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Key Documents

SAB5500113

Sigma-Aldrich

Anti-GFAP antibody, Rabbit monoclonal

recombinant, expressed in proprietary host, clone SP78, affinity isolated antibody

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

Quality Level

recombinant

expressed in proprietary host

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

SP78, monoclonal

species reactivity

human (tested)

species reactivity (predicted by homology)

mouse, bovine, dog, rabbit, pig, rat

technique(s)

immunohistochemistry: 1:100

isotype

IgG

UniProt accession no.

shipped in

wet ice

storage temp.

2-8°C

target post-translational modification

unmodified

Gene Information

human ... GFAP(2670)

General description

Glial fibrillary acidic protein (GFAP) is a member of the class III intermediate filament protein family. It is heavily, and specifically, expressed in astrocytes and certain other astroglia in the central nervous system, in satellite cells in peripheral ganglia, and in non myelinating Schwann cells in peripheral nerves. In addition, neural stem cells frequently strongly express GFAP. Antibodies to GFAP are therefore very useful as markers of astrocytic cells. In addition, many types of brain tumors presumably derived from astrocytic cells, heavily express GFAP. GFAP is also found in the lens epithelium, Kupffer cells of the liver, in some cells in salivary tumors and has been reported in erythrocytes. GFAP is particular expressed in auricular chondrocytes.

Immunogen

Synthetic peptide corresponding to C-terminus of human GFAP protein.

Application

Anti-GFAP antibody, Rabbit monoclonal has been used in immunocytochemistry and Immunohistochemistry.

Biochem/physiol Actions

Glial fibrillary acidic protein (GFAP) maintains the structure and motility of astrocytes. Gfap mediates the interaction between neurons and glial cells. It is responsible for the integrity and function of blood-brain barrier. Myelination and brain injury induced astrogliosis is controlled by Gfap. Cytoskeleton disintegration is known to stimulate the release of Gfap. Upregulation of this gene is observed in traumatic brain injury such as intracerebral hemorrhage and thus serves as a biomarker. Mutation in the GFAP gene causes Alexander disease.

Features and Benefits

Evaluate our antibodies with complete peace of mind. If the antibody does not perform in your application, we will issue a full credit or replacement antibody. Learn more.

Physical form

0.1 ml rabbit monoclonal antibody purified by protein A/G in PBS/1% BSA buffer pH 7.6 with less than 0.1% sodium azide.

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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Visite la Librería de documentos

Increases of Plasma Levels of Glial Fibrillary Acidic Protein, Tau, and Amyloid β up to 90 Days after Traumatic Brain Injury.
Tanya B, et al.
Journal of Neurotrauma, 34(1), 66?73-66?73 (2017)
The predominant neural stem cell isolated from postnatal and adult forebrain but not early embryonic forebrain expresses GFAP.
Imura T, et al.
The Journal of Neuroscience, 23(7), 2824-2832 (2003)
Qiang Zhang et al.
The European journal of neuroscience, 46(9), 2507-2518 (2017-09-19)
Injury to the adult central nervous system (CNS) results in the formation of glial scar tissues. Glial scar-induced failure of regenerative axon pathfinding may limit axon regrowth beyond the lesion site and cause incorrect reinnervation and dystrophic appearance of stalled
Time-dependent activity of Na+/H+ exchanger isoform 1 and homeostasis of intracellular pH in astrocytes exposed to CoCl2 treatment.
Wang P, et al.
Molecular Medicine Reports, 13(5), 4443-4450 (2016)
HIV-1 Tat Induces Unfolded Protein Response and Endoplasmic Reticulum Stress in Astrocytes and Causes Neurotoxicity through Glial Fibrillary Acidic Protein (GFAP) Activation and Aggregation.
Yan F and Johnny J H
The Journal of Biological Chemistry, 291(43), 22819- 22829 (2016)

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