catalog number :
MBS670159
products full name :
Mouse Anti-Human GFAP-UNLB
products short name :
GFAP
products name syn :
Mouse Anti-Human GFAP - Purified, Unlabeled Antibody; Mouse Anti-Human GFAP
other names :
glial fibrillary acidic protein; Glial fibrillary acidic protein; glial fibrillary acidic protein; glial fibrillary acidic protein
other gene names :
GFAP; GFAP; FLJ45472; GFAP
uniprot entry name :
GFAP_HUMAN
isotype :
Mouse (BALB/c) IgG1, kappa
specificity :
Reacts with human GFAP (~ 50 kDa)1. Glial Fibrillary Acid Protein (GFAP) was discovered by Bignami et al 2 as a major fibrous protein of multiple sclerosis plaques. It was subsequently found to be a member of the 10 nm or intermediate filament protein family, specifically the intermediate filament protein family Class III, which also includes peripherin, desmin and vimentin. GFAP 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.3 Many types of brain tumors, presumably of astrocytic origin, heavily express GFAP. In addition, neural stem cells frequently strongly express GFAP. It is also found in the lens epithelium, Kupffer cells of the liver, in some cells of salivary tumors, and has been reported in erythrocytes. Therefore, antibodies to GFAP are very useful as markers of astrocytic cells and neural stem cells, and for distinguishing neoplasms of astrocytic origin from other neoplasms in the central nervous system. Although its function is not fully understood, GFAP protein is probably involved in controlling the shape and movement of astrocytes. The protein may also play a significant role in the interactions of astrocytes with other cells, which are required for the formation and maintenance of the myelin layer that covers nerve cells. Additionally, GFAP may assist in maintaining the protective blood-brain barrier. In adults, GFAP levels increase as a result of the proliferation of astrocytes that occurs in response to a variety of physical, chemical and etiological insults, including Alzheimer's disease, epilepsy and multiple sclerosis. Alexander's disease was recently shown to be caused by point mutations in the protein-coding region of the GFAP gene.4 All forms of Alexander's disease are characterized by the presence of Rosenthal fibers, which are GFAP-containing cytoplasmic inclusions found in astrocytes.
form :
Purified (UNLB) Antibody
storage stability :
The purified (UNLB) antibody is supplied as 0.5 mg purified immunoglobulin in 1.0 mL of borate buffered saline, pH 8.2; store at 2-8 degree C.
tested application :
ELISA
app notes :
Research Application(s): Enzyme Linked Immunosorbent Assay (ELISA) as a capture antibody. ELISA Suggested Dilution: 1ug
other info1 :
Immunogen: Recombinant human Glial Fibrillary Acid Protein (GFAP)
other info2 :
Characterization: To ensure acceptable performance, each batch of product is tested by ELISA to conform to characteristics of a standard reference reagent.
products description :
First described in 1971, glial fibrillary acid protein (GFAP) is a member of the type III intermediate filament family of proteins. GFAP is heavily 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. It is closely related to its non-epithelial family members, vimentin, desmini and peripherin, which are all involved in the structure and functions of the cell’s cytoskeleton. GFAP is thought to help to maintain astrocyte mechanical strength, as well as the shape of cell; however, its, precise function remains poorly understood. In adults, GFAP levels increase in response to the proliferation of astrocytes associated with Alzheimer’s disease, epilepsy and multiple sclerosis. Antibodies specific for GFAP are useful as markers of astrocytic cells and neural stem cells, as well as for distinguishing neoplasms of astrocytic origin from other neoplasms in the central nervous system.
products references :
1) Lukas, Z. et al. 1989. Expression of vimentin and glial fibrillary acid protein in human developing spinal cord. Histochem. J. 21:693. 3) Brenner, M. et al. 2001. Mutations in GFAP, encoding glial fibrillary acid protein, are associated with Alexander's Disease. Nat. Genet. 7:118-120.
ncbi mol weight :
49,880 Da
ncbi pathways :
Nuclear Signaling By ERBB4 Pathway (530744); Signal Transduction Pathway (477114); Signaling By ERBB4 Pathway (530741)
ncbi summary :
This gene encodes one of the major intermediate filament proteins of mature astrocytes. It is used as a marker to distinguish astrocytes from other glial cells during development. Mutations in this gene cause Alexander disease, a rare disorder of astrocytes in the central nervous system. Alternative splicing results in multiple transcript variants encoding distinct isoforms. [provided by RefSeq]
uniprot summary :
Function: GFAP, a class-III intermediate filament, is a cell-specific marker that, during the development of the central nervous system, distinguishes astrocytes from other glial cells. Subunit structure: Interacts with SYNM. By similarity. Isoform 3 interacts with PSEN1 (via N-terminus). Ref.15. Subcellular location: Cytoplasm. Note: Associated with intermediate filaments. Ref.15. Tissue specificity: Expressed in cells lacking fibronectin. Ref.3. Post-translational modification: Phosphorylated by PKN1. Ref.17. Involvement in disease: Defects in GFAP are a cause of Alexander disease (ALEXD) [. MIM:203450]. Alexander disease is a rare disorder of the central nervous system. It is a progressive leukoencephalopathy whose hallmark is the widespread accumulation of Rosenthal fibers which are cytoplasmic inclusions in astrocytes. The most common form affects infants and young children, and is characterized by progressive failure of central myelination, usually leading to death usually within the first decade. Infants with Alexander disease develop a leukoencephalopathy with macrocephaly, seizures, and psychomotor retardation. Patients with juvenile or adult forms typically experience ataxia, bulbar signs and spasticity, and a more slowly progressive course. Ref.19 Ref.20 Ref.21 Ref.22 Ref.23 Ref.24. Sequence similarities: Belongs to the intermediate filament family.