Anti-Tau antibody [TAU-5] - BSA and Azide free (ab80579)
- Product nameAnti-Tau antibody [TAU-5] - BSA and Azide freeSee all Tau primary antibodies ...
- DescriptionMouse monoclonal [TAU-5] to Tau - BSA and Azide free
- SpecificityThis antibody reacts with the non-phosphorylated as well as the phosphorylated forms of tau. It intensely stains the human neurofibrillary tangles, neuropil threads, and neuritic plaques associated with Alzheimer’s disease and shows no cross reaction with other MAPs or tubulin.
- Tested applicationsFlow Cyt, WB, IP, ICC/IF more details
- Species reactivityReacts with: Mouse, Rat, Sheep, Cow, Human
Purified bovine microtubule associated proteins.
- EpitopeMiddle of Tau.
- Positive controlIMR5 cells, human T98G glioblastoma cells or Alzheimer’s disease brain tissue.
- Storage instructionsShipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles.
- Storage bufferPreservative: None
Constituents: 10mM PBS, pH 7.4
- Concentration information loading...
- PurityProtein G purified
- Purification notesPurified from the ascites fluid by Protein G chromatography.
- Clonality Monoclonal
- Clone numberTAU-5
Our Abpromise guarantee covers the use of ab80579 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|Flow Cyt||Flow Cyt: Use 1µg for 106 cells.|
|WB||WB: Use a concentration of 1 - 2 µg/ml. Predicted molecular weight: 79 kDa.|
|IP||IP: Use at 2 µg/mg of lysate.|
|ICC/IF||ICC/IF: Use at an assay dependent dilution.|
- FunctionPromotes microtubule assembly and stability, and might be involved in the establishment and maintenance of neuronal polarity. The C-terminus binds axonal microtubules while the N-terminus binds neural plasma membrane components, suggesting that tau functions as a linker protein between both. Axonal polarity is predetermined by tau localization (in the neuronal cell) in the domain of the cell body defined by the centrosome. The short isoforms allow plasticity of the cytoskeleton whereas the longer isoforms may preferentially play a role in its stabilization.
- Tissue specificityExpressed in neurons. Isoform PNS-tau is expressed in the peripheral nervous system while the others are expressed in the central nervous system.
- Involvement in diseaseNote=In Alzheimer disease, the neuronal cytoskeleton in the brain is progressively disrupted and replaced by tangles of paired helical filaments (PHF) and straight filaments, mainly composed of hyperphosphorylated forms of TAU (PHF-TAU or AD P-TAU).
Defects in MAPT are a cause of frontotemporal dementia (FTD) [MIM:600274]; also called frontotemporal dementia (FTD), pallido-ponto-nigral degeneration (PPND) or historically termed Pick complex. This form of frontotemporal dementia is characterized by presenile dementia with behavioral changes, deterioration of cognitive capacities and loss of memory. In some cases, parkinsonian symptoms are prominent. Neuropathological changes include frontotemporal atrophy often associated with atrophy of the basal ganglia, substantia nigra, amygdala. In most cases, protein tau deposits are found in glial cells and/or neurons.
Defects in MAPT are a cause of Pick disease of the brain (PIDB) [MIM:172700]. It is a rare form of dementia pathologically defined by severe atrophy, neuronal loss and gliosis. It is characterized by the occurrence of tau-positive inclusions, swollen neurons (Pick cells) and argentophilic neuronal inclusions known as Pick bodies that disproportionally affect the frontal and temporal cortical regions. Clinical features include aphasia, apraxia, confusion, anomia, memory loss and personality deterioration.
Note=Defects in MAPT are a cause of corticobasal degeneration (CBD). It is marked by extrapyramidal signs and apraxia and can be associated with memory loss. Neuropathologic features may overlap Alzheimer disease, progressive supranuclear palsy, and Parkinson disease.
Defects in MAPT are a cause of progressive supranuclear palsy type 1 (PSNP1) [MIM:601104, 260540]; also abbreviated as PSP and also known as Steele-Richardson-Olszewski syndrome. PSNP1 is characterized by akinetic-rigid syndrome, supranuclear gaze palsy, pyramidal tract dysfunction, pseudobulbar signs and cognitive capacities deterioration. Neurofibrillary tangles and gliosis but no amyloid plaques are found in diseased brains. Most cases appear to be sporadic, with a significant association with a common haplotype including the MAPT gene and the flanking regions. Familial cases show an autosomal dominant pattern of transmission with incomplete penetrance; genetic analysis of a few cases showed the occurrence of tau mutations, including a deletion of Asn-613.
- Sequence similaritiesContains 4 Tau/MAP repeats.
- Developmental stageFour-repeat (type II) tau is expressed in an adult-specific manner and is not found in fetal brain, whereas three-repeat (type I) tau is found in both adult and fetal brain.
- DomainThe tau/MAP repeat binds to tubulin. Type I isoforms contain 3 repeats while type II isoforms contain 4 repeats.
modificationsPhosphorylation at serine and threonine residues in S-P or T-P motifs by proline-directed protein kinases (PDPK: CDK1, CDK5, GSK-3, MAPK) (only 2-3 sites per protein in interphase, seven-fold increase in mitosis, and in PHF-tau), and at serine residues in K-X-G-S motifs by MAP/microtubule affinity-regulating kinase (MARK) in Alzheimer diseased brains. Phosphorylation decreases with age. Phosphorylation within tau's repeat domain or in flanking regions seems to reduce tau's interaction with, respectively, microtubules or plasma membrane components. Phosphorylation on Ser-610, Ser-622, Ser-641 and Ser-673 in several isoforms during mitosis.
Polyubiquitinated. Requires functional TRAF6 and may provoke SQSTM1-dependent degradation by the proteasome (By similarity). PHF-tau can be modified by three different forms of polyubiquitination. 'Lys-48'-linked polyubiquitination is the major form, 'Lys-6'-linked and 'Lys-11'-linked polyubiquitination also occur.
Glycation of PHF-tau, but not normal brain tau. Glycation is a non-enzymatic post-translational modification that involves a covalent linkage between a sugar and an amino group of a protein molecule forming ketoamine. Subsequent oxidation, fragmentation and/or cross-linking of ketoamine leads to the production of advanced glycation endproducts (AGES). Glycation may play a role in stabilizing PHF aggregation leading to tangle formation in AD.
- Cellular localizationCytoplasm > cytosol. Cell membrane. Cytoplasm > cytoskeleton. Cell projection > axon. Mostly found in the axons of neurons, in the cytosol and in association with plasma membrane components.
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Anti-Tau antibody [TAU-5] - BSA and Azide free images
Denatured IP using Human cells:IP 2µg/mg lysate.WB at 2µg/ml.
ICC/IF image of ab80579 stained SKNSH cells. The cells were 100% methanol fixed (5 min) and then incubated in 1%BSA / 10% normal goat serum / 0.3M glycine in 0.1% PBS-Tween for 1h to permeabilise the cells and block non-specific protein-protein interactions. The cells were then incubated with the antibody (ab80579, 10µg/ml) overnight at +4°C. The secondary antibody (green) was ab96879, DyLight® 488 goat anti-mouse IgG (H+L) used at a 1/250 dilution for 1h. Alexa Fluor® 594 WGA was used to label plasma membranes (red) at a 1/200 dilution for 1h. DAPI was used to stain the cell nuclei (blue) at a concentration of 1.43µM.
Overlay histogram showing SH-SY5Y cells stained with ab80579 (red line). The cells were fixed with 80% methanol (5 min) and then permeabilized with 0.1% PBS-Tween for 20 min. The cells were then incubated in 1x PBS / 10% normal goat serum / 0.3M glycine to block non-specific protein-protein interactions followed by the antibody (ab80579, 1µg/1x106 cells) for 30 min at 22ºC. The secondary antibody used was DyLight® 488 goat anti-mouse IgG (H+L) (ab96879) at 1/500 dilution for 30 min at 22ºC. Isotype control antibody (black line) was mouse IgG1 [ICIGG1] (ab91353, 2µg/1x106 cells) used under the same conditions. Acquisition of >5,000 events was performed. This antibody gave a positive signal in SH-SY5Y cells fixed with 4% paraformaldehyde (10 min)/permeabilized with 0.1% PBS-Tween for 20 min used under the same conditions.
References for Anti-Tau antibody [TAU-5] - BSA and Azide free (ab80579)
This product has been referenced in:
- Das V & Miller JH Non-taxoid site microtubule-stabilizing drugs work independently of tau overexpression in mouse N2a neuroblastoma cells. Brain Res 1489:121-32 (2012). WB . Read more (PubMed: 23085090) »
- Yang M et al. Precursor of Brain-derived Neurotrophic Factor (proBDNF) Forms a Complex with Huntingtin-associated Protein-1 (HAP1) and Sortilin That Modulates proBDNF Trafficking, Degradation, and Processing. J Biol Chem 286:16272-84 (2011). ICC/IF ; Mouse . Read more (PubMed: 21357693) »