporosis, bone metastasis, and osteolytic disease mechanisms.
- Neuro‑immune Interaction & Microglia Studies: Microglia‑specific conditional manipulation to explore CNS homeostasis, neuroinflammation (Alzheimer’s, Parkinson’s, MS), and brain tumor microenvironment.
- Inflammatory & Fibrotic Disease Modeling: Myeloid‑specific gene ablation in models of rheumatoid arthritis, colitis, hepatic/skin repair, and macrophage polarization (M1/M2 switching).
Key Features
- P2A Self‑Cleavage Preserves Native Protein: Csf1rORF and regulatory elements remain intact; P2A mediates stoichiometric release of functional CSF‑1R and CreERT2—no fusion‑protein artifacts, normal myeloid development maintained.
- Faithful Myeloid Lineage Specificity: CreERT2 expression mirrors endogenous Csf1r, targeting monocytes/macrophages, osteoclasts, and microglia with minimal leak; validated by mT/mG reporter showing recombination only in brain microglia, splenic red‑pulp/window‑zone macrophages—no signal in non‑target tissues (e.g., heart).
- Tamoxifen‑Inducible Temporal Control: Cytoplasm‑sequestered CreERT2 enters nucleus upon 4‑OHT/tamoxifen treatment, allowing postnatal/post‑developmental gene deletion to circumvent embryonic lethality or systemic phenotypes.
- Avoids Off‑Target & Developmental Confounds: Inducible design eliminates interpretive ambiguity from constitutive knockout; high recombination efficiency with low background in standard tamoxifen dosing regimens.
Strain Description
Csf1r‑P2A‑CreERT2 Inducible Knock‑in Mouse Model (C57BL/6N‑Csf1rtm1(P2A‑CreERT2)/MCL)
This model is generated by precise insertion of a P2A‑CreERT2 (tamoxifen‑inducible Cre recombinase fused to estrogen receptor ligand‑binding domain) cassette immediately after the stop codon of the endogenous Csf1rgene on the C57BL/6N background. Csf1rand CreERT2 are co‑translated as a single polypeptide and cleaved by the P2A peptide in vivo, ensuring faithful, myeloid‑lineage‑specific Cre expression without disrupting endogenous CSF‑1R function. Tamoxifen administration triggers nuclear translocation of CreERT2, enabling spatiotemporally controlled conditional gene recombination exclusively in Csf1r‑positive cells (monocytes, macrophages, osteoclasts, microglia).
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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