Recombinant Anti-Tau antibody [TAU-5] - BSA and Azide free (ab80579)
Key features and details
- Produced recombinantly (animal-free) for high batch-to-batch consistency and long term security of supply
- Mouse monoclonal [TAU-5] to Tau - BSA and Azide free
- Suitable for: WB, ICC/IF
- Reacts with: Mouse, Rat, Human
Overview
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Product name
Anti-Tau antibody [TAU-5] - BSA and Azide free
See all Tau primary antibodies -
Description
Mouse monoclonal [TAU-5] to Tau - BSA and Azide free -
Host species
Mouse -
Specificity
The specificity of this antibody refers to P29172.
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Tested applications
Suitable for: WB, ICC/IFmore details -
Species reactivity
Reacts with: Mouse, Rat, Human -
Immunogen
Full length native protein (purified). This information is proprietary to Abcam and/or its suppliers.
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Epitope
The epitope has been mapped to the Human tau sequence 218-225 (doi:10.1016/j.bbrc.2007.04.187) -
Positive control
- WB: Human, mouse and rat brain tissue lysate. ICC: primary hippocampal rat neurons/glia, DIV14.
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General notes
This product is a recombinant monoclonal antibody, which offers several advantages including:
- - High batch-to-batch consistency and reproducibility
- - Improved sensitivity and specificity
- - Long-term security of supply
- - Animal-free production
Properties
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Form
Liquid -
Storage instructions
Shipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C. Avoid freeze / thaw cycle. -
Storage buffer
Constituent: 100% PBS -
Carrier free
Yes -
Concentration information loading...
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Purity
Protein G purified -
Clonality
Monoclonal -
Clone number
TAU-5 -
Isotype
IgG1 -
Light chain type
kappa -
Research areas
Associated products
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Compatible Secondaries
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Conjugation kits
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Isotype control
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Related Products
Applications
The Abpromise guarantee
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.
Application | Abreviews | Notes |
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WB | (4) |
Use a concentration of 1 µg/ml. Predicted molecular weight: 79 kDa.
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ICC/IF |
Use a concentration of 1 µg/ml.
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Notes |
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WB
Use a concentration of 1 µg/ml. Predicted molecular weight: 79 kDa. |
ICC/IF
Use a concentration of 1 µg/ml. |
Target
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Function
Promotes 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 specificity
Expressed in neurons. Isoform PNS-tau is expressed in the peripheral nervous system while the others are expressed in the central nervous system. -
Involvement in disease
Note=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 similarities
Contains 4 Tau/MAP repeats. -
Developmental stage
Four-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. -
Domain
The tau/MAP repeat binds to tubulin. Type I isoforms contain 3 repeats while type II isoforms contain 4 repeats. -
Post-translational
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 localization
Cytoplasm > 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. - Information by UniProt
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Database links
- Entrez Gene: 4137 Human
- Entrez Gene: 17762 Mouse
- Entrez Gene: 29477 Rat
- Omim: 157140 Human
- SwissProt: P10636 Human
- SwissProt: P10637 Mouse
- SwissProt: P19332 Rat
- Unigene: 101174 Human
see all -
Form
There are 9 isoforms produced by alternative splicing. -
Alternative names
- AI413597 antibody
- AW045860 antibody
- DDPAC antibody
see all
Images
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All lanes : ab80579 at 1 ug/ml and ab181602 at 1/20000 overnight at 4ºC
Lane 1 : Human Brain Tissue Lysate at 40 µg with Milk in TBS-T (0.1% Tween®)
Lane 2 : Mouse Brain Tissue Lysate at 40 µg with Milk in TBS-T (0.1% Tween®)
Lane 3 : Rat Brain Tissue Lysate with Milk in TBS-T (0.1% Tween®)
Blocking peptides at 3 % per lane.
Secondary
All lanes : ab216772 and ab216777, for 1 hour at room temperature at 1/20000 dilution
Predicted band size: 79 kDa
Observed band size: 55 kDa why is the actual band size different from the predicted?
Additional bands at: 37 kDa (possible Loading Control)Green - ab80579.
Red - Loading control.
Binding at expected molecular weights consistent with Tau protein across the various species.
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ab80579 staining Tau in primary hippocampal rat neurons/glia, DIV14. The cells were fixed with 4% paraformaldehyde (10 min), permeabilized with 0.1% PBS-Tween for 5 minutes and then blocked with 1% BSA/10% normal goat serum/0.3M glycine in 0.1%PBS-Tween for 1h. The cells were then incubated overnight at 4°C with ab80579 at 1μg/ml and ab6046, Rabbit polyclonal to beta Tubulin - Loading Control. Cells were then incubated with ab150117, Goat polyclonal Secondary Antibody to Mouse IgG H&L (Alexa Fluor® 488) preadsorbed at 1/1000 dilution (shown in green) and ab150080, Goat polyclonal secondary to Rabbit IgG H&L (Alexa Fluor® 594) at 1/1000 dilution (shown in pseudocolour red). Nuclear DNA was labelled with DAPI (shown in blue). Image was acquired with a high-content analyser (Operetta CLS, Perkin Elmer) and a maximum intensity projection of confocal sections is shown.
Protocols
Datasheets and documents
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Datasheet download
References (131)
ab80579 has been referenced in 131 publications.
- Liang Z et al. Long-Term High-Fat Diet Consumption Induces Cognitive Decline Accompanied by Tau Hyper-Phosphorylation and Microglial Activation in Aging. Nutrients 15:N/A (2023). PubMed: 36615907
- Guo SL et al. Promotion of the Differentiation of Dental Pulp Stem Cells into Oligodendrocytes by Knockdown of Heat Shock Protein 27. Dev Neurosci 44:91-101 (2022). PubMed: 34986480
- Hu T et al. Inhibition of Exosome Release Alleviates Cognitive Impairment After Repetitive Mild Traumatic Brain Injury. Front Cell Neurosci 16:832140 (2022). PubMed: 35153676
- Xie Z et al. Microglial cathepsin E plays a role in neuroinflammation and amyloid β production in Alzheimer's disease. Aging Cell 21:e13565 (2022). PubMed: 35181976
- Yoshida N et al. Relationship between Cognitive Dysfunction and Age-Related Variability in Oxidative Markers in Isolated Mitochondria of Alzheimer's Disease Transgenic Mouse Brains. Biomedicines 10:N/A (2022). PubMed: 35203488