{"id":"CU26299","slug":"ank3-e35-deletion-mouse-model--CU26299","source":{"id":"CU26299","dataset":"techtransfer","title":"Ank3 E35 deletion mouse model for neuronal excitability research","description_":"<p>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.</p>\r\r<h2>Unmet Need: Translational models for ANK3-linked psychiatric disease mechanisms</h2>\r\r<p>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.</p>\r\r<h2>The Technology: ANK3 microexon deletion mouse model for psychiatric disease research</h2>\r\r<p>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.</p>\r\r<h2>Applications:</h2>\r\r<ul>\r<li>Preclinical model for ANK3-linked psychiatric disorder research</li>\r<li>Drug screening model for normalizing neuronal excitability</li>\r<li>Biomarker discovery platform</li>\r<li>Research tool for studying inhibitory interneuron dysfunction, alternative splicing, and calcium signaling</li>\r</ul>\r\r<h2>Advantages:</h2>\r\r<ul>\r<li>Models specific ANK3-linked disease mechanisms with greater precision than knockout models</li>\r<li>Preserves broader ankyrin-G neuronal function</li>\r<li>Enables cell type-specific disease analysis</li>\r<li>Provides quantitative electrophysiology and calcium signaling readouts</li>\r</ul>\r\r<h2>Lead Inventor:</h2>\r\r<p><a href=\"https://systemsbiology.columbia.edu/faculty/chaolin-zhang\">Chaolin Zhang, Ph.D.</a></p>\r\r<h2>Related Publications:</h2>\r\r<ul>\r<li><a href=\"https://www.nature.com/articles/s41467-026-69486-x\">Alam S, Dermentzaki G, Cabrera-Garcia D, Li M, Wang R, Campbell M, et al. “A neuron type-specific microexon in Ank3/ankyrin-G modulates calcium activity and neuronal excitability” Nature Communications. 2026 Apr 6; 17(1): 3173.</a></li>\r</ul>\r\r<h2>Tech Ventures Reference:</h2>\r\r<ul>\r<li><p>IR CU26299</p></li>\r<li><p>Licensing Contact: <a href=\"mailto:techtransfer@columbia.edu\">Joan Martinez</a> </p></li>\r</ul>\r","tags":[],"file_number":"CU26299","collections":[],"meta_description":"Neuron-type Ank3 E35a deletion mouse enables precise study of interneuron excitability, calcium signaling, and psychiatric disease mechanisms.","apriori_judge_output":"{\"scores\":{\"novelty\":4.0,\"potential_impact\":4.0,\"readiness\":3.0,\"scalability\":3.0,\"timeliness\":3.0},\"weighted_score\":3.7,\"risks\":[\"Model specificity may be niche to Ank3 isoforms; translational relevance to humans requires validation\",\"Potential regulatory considerations for animal models in preclinical use\",\"Need for broader validation across neuronal subtypes to ensure generalizability\"],\"one_sentence_take\":\"A technically solid, moderately novel neuronal isoform-focused model with good readiness but limited near-term scalability and translational breadth; cost-effective for mechanism-driven screening but requires broader validation for broad commercial impact.\"}","inventors":["Chaolin Zhang PhD"],"manager":"Joan Martinez","depts":["Systems Biology"],"divs":["Columbia University Medical Center (CUMC)"],"date_released":"2026-05-22"},"highlight":{},"matched_queries":null,"score":0.0}