Aldh1l1-P2A-CreERT2 Mouse Model
| Starin Name | C57BL/6N‑Aldh1l1<sup>tm1(P2A‑CreERT2)</sup> |
|---|---|
| Strain Background | C57BL/6N |
Applications
- Astrocyte Physiology & Lineage Tracing: Crossing with Cre‑dependent reporter strains (e.g., mT/mG, Rosa26tdTomato) to trace astrocyte development, heterogeneity, and fate mapping across all brain regions—including GFAP‑low areas (thalamus, cerebellum).
- Neurodegenerative Disease Research: Astrocyte‑specific conditional knockout in models of Alzheimer’s disease, Parkinson’s disease, ALS, and aging‑related neurodegeneration.
- CNS Injury & Neuroinflammation: Studying astrocytic roles in traumatic brain injury, spinal cord injury, encephalitis, multiple sclerosis, and blood‑brain barrier maintenance.
- Liver & Kidney Metabolic Disease: Hepatocyte‑ or renal proximal tubule‑specific gene manipulation to investigate NAFLD/NASH, oxidative stress, one‑carbon metabolism, and drug‑induced organ injury.
- Glia‑Neuron Interaction & Neural Microenvironment: Dissecting astrocyte‑to‑neuron signaling and astrocytic contribution to synaptic modulation and neural homeostasis.
Key Features
- P2A Self‑Cleavage Preserves Native Protein: Aldh1l1ORF and regulatory elements remain intact; P2A mediates >90% efficient stoichiometric release of functional ALDH1L1 and CreERT2—no fusion‑protein artifacts, normal metabolism and development maintained.
- Faithful Aldh1l1 Lineage Specificity: CreERT2 expression mirrors endogenous Aldh1l1—highly specific to astrocytes (including GFAP‑low brain regions), hepatocytes, and renal proximal tubules—with minimal leak and no off‑target recombination in neurons or non‑target tissues (e.g., spleen).
- Tamoxifen‑Inducible Temporal Control: Cytoplasm‑sequestered CreERT2 enters nucleus upon tamoxifen/4‑OHT treatment, allowing postnatal/time‑defined gene deletion to circumvent embryonic lethality or systemic phenotypes.
- Broad Brain Coverage Beyond GFAP‑Cre: Overcomes regional blind spots of GFAP‑driven Cre tools; efficiently targets astrocytes throughout the CNS (cortex, hippocampus, thalamus, cerebellum, brainstem).
Strain Description
Aldh1l1‑P2A‑CreERT2 Inducible Knock‑in Mouse Model (C57BL/6N‑Aldh1l1tm1(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 Aldh1l1gene on the C57BL/6N background. Aldh1l1and CreERT2 are co‑translated as a single polypeptide and cleaved by the P2A peptide in vivo, ensuring faithful, Aldh1l1‑lineage‑specific Cre expression (CNS astrocytes, hepatocytes, renal proximal tubule epithelial cells) while preserving native Aldh1l1 function. Tamoxifen administration triggers nuclear translocation of CreERT2, enabling spatiotemporally controlled conditional gene recombination exclusively in Aldh1l1‑positive cells.
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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