Tau 2N Antibody: ATTO 594

Tau is a microtubule-associated protein encoded by the MAPT gene, which undergoes complex alternative splicing to produce six isoforms in the adult human brain. These isoforms differ by the presence of zero, one, or two N-terminal inserts (0N, 1N, 2N) and either three (3R) or four (4R) microtubule-binding repeat domains. The 2N isoform, characterized by two N-terminal inserts, exists in both 2N3R and 2N4R variants. These isoforms are involved in modulating tau’s interaction with microtubules and other cellular components. The 3R/4R ratio is tightly regulated in the healthy brain but becomes disrupted in tauopathies. For example, Alzheimer’s disease (AD) exhibits a mixed 3R/4R tau pathology, while other disorders such as Pick’s disease or progressive supranuclear palsy show isoform-specific accumulation. Tau 2N isoforms are of particular interest in neurodegenerative research due to their distinct expression patterns and potential contributions to disease-specific tau aggregation. Tools that selectively detect human 2N isoforms—such as isoform-specific antibodies like StressMarq's Tau 2N Antibody—are valuable for distinguishing pathological tau species and for developing targeted diagnostics and therapeutics. Our human Tau 2N3R/4R polyclonal antibody has demonstrated specificity to human 2N isoforms and does not detect rodent isoforms. Understanding the role of Tau 2N in isoform imbalance and aggregation provides critical insight into the molecular mechanisms driving neurodegeneration.

1. Goedert, M., Spillantini, M. G., Jakes, R., Rutherford, D., & Crowther, R. A. (1989) . Multiple isoforms of human microtubule-associated protein tau: sequences and localization in neurofibrillary tangles of Alzheimer's disease. Neuron, 3 (4), 519–526. DOI: 10.1016/0896-6273 (89) 90210-9 2. Spillantini, M. G., & Goedert, M. (2013) . Tau pathology and neurodegeneration. The Lancet Neurology, 12 (6), 609–622. DOI: 10.1016/S1474-4422 (13) 70090-5 3. Kovacs, G. G. (2017) . Tauopathies. Handbook of Clinical Neurology, 145, 355–368. DOI: 10.1016/B978-0-12-802395-2.00025-3