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MAB5430

Sigma-Aldrich

Anti-Tau Antibody, Caspase Cleaved (truncated at Asp421)

clone tau-C3, Chemicon®, from mouse

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About This Item

UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41

biological source

mouse

Quality Level

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

tau-C3, monoclonal

species reactivity

human

manufacturer/tradename

Chemicon®

technique(s)

ELISA: suitable
immunohistochemistry: suitable
western blot: suitable

isotype

IgG1

UniProt accession no.

shipped in

wet ice

target post-translational modification

unmodified

Gene Information

human ... MAPT(4137)

Specificity

Reacts with Tau, caspase cleaved (truncated at Asp421). The antibody shows no reactivity with full length tau nor other tau C-terminal truncations. The antibody stains amyloid beta treated neurons and brain tissue in Alzheimer′s disease, more specifically it stains a subset of neurofibrillary tangles, tau-containing neuritic plaques and neuropil threads.

Immunogen

Epitope: Caspase Cleaved (truncated at Asp421)
Peptide corresponding to the C-terminus of tau truncated as aspartic acid 421.

Application

Anti-Tau Antibody, Caspase Cleaved (truncated at Asp421) is an antibody against Tau for use in ELISA, WB, IH.
Research Category
Neuroscience
Research Sub Category
Neurodegenerative Diseases
Western blot

Immunohistochemistry

ELISA

Optimal working dilutions must be determined by end user.

Target description

43 kDa (aa 1 to 421) or smaller fragments with Asp421 as the c-terminus

Physical form

Format: Purified
Purified immunoglobulin. Liquid in PBS. Contains no preservative.

Storage and Stability

Maintain at 2-8°C in undiluted aliquots for up to 6 months after date of receipt.

Other Notes

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

Legal Information

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Storage Class

10 - Combustible liquids

wgk_germany

WGK 2

flash_point_f

Not applicable

flash_point_c

Not applicable


Certificados de análisis (COA)

Busque Certificados de análisis (COA) introduciendo el número de lote del producto. Los números de lote se encuentran en la etiqueta del producto después de las palabras «Lot» o «Batch»

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Patrice Delobel et al.
The American journal of pathology, 172(1), 123-131 (2007-12-15)
Recent evidence has suggested that truncation of tau protein at the caspase cleavage site D421 precedes hyperphosphorylation and may be necessary for the assembly of tau into filaments in Alzheimer's disease and other tauopathies. Here we have investigated the time
Debra K Kumasaka et al.
International journal of physiology, pathophysiology and pharmacology, 1(1), 48-56 (2009-01-12)
A recent study demonstrated the lack of beta-amyloid (Abeta) plaque formation and accumulation of the amyloid precursor protein (APP) in a triple transgenic mouse model of Alzheimer's disease (3xTg-AD) following overexpression of the anti-apoptotic protein, Bcl-2 (Rohn et al., J.
Tau pathogenesis is promoted by A?1-42 but not A?1-40.
Hu, X; Li, X; Zhao, M; Gottesdiener, A; Luo, W; Paul, S
Mol. Neurodegener. null
John C Means et al.
Cellular and molecular neurobiology, 40(6), 911-926 (2020-01-11)
Optic nerve head astrocytes (ONHAs) are the major cell type within the optic nerve head, providing both structural and nutrient support to the optic nerve. Astrocytes are necessary for the survival of neurons with controlled activation of astrocytes being beneficial
John C Means et al.
Neurochemical research, 41(9), 2278-2288 (2016-05-26)
Mouse models of neurodegenerative diseases such as Alzheimer's disease (AD) are important for understanding how pathological signaling cascades change neural circuitry and with time interrupt cognitive function. Here, we introduce a non-genetic preclinical model for aging and show that it

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