Anti-Tau – Purified

This purified antibody is formulated in 0.01 M phosphate buffered saline (150 mM NaCl) PBS pH 7.4, 1% BSA and 0.09% sodium azide as a preservative.

This purified antibody is stable when stored at 2-8°C. Do not freeze.

Next Day Ambient

Mouse Anti Tau (Clone Tau-2) recognizes the microtubule associated protein τ-Tau. This monoclonal antibody was purified using multi-step affinity chromatography methods such as Protein A or G depending on the species and isotype.

The Tau protein is a critical microtubule-associated protein in neurons, encoded by the MAPT gene. Its normal function is stabilizing neuronal microtubules.

In Alzheimer's disease (AD) and other tauopathies, Tau undergoes abnormal processing, specifically hyperphosphorylation and truncation by proteases like caspases and calpains. This results in the formation of intracellular aggregates known as Neurofibrillary Tangles (NFTs), which are considered a neuropathological hallmark.

Critically, tauopathy correlates strongly with clinical dementia in AD. Key kinases, including MAPK, GSK-3, and Cdk-5, regulate Tau's phosphorylation state. Understanding these modifications, along with other post-translational changes like ubiquitination, is essential for studying Tau toxicity and developing new therapeutic strategies.

Clone-Specific Utility (Tau-2):

The Anti-Tau Monoclonal Antibody (Clone Tau-2) is a crucial tool for comprehensive Tau research. It is known in the literature for its ability to bind to the heterogeneous Tau protein in a phosphatase-independent manner, meaning it detects Tau in both phosphorylated and non-phosphorylated forms.

Raised against bovine MAPs, Tau-2 robustly recognizes the protein across multiple species (Human, Bovine, Monkey) and is commonly used to stain and localize Tau along microtubules in healthy cells, and to detect the filamentous structures comprising NFTs in post-mortem AD brain tissue. This specificity makes it highly effective for applications like IHC FFPE and Western Blotting to analyze total Tau levels and pathology progression.

1. Binder, L. I. et al. (1985) J. Cell Biol. 101:1371 2. Papasozomenos, S. C. et al. (1987) Cell Motility and the Cytoskeleton 8:210 3. Lewis, S. A. et al. (1989) Nature 342:498