Ank3 E35 deletion mouse model for neuronal excitability research
This technology is a CRISPR-generated Ank3 E35a deletion mouse model that enables research into neuron type-specific calcium signaling, interneuron excitability, and neuropsychiatric disease relevant brain circuitry.
Unmet Need: Translational models for ANK3-linked psychiatric disease mechanisms
ANK3 is a major genetic risk factors for bipolar disorder and has also been implicated in other neuropsychiatric conditions, including schizophrenia and autism, yet the mechanisms linking ANK3 variation to disease-relevant brain dysfunction remain poorly defined. Current psychiatric disease models often rely on broad gene disruption or behavioral readouts, which fail to capture neuron type-specific effects of ANK3 isoforms excitability, calcium signaling, and cortical circuit function. This limits the ability to connect ANK3-associated molecular changes to measurable neuronal phenotypes for target validation, biomarker discovery, and therapeutic screening. Such models could help identify interventions that normalize disease-relevant interneuron activity and calcium signaling rather than broadly targeting psychiatric symptoms after they emerge.
The Technology: ANK3 microexon deletion mouse model for psychiatric disease research
This technology is a mouse model that carries a targeted deletion of Ank3 microexon E35a, a neuron type-specific exon that is included in select neuronal populations, including cortical inhibitory interneurons. By removing this exon while preserving broader ankyrin-G function, the model enables researchers to study how specific ANK3 isoform changes affect neuronal excitability, calcium signaling, and brain circuit activity relevant to bipolar disorder and other psychiatric diseases.
Applications:
- Preclinical model for ANK3-linked psychiatric disorder research
- Drug screening model for normalizing neuronal excitability
- Biomarker discovery platform
- Research tool for studying inhibitory interneuron dysfunction, alternative splicing, and calcium signaling
Advantages:
- Models specific ANK3-linked disease mechanisms with greater precision than knockout models
- Preserves broader ankyrin-G neuronal function
- Enables cell type-specific disease analysis
- Provides quantitative electrophysiology and calcium signaling readouts
Lead Inventor:
Related Publications:
Tech Ventures Reference:
IR CU26299
Licensing Contact: Joan Martinez