产品名称
Anti-GFAP antibody, Rabbit monoclonal, clone SP78, recombinant, expressed in proprietary host, affinity isolated antibody
biological source
rabbit
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
Quality Level
Gene Information
human ... GFAP(2670)
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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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存储类别
10 - Combustible liquids
wgk
WGK 2
flash_point_f
Not applicable
flash_point_c
Not applicable
法规信息
常规特殊物品
低风险生物材料
此项目有
Glial Fibrillary Acidic Protein for Prehospital Diagnosis of Intracerebral Hemorrhage.
Rozanski M, et al.
Cerebrovascular Diseases (Basel, Switzerland), 43(1-2), 76-81 (2017)
Biological roles of glial fibrillary acidic protein as a biomarker in cartilage regenerative medicine.
Kanazawa S, et al.
Journal of Cellular Physiology, 232(11), 3182-3193 (2017)
Protective Effect of Curcumin Against Oxidative Stress-Induced Injury in Rats with Parkinson?s Disease Through the Wnt/β-Catenin Signaling Pathway
Wang Y L, et al.
Cellular Physiology and Biochemistry, 43(6), 2226-2241 (2017)
Peng Wang et al.
Molecular medicine reports, 13(5), 4443-4450 (2016-04-02)
Hypoxia causes injury to the central nervous system during stroke and has significant effects on pH homeostasis. Na+/H+ exchanger isoform 1 (NHE1) is important in the mechanisms of hypoxia and intracellular pH (pHi) homeostasis. As a well-established hypoxia-mimetic agent, CoCl2 stabilizes
QKI6B mRNA levels are upregulated in schizophrenia and predict GFAP expression.
Farnsworth B, et al.
Brain Research, 1669, 63-68 (2017)
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