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Key Documents

MAB3402B

Sigma-Aldrich

Anti-GFAP Antibody, Biotin Conjugate | MAB3402B

from mouse, biotin conjugate

Sinónimos:

Glial fibrillary acidic protein, GFAP

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About This Item

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

biological source

mouse

Quality Level

100

conjugate

biotin conjugate

antibody form

purified antibody

antibody product type

primary antibodies

clone

monoclonal

species reactivity

pig, mouse

species reactivity (predicted by homology)

porcine (based on 100% sequence homology), human (based on 100% sequence homology), chicken (based on 100% sequence homology), rat (based on 100% sequence homology)

technique(s)

immunohistochemistry: suitable

isotype

IgG1

NCBI accession no.

NP_002046

UniProt accession no.

P14136

shipped in

wet ice

target post-translational modification

unmodified

Gene Information

human ... GFAP(2670)

Categorías relacionadas

General description

Glial fibrillary acidic protein is a class-III intermediate filament. GFAP is the main constituent of intermediate filaments in astrocytes and serves as a cell specific marker that distinguishes differentiated astrocytes from other glial cells during the development of the central nervous system.

Immunogen

Purified glial filament protein (Debus, E., et al. (1983) Differentiation. 25:193-203.)

Application

Anti-GFAP Antibody, Biotin Conjugate detects level of GFAP & has been published & validated for use in IH.
Research Category
Neuroscience
Research Sub Category
Developmental Neuroscience

Quality

Evaluated by Immunohistochemistry in mouse adult brain tissue.

Immunohistochemistry Analysis: 1:100 dilution of this antibody detected GFAP in mouse adult brain tissue.

Target description

50 kDa calculated

Physical form

Protein A purified
Purified mouse monoclonal IgG1 conjugated to Biotin in PBS with 0.1% sodium azide and 15 mg/mL BSA.

Storage and Stability

Maintain refrigerated at 2-8 °C protected from light in undiluted aliquots for up to 6 months from date of receipt.

Analysis Note

Control
Mouse adult brain tissue

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

12 - Non 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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Molecular neurodegeneration, 17(1), 13-13 (2022-02-04)
One of the key pathological hallmarks of Alzheimer disease (AD) is the accumulation of the amyloid-β (Aβ) peptide into amyloid plaques. The apolipoprotein E (APOE) gene is the strongest genetic risk factor for late-onset AD and has been shown to
Monica Xiong et al.
Science translational medicine, 13(581) (2021-02-19)
The ε4 allele of the apolipoprotein E (APOE) gene is the strongest genetic risk factor for late-onset Alzheimer's disease (AD) and greatly influences the development of amyloid-β (Aβ) pathology. Our current study investigated the potential therapeutic effects of the anti-human
Chao Wang et al.
Neuron, 109(10), 1657-1674 (2021-04-09)
The apolipoprotein E (APOE) gene is the strongest genetic risk factor for Alzheimer's disease and directly influences tauopathy and tau-mediated neurodegeneration. ApoE4 has strong deleterious effects on both parameters. In the brain, apoE is produced and secreted primarily by astrocytes
Avital Licht-Murava et al.
Science advances, 9(16), eade1282-eade1282 (2023-04-19)
Transactivating response region DNA binding protein 43 (TDP-43) pathology is prevalent in dementia, but the cell type-specific effects of TDP-43 pathology are not clear, and therapeutic strategies to alleviate TDP-43-linked cognitive decline are lacking. We found that patients with Alzheimer's

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