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MAB3402B

Sigma-Aldrich

Anti-GFAP Antibody, Biotin Conjugate | MAB3402B

from mouse, biotin conjugate

Synonym(e):

Glial fibrillary acidic protein, GFAP

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About This Item

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

Biologische Quelle

mouse

Qualitätsniveau

Konjugat

biotin conjugate

Antikörperform

purified antibody

Antikörper-Produkttyp

primary antibodies

Klon

monoclonal

Speziesreaktivität

pig, mouse

Speziesreaktivität (Voraussage durch Homologie)

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

Methode(n)

immunohistochemistry: suitable

Isotyp

IgG1

NCBI-Hinterlegungsnummer

UniProt-Hinterlegungsnummer

Versandbedingung

wet ice

Posttranslationale Modifikation Target

unmodified

Angaben zum Gen

human ... GFAP(2670)

Allgemeine Beschreibung

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.)

Anwendung

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

Qualität

Evaluated by Immunohistochemistry in mouse adult brain tissue.

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

Zielbeschreibung

50 kDa calculated

Physikalische Form

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

Lagerung und Haltbarkeit

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

Hinweis zur Analyse

Control
Mouse adult brain tissue

Haftungsausschluss

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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Lagerklassenschlüssel

12 - Non Combustible Liquids

WGK

WGK 2

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable


Analysenzertifikate (COA)

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Die Dokumentenbibliothek aufrufen

Guo-Qiang Wang et al.
Journal of neuroscience research, 100(10), 1908-1920 (2022-07-08)
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Thomas E Mahan et al.
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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